subject:(Caloric restriction)

Texas A&M University

1. Huang, Pei-San. Effects of Chronic Nicotine Exposure and Lack of High Affinity Nicotinic Receptors on Cortico-Hippocampal Areas in the Aging Mouse Brain.

Degree: PhD, Biomedical Sciences, 2012, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-2012-05-11067

► Nicotine, the major psychoactive ingredient of tobacco smoke, underlies numerous effects by activating neuronal nicotinic acetylcholine receptors. Both in vitro and in vivo studies suggest… (more)

▼ Nicotine, the major psychoactive ingredient of tobacco smoke, underlies numerous effects by activating neuronal nicotinic acetylcholine receptors. Both in vitro and in vivo studies suggest that nicotine is neuroprotective and improves cognitive performance. Epidemiology studies show that smoking is negatively correlated with the incidence of Parkinson's disease and Alzheimer's disease. Postmortem research and neuroimaging studies show that loss of nicotinic binding sites in the brain is the major feature of neurodegenerative diseases related to dementia and cognitive impairment. Caloric restriction, a regimen that extends the lifespan in all mammalian species studied so far including rodents and primates, is a highly regulated response to food deprivation. It is believed that the longevity effect of caloric restriction is mediated by SIRT1, a NAD-dependent deacetylase, and its related genes. Nicotine's effect on body weight could also lead to weight loss by decreasing caloric absorption consumption. The goal of this study was to find the possible correlation between nicotine's effects and the activation of SIRT1 and its related genes. Using beta2-/- mice that lack high affinity beta2 nicotinic acetylcholine receptors (nAChRs), we first demonstrated that beta2* nAChRs do not directly regulate expression of survival genes. However, we found that loss of beta2* nAChRs could result in augmented cellular stress, which indirectly increased expression of SIRT1, Nampt, and Ku70, possibly as an adaptive response to provide protection against neurodegeneration. We also found that loss of endogenous activation of beta2* nAChRs had less effect on synaptic connections but strongly impaired survival of hippocampal GABAergic neurons. To activate beta2* nAChRs in normal mice, we administered nicotine through drinking water. In a short-term exposure study, we determined the dose of nicotine to be used in young adult mice, and found that chronic nicotine treatment was anxiolytic, decreased caloric consumption, increased nAChR binding sites, and most importantly, increased expression of SIRT1 and its related genes. Finally, we compared long-term nicotine treatment with caloric restriction in middle-aged mice to examine their effects to brain aging, and our results indicated that in mice long term caloric restriction and nicotine treatment both tend to improve memory in aging mice, but appear to act through different mechanisms. Advisors/Committee Members: Winzer-Serhan, Ursula H. (advisor), Abbott, Louise C. (advisor), Welsh, C. Jane (committee member), Griffith, William H. (committee member).

Subjects/Keywords: nicotine; neuroprotection; aging; nAChRs; neurodegeneration; caloric restriction

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Huang, P. (2012). Effects of Chronic Nicotine Exposure and Lack of High Affinity Nicotinic Receptors on Cortico-Hippocampal Areas in the Aging Mouse Brain. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2012-05-11067

Chicago Manual of Style (16^th Edition):

Huang, Pei-San. “Effects of Chronic Nicotine Exposure and Lack of High Affinity Nicotinic Receptors on Cortico-Hippocampal Areas in the Aging Mouse Brain.” 2012. Doctoral Dissertation, Texas A&M University. Accessed January 18, 2021. http://hdl.handle.net/1969.1/ETD-TAMU-2012-05-11067.

MLA Handbook (7^th Edition):

Huang, Pei-San. “Effects of Chronic Nicotine Exposure and Lack of High Affinity Nicotinic Receptors on Cortico-Hippocampal Areas in the Aging Mouse Brain.” 2012. Web. 18 Jan 2021.

Vancouver:

Huang P. Effects of Chronic Nicotine Exposure and Lack of High Affinity Nicotinic Receptors on Cortico-Hippocampal Areas in the Aging Mouse Brain. [Internet] [Doctoral dissertation]. Texas A&M University; 2012. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-05-11067.

Council of Science Editors:

Huang P. Effects of Chronic Nicotine Exposure and Lack of High Affinity Nicotinic Receptors on Cortico-Hippocampal Areas in the Aging Mouse Brain. [Doctoral Dissertation]. Texas A&M University; 2012. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-05-11067

University of Minnesota

2. Ploeger, Jonathan. Dietary and Cellular Mechanisms Regulating Hepatocyte Proliferation and Cancer.

Degree: PhD, Nutrition, 2017, University of Minnesota

URL: http://hdl.handle.net/11299/198372

► Obesity is well-documented to promote the development of nonalcoholic fatty liver disease (NAFLD) including its more advanced stages such as non-alcoholic steatohepatitis, cirrhosis and hepatocellular… (more)

▼ Obesity is well-documented to promote the development of nonalcoholic fatty liver disease (NAFLD) including its more advanced stages such as non-alcoholic steatohepatitis, cirrhosis and hepatocellular carcinoma (HCC). While metabolic perturbations describing obesogenic progression from NAFLD to HCC have largely been investigated, our knowledge of the role lipolysis plays in this process is scant. This research project is aimed at understanding the role fasting lipid metabolism plays in pathologic features of carcinogenesis as well as synergistically combining with lifestyle factors to prevent obesity driven progression of NAFLD to HCC. To elucidate these features, we employed two seminal studies. The first study characterized the role of adipose triglyceride lipase (ATGL) in limiting a major cell cycle regulator, cyclin D1, and hepatocellular proliferation both in vitro and in vivo. We show that lipid catabolism via ATGL antagonizes cell proliferation. Additionally, we recapitulate these findings using a partial hepatectomy model to drive hepatocellular proliferation in vivo. In the second study, we conduct a long-term carcinogenesis study that examines the role of dietary fat composition and lifestyle factors that promote fasting lipid metabolism. Animals were calorically restricted (CR) or exposed to regular endurance exercise. Using the hepatic carcinogen diethylnitrosamine (DEN), we show CR prevents hepatic tumor formation independent of dietary fat composition. RNA sequencing of non-transformed liver tissues revealed changes in metabolic pathways and reduced inflammation, cytokine production, stellate cell activation and migration, and genes associated with liver injury and oncogenesis. Taken together, fasting hepatic lipid metabolism plays a significant role in mitigating proliferative effects often associated with overconsumption of calories. Furthermore, lifestyle factors that promote lipolysis in the liver robustly protected mice from developing tumors. Further investigation is warranted to define the molecular mechanisms ATGL plays in limiting hepatic proliferation as well as characterizing the role of ATGL and fasting in hepatic tumorigenesis.

Subjects/Keywords: Caloric Restriction; Cancer; Liver; NAFLD; Obesity; Proliferation

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ploeger, J. (2017). Dietary and Cellular Mechanisms Regulating Hepatocyte Proliferation and Cancer. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/198372

Chicago Manual of Style (16^th Edition):

Ploeger, Jonathan. “Dietary and Cellular Mechanisms Regulating Hepatocyte Proliferation and Cancer.” 2017. Doctoral Dissertation, University of Minnesota. Accessed January 18, 2021. http://hdl.handle.net/11299/198372.

MLA Handbook (7^th Edition):

Ploeger, Jonathan. “Dietary and Cellular Mechanisms Regulating Hepatocyte Proliferation and Cancer.” 2017. Web. 18 Jan 2021.

Vancouver:

Ploeger J. Dietary and Cellular Mechanisms Regulating Hepatocyte Proliferation and Cancer. [Internet] [Doctoral dissertation]. University of Minnesota; 2017. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/11299/198372.

Council of Science Editors:

Ploeger J. Dietary and Cellular Mechanisms Regulating Hepatocyte Proliferation and Cancer. [Doctoral Dissertation]. University of Minnesota; 2017. Available from: http://hdl.handle.net/11299/198372

University of Melbourne

3. Ng Tang Fui, Mark Andrew. Effect of testosterone therapy combined with a very low caloric diet in obese men: a randomised controlled trial.

Degree: 2017, University of Melbourne

URL: http://hdl.handle.net/11343/194799

► Context: Whilst testosterone treatment is indicated for men with classical hypogonadism, there is no consensus as to whether treatment should be given to men with… (more)

▼ Context: Whilst testosterone treatment is indicated for men with classical hypogonadism, there is no consensus as to whether treatment should be given to men with functional hypogonadism due to paucity of high-quality randomised controlled trials (RCT) of long duration. Obesity is commonly associated with low testosterone with approximately one third of adult men in developed countries classified as obese and one third of these men have low testosterone levels. Weight loss through diet and exercise can lead to modest increases in testosterone levels and improve quality of life but whether the addition of testosterone treatment has additional benefits on body composition and constitutional symptoms is unknown. Objective and methods: In this 56-week RCT of 100 obese men with low total testosterone levels subjected to a rigorous weight loss program, we investigated the effect of intramuscular testosterone undecanoate treatment on fat mass, lean mass, body weight, metabolic parameters, constitutional symptoms, adipokines, gut-derived hormonal mediators of appetite, bone mineral density and bone remodelling markers. A pre-specified blinded follow-up study was conducted for a duration of at least one year following the end of the RCT to determine whether any changes in the RCT were maintained following treatment withdrawal. Results: Testosterone treatment led to reductions in total fat mass (mean adjusted difference, MAD, -2.9kg, [ 95% CI -5.7, -0.20], P=0.04) and visceral fat (-2,678mm2 [-5,180, -176], P=0.04) over and above that achieved with dieting. Diet-induced loss of muscle mass was mitigated (MAD 3.4kg [1.3, 5.5], P=0.002) following testosterone treatment. Testosterone treatment improved Aging Males Symptoms (AMS) score (MAD -0.34, [-0.65, -0.02], P=0.04) and international index of erectile function version 5 (IIEF-5) scores (MAD -0.32 [-0.59, -0.05], P=0.025). Testosterone treatment led to a reduction in circulating leptin levels, MAD -3.6ng/ml [-5.3, -1.9], P<0.001. The changes in gut-derived hormonal mediators of appetite following weight loss in men receiving placebo was not modified by the addition of testosterone treatment. There was a reduction in c-telopeptide, MAD -66ng/L [-113, -19], P=0.018 and in procollagen type 1 N propeptide, MAD -5.6ug/L [-10.1, -1.1], P=0.03, but no change in bone mineral density between testosterone and placebo-treated men. The changes in fat mass and lean mass following testosterone treatment in the RCT were not preserved in the follow-up observation period. Twelve months after RCT completion, total testosterone levels were no different in previously testosterone and placebo-treated (P=0.71) men. Conclusions: In this rigorously conducted RCT comprehensively examining testosterone treatment in obese men, the use of testosterone treatment in obese men promoted favourable changes in body composition and improved constitutional symptoms over and above those achieved with diet alone. As the benefits of testosterone treatment are not maintained following treatment…

Subjects/Keywords: testosterone; obesity; caloric restriction; body composition

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ng Tang Fui, M. A. (2017). Effect of testosterone therapy combined with a very low caloric diet in obese men: a randomised controlled trial. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/194799

Chicago Manual of Style (16^th Edition):

Ng Tang Fui, Mark Andrew. “Effect of testosterone therapy combined with a very low caloric diet in obese men: a randomised controlled trial.” 2017. Doctoral Dissertation, University of Melbourne. Accessed January 18, 2021. http://hdl.handle.net/11343/194799.

MLA Handbook (7^th Edition):

Ng Tang Fui, Mark Andrew. “Effect of testosterone therapy combined with a very low caloric diet in obese men: a randomised controlled trial.” 2017. Web. 18 Jan 2021.

Vancouver:

Ng Tang Fui MA. Effect of testosterone therapy combined with a very low caloric diet in obese men: a randomised controlled trial. [Internet] [Doctoral dissertation]. University of Melbourne; 2017. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/11343/194799.

Council of Science Editors:

Ng Tang Fui MA. Effect of testosterone therapy combined with a very low caloric diet in obese men: a randomised controlled trial. [Doctoral Dissertation]. University of Melbourne; 2017. Available from: http://hdl.handle.net/11343/194799

4. Castoldi, Francesca. L'aspirine récapitule les caractéristiques de la restriction calorique : Aspirin recapitulates features of caloric restriction.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2018, Université Paris-Saclay (ComUE)

URL: http://www.theses.fr/2018SACLS440

►

L'autophagie est un processus d'auto-digestion durant lequel les cellule dégradent leurs propres composants afin de maintenir l’homéostasie en conditions basales. L'autophagie est donc nécessaire à… (more)

▼

L'autophagie est un processus d'auto-digestion durant lequel les cellule dégradent leurs propres composants afin de maintenir l’homéostasie en conditions basales. L'autophagie est donc nécessaire à l’échelle de la cellule et de l’organisme car elle joue un rôle dans l’élimination des organites endommagés et des agrégats de protéines potentiellement nocifs et a la capacité de mobiliser les métabolites essentiels des réserves énergétiques en conditions de stressLa détérioration des fonctions cellulaires et au niveau de l’organisme liée à l'âge est associée à une dérégulation des voies de détection des nutriments ainsi qu’à une autophagie déficiente. La réactivation du flux autophagique peut prévenir ou améliorer ces dysfonctionnements métaboliques liés à l'âge. Les composés non toxiques capables de réduire les taux globaux d'acétylation des protéines et d'induire l'autophagie ont été classés dans la catégorie des agents mimétiques de restriction calorique (CRMs, de l’anglais « caloric restriction mimetic »). Nous montrons ici que l'aspirine et son métabolite actif, le salicylate, induisent une autophagie en raison de leur capacité à inhiber l'activité acétyltransférase de EP300. Alors que le salicylate stimule le flux autophagique dans les cellules « Wild Type », il ne permet pas d’augmenter le niveau d'autophagie dans les cellules déficientes en EP300, ni dans les cellules dans lesquelles EP300 endogène a été remplacé par les mutants EP300 résistants au salicylate. En conséquence, l'activité pro-autophagique de l'aspirine et du salicylate sur le nématode Caenorhabditis elegans est perdue lorsque l'expression de l'orthologue EP300 cpb-1 est réduite. Ces résultats permettent de conclure que l'aspirine est un CRM dont le mécanisme est conservé au cours de l’évolution.

Autophagy is a self-digestion process in which cell degrades its own components in order to maintain homeostasis in basal conditions; autophagy is required for the maintenance of cellular and organismal fitness due to its role in eliminating damaged organelles and potentially harmful protein aggregates, as well as its unique capacity to mobilize essential metabolites from complex energy stores in conditions of stress.The age-associated deterioration in cellular and organismal functions associates with dysregulation of nutrient-sensing pathways and disabled autophagy. The reactivation of autophagic flux may prevent or ameliorate age-related metabolic dysfunctions. Non-toxic compounds endowed with the capacity to reduce the overall levels of protein acetylation and to induce autophagy have been categorized as caloric restriction mimetics (CRMs). Here, we show that aspirin or its active metabolite salicylate induce autophagy by virtue of their capacity to inhibit the acetyltransferase activity of EP300. While salicylate readily stimulates autophagic flux in control cells, it fails to further increase autophagy levels in EP300-deficient cells, as well as in cells in which endogenous EP300 has been replaced by salicylate-resistant EP300 mutants. Accordingly,…

Advisors/Committee Members: Kroemer, Guido (thesis director).

Subjects/Keywords: Autophagie; Aspirine; Restriction calorique; Autophagy; Aspirin; Caloric restriction mimetics

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Castoldi, F. (2018). L'aspirine récapitule les caractéristiques de la restriction calorique : Aspirin recapitulates features of caloric restriction. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2018SACLS440

Chicago Manual of Style (16^th Edition):

Castoldi, Francesca. “L'aspirine récapitule les caractéristiques de la restriction calorique : Aspirin recapitulates features of caloric restriction.” 2018. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed January 18, 2021. http://www.theses.fr/2018SACLS440.

MLA Handbook (7^th Edition):

Castoldi, Francesca. “L'aspirine récapitule les caractéristiques de la restriction calorique : Aspirin recapitulates features of caloric restriction.” 2018. Web. 18 Jan 2021.

Vancouver:

Castoldi F. L'aspirine récapitule les caractéristiques de la restriction calorique : Aspirin recapitulates features of caloric restriction. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2018. [cited 2021 Jan 18]. Available from: http://www.theses.fr/2018SACLS440.

Council of Science Editors:

Castoldi F. L'aspirine récapitule les caractéristiques de la restriction calorique : Aspirin recapitulates features of caloric restriction. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2018. Available from: http://www.theses.fr/2018SACLS440

University of Rochester

5. Frattini, Gregory D. (1981 - ). Chapter I: Studies of the catalytic Mukaiyama aldol reactions of trimethylsilyoxyfuran ; Chapter II: The synthesis of a photoaffinity probe for a caloric restriction mimic.

Degree: PhD, 2011, University of Rochester

URL: http://hdl.handle.net/1802/14816

► Chapter I: Studies of the catalytic Mukaiyama aldol reactions of trimethylsilyoxyfuran. The applicability of the Corey-Bakshi-Shibata reagent as an asymmetric catalyst for Mukaiyama type aldol… (more)

Subjects/Keywords: Mukaiyama aldol; CBS; Caloric restriction; Diazarine photoaffinity probe; Catalytic

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Frattini, G. D. (. -. ). (2011). Chapter I: Studies of the catalytic Mukaiyama aldol reactions of trimethylsilyoxyfuran ; Chapter II: The synthesis of a photoaffinity probe for a caloric restriction mimic. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/14816

Chicago Manual of Style (16^th Edition):

Frattini, Gregory D (1981 - ). “Chapter I: Studies of the catalytic Mukaiyama aldol reactions of trimethylsilyoxyfuran ; Chapter II: The synthesis of a photoaffinity probe for a caloric restriction mimic.” 2011. Doctoral Dissertation, University of Rochester. Accessed January 18, 2021. http://hdl.handle.net/1802/14816.

MLA Handbook (7^th Edition):

Frattini, Gregory D (1981 - ). “Chapter I: Studies of the catalytic Mukaiyama aldol reactions of trimethylsilyoxyfuran ; Chapter II: The synthesis of a photoaffinity probe for a caloric restriction mimic.” 2011. Web. 18 Jan 2021.

Vancouver:

Frattini GD(-). Chapter I: Studies of the catalytic Mukaiyama aldol reactions of trimethylsilyoxyfuran ; Chapter II: The synthesis of a photoaffinity probe for a caloric restriction mimic. [Internet] [Doctoral dissertation]. University of Rochester; 2011. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1802/14816.

Council of Science Editors:

Frattini GD(-). Chapter I: Studies of the catalytic Mukaiyama aldol reactions of trimethylsilyoxyfuran ; Chapter II: The synthesis of a photoaffinity probe for a caloric restriction mimic. [Doctoral Dissertation]. University of Rochester; 2011. Available from: http://hdl.handle.net/1802/14816

6. 島内, 誠一郎. Bone structural and metabolic response of caloric restriction in Wistar rats and a GH-IGF-1 axis-suppressed transgenic rat model. : カロリー制限を行ったWistar ratとGH-IGF-1系を抑制したトランスジェニックラットの骨構造および骨代謝の変化についての検討.

Degree: 博士(医学), 2017, Nagasaki University / 長崎大学

URL: http://hdl.handle.net/10069/37825

► The growth hormone–insulin-like growth factor-1 (GH–IGF-1) axis plays an important role in the effects of caloric restriction (CR) on lifespan extension and may elicit effects… (more)

Subjects/Keywords: bone metabolism; caloric restriction; GH-IGF-1 axis; micro CT; aging

10 more images…

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

島内, �. (2017). Bone structural and metabolic response of caloric restriction in Wistar rats and a GH-IGF-1 axis-suppressed transgenic rat model. : カロリー制限を行ったWistar ratとGH-IGF-1系を抑制したトランスジェニックラットの骨構造および骨代謝の変化についての検討. (Thesis). Nagasaki University / 長崎大学. Retrieved from http://hdl.handle.net/10069/37825

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

島内, 誠一郎. “Bone structural and metabolic response of caloric restriction in Wistar rats and a GH-IGF-1 axis-suppressed transgenic rat model. : カロリー制限を行ったWistar ratとGH-IGF-1系を抑制したトランスジェニックラットの骨構造および骨代謝の変化についての検討.” 2017. Thesis, Nagasaki University / 長崎大学. Accessed January 18, 2021. http://hdl.handle.net/10069/37825.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

島内, 誠一郎. “Bone structural and metabolic response of caloric restriction in Wistar rats and a GH-IGF-1 axis-suppressed transgenic rat model. : カロリー制限を行ったWistar ratとGH-IGF-1系を抑制したトランスジェニックラットの骨構造および骨代謝の変化についての検討.” 2017. Web. 18 Jan 2021.

Vancouver:

島内 �. Bone structural and metabolic response of caloric restriction in Wistar rats and a GH-IGF-1 axis-suppressed transgenic rat model. : カロリー制限を行ったWistar ratとGH-IGF-1系を抑制したトランスジェニックラットの骨構造および骨代謝の変化についての検討. [Internet] [Thesis]. Nagasaki University / 長崎大学; 2017. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10069/37825.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

島内 �. Bone structural and metabolic response of caloric restriction in Wistar rats and a GH-IGF-1 axis-suppressed transgenic rat model. : カロリー制限を行ったWistar ratとGH-IGF-1系を抑制したトランスジェニックラットの骨構造および骨代謝の変化についての検討. [Thesis]. Nagasaki University / 長崎大学; 2017. Available from: http://hdl.handle.net/10069/37825

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Universidade Estadual de Campinas

7. Dorighello, Gabriel Gabriel, 1982-. Efeitos da restrição calórica e do 2,4 dinitrofenol sobre o metabolismo e desenvolvimento da aterosclerose em camundongos hipercolesterolêmicos: Effects of caloric restriction and 2,4-dinitrophenol on the metabolism and development of atherosclerosis in hypercholesterolemic mice.

Degree: 2013, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314294

► Abstract: Cardiovascular diseases (CVD) are the major cause of death in the occidental world. Atherosclerosis is the main process responsible for the pathogenesis of these… (more)

▼ Abstract: Cardiovascular diseases (CVD) are the major cause of death in the occidental world. Atherosclerosis is the main process responsible for the pathogenesis of these diseases. Metabolic disturbances such as dyslipidemias, hypertension, insulin resistance and obesity are well established atherosclerosis risk factors. Currently, different pharmacological and dietetic interventions have been used to reduce and avoid CVD. Caloric restriction is one of these strategies, which is associated with increases in life span and reductions of age related chronic diseases. The mitochondrial uncoupler 2,4 dinitrophenol (DNP) has been considered as a caloric restriction mimetic tool. We have demonstrated that a mouse model of human familial hypercholesterolemia exhibits metabolic and redox disturbances highly relevant for metabolic syndrome and atherosclerosis. Thus, the aim of this study was to evaluate the effects of caloric restriction and mild mitochondrial uncoupling induced by DNP on the metabolism and atherosclerosis development in hypercholesterolemic LDL receptor deficient mice (R0). Thus, R0 mice were compared after 3 months in three conditions: R0 fed ad libitum (control), R0 under caloric restriction (R0-RC) obtained by providing food in alternate days, and R0-DNP fed ad libitum and treated with DNP 1 mg/L in the drinking water. The caloric restriction regimen, despite reducing food intake, induced unexpected adverse metabolic effects, namely, increased plasma total-, VLDL- and LDL-cholesterol, and increased visceral and subcutaneous adipose tissue masses. In addition, R0-RC mice became hyperglycemic, hyperinsulinemic, glucose intolerant and insulin resistant. Moreover, R0-RC mice presented elevated plasma levels of the inflammatory markers TNF? and C-reactive protein. Some benefits regarding systemic and tissue redox state were observed in R0-RC, however, atherosclerosis lesion areas were increased about 3 fold in R0-RC mice. DNP treatment had minimal effects on the lipid and glucose metabolism of R0-DNP mice. It decreased plasma free fatty acids, but did not change other plasma lipids, inflammatory markers, glucose homeostasis, and the size of adipose depots. On the other hand, marked effects of DNP treatment on the tissue redox state were observed, namely, reduction in the generation of mitochondrial oxidative reactive species and in the liver content of carbonyl protein. The spontaneous atherosclerosis development was significantly reduced in the R0-DNP mice, independently other well established risk factors such as plasma cholesterol and inflammatory mediators. Therefore, the caloric restriction regimen is not indicated for the condition of familial hypercholesterolemia due to LDL receptor deficiency. On the other hand, DNP treatment, possibly via mild mitochondrial uncoupling, evidences the relevance of mitochondrial source of reactive oxygen for the atherosclerosis development independently of other risk factors Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Oliveira, Helena Coutinho Franco de, 1958- (advisor), Universidade Estadual de Campinas. Instituto de Biologia (institution), Programa de Pós-Graduação em Biologia Funcional e Molecular (nameofprogram), Davel, Ana Paula Couto (committee member), Castilho, Roger Frigério (committee member), Amaral, Maria Esmeria Corezola do (committee member), Quintilho, Eder Carlos Rocha (committee member).

Subjects/Keywords: Hipercolesterolemia; Aterosclerose; Restrição calórica; Diabetes Mellitus; Hypercholesterolemia; Atherosclerosis; Caloric restriction; Diabetes

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dorighello, Gabriel Gabriel, 1. (2013). Efeitos da restrição calórica e do 2,4 dinitrofenol sobre o metabolismo e desenvolvimento da aterosclerose em camundongos hipercolesterolêmicos: Effects of caloric restriction and 2,4-dinitrophenol on the metabolism and development of atherosclerosis in hypercholesterolemic mice. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/314294

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Dorighello, Gabriel Gabriel, 1982-. “Efeitos da restrição calórica e do 2,4 dinitrofenol sobre o metabolismo e desenvolvimento da aterosclerose em camundongos hipercolesterolêmicos: Effects of caloric restriction and 2,4-dinitrophenol on the metabolism and development of atherosclerosis in hypercholesterolemic mice.” 2013. Thesis, Universidade Estadual de Campinas. Accessed January 18, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314294.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Dorighello, Gabriel Gabriel, 1982-. “Efeitos da restrição calórica e do 2,4 dinitrofenol sobre o metabolismo e desenvolvimento da aterosclerose em camundongos hipercolesterolêmicos: Effects of caloric restriction and 2,4-dinitrophenol on the metabolism and development of atherosclerosis in hypercholesterolemic mice.” 2013. Web. 18 Jan 2021.

Vancouver:

Dorighello, Gabriel Gabriel 1. Efeitos da restrição calórica e do 2,4 dinitrofenol sobre o metabolismo e desenvolvimento da aterosclerose em camundongos hipercolesterolêmicos: Effects of caloric restriction and 2,4-dinitrophenol on the metabolism and development of atherosclerosis in hypercholesterolemic mice. [Internet] [Thesis]. Universidade Estadual de Campinas; 2013. [cited 2021 Jan 18]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314294.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Dorighello, Gabriel Gabriel 1. Efeitos da restrição calórica e do 2,4 dinitrofenol sobre o metabolismo e desenvolvimento da aterosclerose em camundongos hipercolesterolêmicos: Effects of caloric restriction and 2,4-dinitrophenol on the metabolism and development of atherosclerosis in hypercholesterolemic mice. [Thesis]. Universidade Estadual de Campinas; 2013. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314294

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

8. Owusu, Priscilla. The role of hepatic kisspeptin as a link between the reproductive axis and metabolic status.

Degree: 2014, Johns Hopkins University

URL: http://jhir.library.jhu.edu/handle/1774.2/37241

► In mammals, the reproductive neuroendocrine axis is a feedback loop system consisting of the hypothalamus, the pituitary, and the gonads. Kisspeptin and its receptor Kiss1R… (more)

Subjects/Keywords: kisspeptin; caloric restriction

…through the following experimental methods: 1) Determined whether caloric restriction… …using fold change = 2ΔΔCT). Effect of caloric restriction on hepatic Kiss1r and ERa mRNA… …expression levels by RT-qPCR as described above. Effect of caloric restriction on serum… …experimental groups. For females, the 24-hour caloric restriction and re-feeding timeframe was set up… …caloric restriction on hepatic Kiss1 and ERα mRNA expression A B b 1.5 8 6 4 a a 0 a 1.0…

7 more images…

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Owusu, P. (2014). The role of hepatic kisspeptin as a link between the reproductive axis and metabolic status. (Thesis). Johns Hopkins University. Retrieved from http://jhir.library.jhu.edu/handle/1774.2/37241

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Owusu, Priscilla. “The role of hepatic kisspeptin as a link between the reproductive axis and metabolic status.” 2014. Thesis, Johns Hopkins University. Accessed January 18, 2021. http://jhir.library.jhu.edu/handle/1774.2/37241.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Owusu, Priscilla. “The role of hepatic kisspeptin as a link between the reproductive axis and metabolic status.” 2014. Web. 18 Jan 2021.

Vancouver:

Owusu P. The role of hepatic kisspeptin as a link between the reproductive axis and metabolic status. [Internet] [Thesis]. Johns Hopkins University; 2014. [cited 2021 Jan 18]. Available from: http://jhir.library.jhu.edu/handle/1774.2/37241.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Owusu P. The role of hepatic kisspeptin as a link between the reproductive axis and metabolic status. [Thesis]. Johns Hopkins University; 2014. Available from: http://jhir.library.jhu.edu/handle/1774.2/37241

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

9. Boilard, Heïdi. Effets d'un déficit calorique sur la compensation énergétique en période post-exercice chez la femme .

Degree: 2016, University of Ottawa

URL: http://hdl.handle.net/10393/34859

► Les études à long-terme confirment que la combinaison d’un déficit calorique et d’un programme d’exercice est une intervention plus profitable quant à la perte de… (more)

▼ Les études à long-terme confirment que la combinaison d’un déficit calorique et d’un programme d’exercice est une intervention plus profitable quant à la perte de poids qu’un régime hypocalorique ou un programme d’exercice seul. Toutefois, la perte de poids moyenne de l’approche combinée est en générale inférieure à celle estimée sur la base du déficit calorique et de la dépense énergétique du programme d’exercice. L’objectif principal de cette étude portait sur l’investigation des effets d’un déficit calorique et de l’exercice sur l’apport calorique, la dépense énergétique totale, la thermogenèse d’origine autre que l’exercice et la compensation alimentaire post-exercice chez les jeunes femmes. Huit jeunes femmes de poids normal et inactives ont participé à quatre conditions expérimentales : contrôle; exercice, où une séance d’exercice à intensité modérée a été réalisée; déficit calorique, où un déficit calorique de 25% pour une période de 3 jours consécutifs a été respecté; et exercice/déficit calorique. À la suite de chaque session, un repas ad libitum à l’heure du dîner a été offert aux participantes et des boîtes à lunch contenant des aliments à volonté choisis par l’entremise de menu ont été remises à ces dernières pour couvrir l’apport calorique pour la journée (jour 1) ainsi que la journée subséquente (jour 2). De plus, un accéléromètre a été remis à chaque participante après chaque séance expérimentale pour être en mesure d’estimer la dépense énergétique liée à l’activité physique pour le jour 1 et jour 2. Aucune différence significative n’a été observée entre les différentes conditions expérimentales pour l’apport calorique au repas ad libitum post-exercice, au jour 1 ainsi qu’au jour 2. De plus, aucune différence significative n’a été notée pour la dépense énergétique totale ainsi que la thermogenèse d’origine autre que l’exercice et aucune compensation alimentaire post-exercice n’a été observée en fonction des conditions expérimentales. Ces résultats suggèrent que la combinaison d’un déficit calorique de 3 journées consécutives avant une séance d’exercice d’intensité modérée n’influence pas l’apport calorique post-exercice, la dépense énergétique totale, la thermogenèse d’origine autre que l’exercice et n’engendre pas de compensation alimentaire post-exercice. Un déficit calorique combiné à l’exercice d’une période plus prolongée pourrait être nécessaire afin d’observer une augmentation de la compensation alimentaire post-exercice pendant une intervention qui vise à induire une perte de poids.

Subjects/Keywords: Caloric restriction; exercise; energy intake; energy expenditure; compensation

15 more images…

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Boilard, H. (2016). Effets d'un déficit calorique sur la compensation énergétique en période post-exercice chez la femme . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/34859

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Boilard, Heïdi. “Effets d'un déficit calorique sur la compensation énergétique en période post-exercice chez la femme .” 2016. Thesis, University of Ottawa. Accessed January 18, 2021. http://hdl.handle.net/10393/34859.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Boilard, Heïdi. “Effets d'un déficit calorique sur la compensation énergétique en période post-exercice chez la femme .” 2016. Web. 18 Jan 2021.

Vancouver:

Boilard H. Effets d'un déficit calorique sur la compensation énergétique en période post-exercice chez la femme . [Internet] [Thesis]. University of Ottawa; 2016. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10393/34859.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Boilard H. Effets d'un déficit calorique sur la compensation énergétique en période post-exercice chez la femme . [Thesis]. University of Ottawa; 2016. Available from: http://hdl.handle.net/10393/34859

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Aberdeen

10. Cameron, Kerry. Regulation of body weight following calorific restriction.

Degree: PhD, 2008, University of Aberdeen

URL: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152784450005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.495026

► The principal aim of this thesis was to investigate the effects of altering the energy density of the diet (kJ/g) on post-restriction weight regain in… (more)

Subjects/Keywords: 571.1; Body weight; Caloric Restriction

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cameron, K. (2008). Regulation of body weight following calorific restriction. (Doctoral Dissertation). University of Aberdeen. Retrieved from https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152784450005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.495026

Chicago Manual of Style (16^th Edition):

Cameron, Kerry. “Regulation of body weight following calorific restriction.” 2008. Doctoral Dissertation, University of Aberdeen. Accessed January 18, 2021. https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152784450005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.495026.

MLA Handbook (7^th Edition):

Cameron, Kerry. “Regulation of body weight following calorific restriction.” 2008. Web. 18 Jan 2021.

Vancouver:

Cameron K. Regulation of body weight following calorific restriction. [Internet] [Doctoral dissertation]. University of Aberdeen; 2008. [cited 2021 Jan 18]. Available from: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152784450005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.495026.

Council of Science Editors:

Cameron K. Regulation of body weight following calorific restriction. [Doctoral Dissertation]. University of Aberdeen; 2008. Available from: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152784450005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.495026

University of Aberdeen

11. Cameron, Kerry. Regulation of body weight following calorific restriction.

Degree: School of Biological Sciences., 2008, University of Aberdeen

URL: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=24710 ; http://digitool.abdn.ac.uk:1801/webclient/DeliveryManager?pid=24710&custom_att_2=simple_viewer

Subjects/Keywords: Body weight; Caloric Restriction.

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cameron, K. (2008). Regulation of body weight following calorific restriction. (Doctoral Dissertation). University of Aberdeen. Retrieved from http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=24710 ; http://digitool.abdn.ac.uk:1801/webclient/DeliveryManager?pid=24710&custom_att_2=simple_viewer

Chicago Manual of Style (16^th Edition):

Cameron, Kerry. “Regulation of body weight following calorific restriction.” 2008. Doctoral Dissertation, University of Aberdeen. Accessed January 18, 2021. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=24710 ; http://digitool.abdn.ac.uk:1801/webclient/DeliveryManager?pid=24710&custom_att_2=simple_viewer.

MLA Handbook (7^th Edition):

Cameron, Kerry. “Regulation of body weight following calorific restriction.” 2008. Web. 18 Jan 2021.

Vancouver:

Cameron K. Regulation of body weight following calorific restriction. [Internet] [Doctoral dissertation]. University of Aberdeen; 2008. [cited 2021 Jan 18]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=24710 ; http://digitool.abdn.ac.uk:1801/webclient/DeliveryManager?pid=24710&custom_att_2=simple_viewer.

Council of Science Editors:

Cameron K. Regulation of body weight following calorific restriction. [Doctoral Dissertation]. University of Aberdeen; 2008. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=24710 ; http://digitool.abdn.ac.uk:1801/webclient/DeliveryManager?pid=24710&custom_att_2=simple_viewer

University of Edinburgh

12. Lovdel, Andrea. Investigating glucocorticoids as mediators of increased bone marrow adiposity and bone loss.

Degree: PhD, 2020, University of Edinburgh

URL: http://hdl.handle.net/1842/36999

► In addition to white and brown adipose tissue (WAT and BAT, respectively), there is a third major adipose depot, called bone marrow adipose tissue (BMAT),… (more)

▼ In addition to white and brown adipose tissue (WAT and BAT, respectively), there is a third major adipose depot, called bone marrow adipose tissue (BMAT), the formation and function of which is poorly understood. In healthy adults, BMAT accounts for up to 70% of bone marrow (BM) volume and further increases during various conditions, such as ageing, osteoporosis, obesity, oestrogen deficiency, glucocorticoid (GC) therapy and, most surprisingly, during caloric restriction (CR) in animals and anorexia nervosa (AN) in humans. Furthermore, such BMAT expansion often coincides with bone loss. However, the mechanisms regulating BMAT expansion in these adverse conditions remain incompletely understood. One possibility is that GCs contribute to BMAT expansion and bone loss during CR and ageing. Long-term GC treatment can induce bone loss and BMAT expansion. One recent study found that CR is associated with elevated circulating GCs in mice, but not in rabbits; the mice also have increased BMAT, whereas the rabbits do not. Furthermore, GCs have been reported to increase during starvation or AN in humans, followed by BMAT expansion. Tissue regeneration of GCs is regulated by 11ß-hydroxysteroid dehydrogenase (11ß-HSD1), which generates active cortisol in humans and corticosterone in rodents, from inactive cortisone and 11-dehydrocorticosterone (11-DHC), respectively. Notably, 11ß-HSD1 KO mice resist the Cushingoid effects of GC excess. Thus, the hypothesis for this thesis is that GC excess contributes to BMAT expansion and bone loss during CR and ageing, and that 11ß-HSD1 KO mice would therefore resist these effects. Herein, I addressed this hypothesis by characterising the BMAT and bone phenotypes of control and 11ß-HSD1 KO mice in response to CR and ageing. To investigate the effects on BMAT and bone remodelling during CR, male and female C57BL/6J mice lacking 11ß-HSD1 (KO) or littermate controls (WT) were fed ad libitum (AL) or 70% of AL intake (CR) from 9-15 weeks of age. Whereas, to investigate the effects of ageing on BMAT and bone remodelling, KO and WT mice of both sexes were characterised at 15, 42 and 70 weeks of age. Following CR, all mice had decreased body mass and increased plasma and BM corticosterone concentrations. Cortical bone loss was present with CR in all mice, and CR significantly increased BMAT in WT males and females, and in KO females. However, KO males resisted CR-induced BMAT expansion. Unexpectedly, the KO males also had significantly increased circulatory and BM progesterone, suggesting that this hormone might be a potential candidate. The aged mice exhibited increased circulating corticosterone and BMAT, and decreased bone mass, compared to young mice. However, unlike during CR, KO males did not resist age-related BMAT expansion, suggesting that the mechanisms for this differ to those responsible for BMAT expansion during CR. Correlation data between BMAT, bone parameters and GCs suggest these factors may be linked, but do not inform cause and effect. Although 11ß-HSD1 may play a role in BMAT…

Subjects/Keywords: bone marrow adipose tissue; BMAT; bone; caloric restriction

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lovdel, A. (2020). Investigating glucocorticoids as mediators of increased bone marrow adiposity and bone loss. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/36999

Chicago Manual of Style (16^th Edition):

Lovdel, Andrea. “Investigating glucocorticoids as mediators of increased bone marrow adiposity and bone loss.” 2020. Doctoral Dissertation, University of Edinburgh. Accessed January 18, 2021. http://hdl.handle.net/1842/36999.

MLA Handbook (7^th Edition):

Lovdel, Andrea. “Investigating glucocorticoids as mediators of increased bone marrow adiposity and bone loss.” 2020. Web. 18 Jan 2021.

Vancouver:

Lovdel A. Investigating glucocorticoids as mediators of increased bone marrow adiposity and bone loss. [Internet] [Doctoral dissertation]. University of Edinburgh; 2020. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1842/36999.

Council of Science Editors:

Lovdel A. Investigating glucocorticoids as mediators of increased bone marrow adiposity and bone loss. [Doctoral Dissertation]. University of Edinburgh; 2020. Available from: http://hdl.handle.net/1842/36999

University of Edinburgh

13. Lovdel, Andrea. Investigating glucocorticoids as mediators of increased bone marrow adiposity and bone loss.

Degree: PhD, 2020, University of Edinburgh

URL: https://doi.org/10.7488/era/300 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.806199

► In addition to white and brown adipose tissue (WAT and BAT, respectively), there is a third major adipose depot, called bone marrow adipose tissue (BMAT),… (more)

▼ In addition to white and brown adipose tissue (WAT and BAT, respectively), there is a third major adipose depot, called bone marrow adipose tissue (BMAT), the formation and function of which is poorly understood. In healthy adults, BMAT accounts for up to 70% of bone marrow (BM) volume and further increases during various conditions, such as ageing, osteoporosis, obesity, oestrogen deficiency, glucocorticoid (GC) therapy and, most surprisingly, during caloric restriction (CR) in animals and anorexia nervosa (AN) in humans. Furthermore, such BMAT expansion often coincides with bone loss. However, the mechanisms regulating BMAT expansion in these adverse conditions remain incompletely understood. One possibility is that GCs contribute to BMAT expansion and bone loss during CR and ageing. Long-term GC treatment can induce bone loss and BMAT expansion. One recent study found that CR is associated with elevated circulating GCs in mice, but not in rabbits; the mice also have increased BMAT, whereas the rabbits do not. Furthermore, GCs have been reported to increase during starvation or AN in humans, followed by BMAT expansion. Tissue regeneration of GCs is regulated by 11ß-hydroxysteroid dehydrogenase (11ß-HSD1), which generates active cortisol in humans and corticosterone in rodents, from inactive cortisone and 11-dehydrocorticosterone (11-DHC), respectively. Notably, 11ß-HSD1 KO mice resist the Cushingoid effects of GC excess. Thus, the hypothesis for this thesis is that GC excess contributes to BMAT expansion and bone loss during CR and ageing, and that 11ß-HSD1 KO mice would therefore resist these effects. Herein, I addressed this hypothesis by characterising the BMAT and bone phenotypes of control and 11ß-HSD1 KO mice in response to CR and ageing. To investigate the effects on BMAT and bone remodelling during CR, male and female C57BL/6J mice lacking 11ß-HSD1 (KO) or littermate controls (WT) were fed ad libitum (AL) or 70% of AL intake (CR) from 9-15 weeks of age. Whereas, to investigate the effects of ageing on BMAT and bone remodelling, KO and WT mice of both sexes were characterised at 15, 42 and 70 weeks of age. Following CR, all mice had decreased body mass and increased plasma and BM corticosterone concentrations. Cortical bone loss was present with CR in all mice, and CR significantly increased BMAT in WT males and females, and in KO females. However, KO males resisted CR-induced BMAT expansion. Unexpectedly, the KO males also had significantly increased circulatory and BM progesterone, suggesting that this hormone might be a potential candidate. The aged mice exhibited increased circulating corticosterone and BMAT, and decreased bone mass, compared to young mice. However, unlike during CR, KO males did not resist age-related BMAT expansion, suggesting that the mechanisms for this differ to those responsible for BMAT expansion during CR. Correlation data between BMAT, bone parameters and GCs suggest these factors may be linked, but do not inform cause and effect. Although 11ß-HSD1 may play a role in BMAT…

Subjects/Keywords: bone marrow adipose tissue; BMAT; bone; caloric restriction

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lovdel, A. (2020). Investigating glucocorticoids as mediators of increased bone marrow adiposity and bone loss. (Doctoral Dissertation). University of Edinburgh. Retrieved from https://doi.org/10.7488/era/300 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.806199

Chicago Manual of Style (16^th Edition):

Lovdel, Andrea. “Investigating glucocorticoids as mediators of increased bone marrow adiposity and bone loss.” 2020. Doctoral Dissertation, University of Edinburgh. Accessed January 18, 2021. https://doi.org/10.7488/era/300 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.806199.

MLA Handbook (7^th Edition):

Lovdel, Andrea. “Investigating glucocorticoids as mediators of increased bone marrow adiposity and bone loss.” 2020. Web. 18 Jan 2021.

Vancouver:

Lovdel A. Investigating glucocorticoids as mediators of increased bone marrow adiposity and bone loss. [Internet] [Doctoral dissertation]. University of Edinburgh; 2020. [cited 2021 Jan 18]. Available from: https://doi.org/10.7488/era/300 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.806199.

Council of Science Editors:

Lovdel A. Investigating glucocorticoids as mediators of increased bone marrow adiposity and bone loss. [Doctoral Dissertation]. University of Edinburgh; 2020. Available from: https://doi.org/10.7488/era/300 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.806199

University of Texas Southwestern Medical Center

14. Zhang, Yuanyuan. From Feast to Famine: A Tale of Satiety and Hunger Hormones.

Degree: 2016, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/7082

►

The general metadata – e.g., title, author, abstract, subject headings, etc. – is publicly available, but access to the submitted files is restricted to UT… (more)

▼

The general metadata – e.g., title, author, abstract, subject headings, etc. – is publicly available, but access to the submitted files is restricted to UT Southwestern campus access and/or authorized UT Southwestern users.

Ghrelin is a peptide hormone secreted mainly from the stomach. It has a unique octanoylation on Ser-3 by Ghrelin-O-Acyltransferase (GOAT). We have previously shown that Goat−/− mice developed severe hypoglycemia under 60% calorie restriction. Liver autophagy has been reported to play a crucial role in maintaining blood glucose during fasting. The present work was carried out to explore whether autophagy plays a role in the onset of hypoglycemia in Goat−/− mice. We observed a deficiency in autophagy in livers of calorie-restricted Goat−/− mice by showing lower expression level of LC3-II, an autophagy marker. This was further demonstrated by showing 10-fold fewer autolysosomes in livers of calorie-restricted Goat−/− mice as compared to the control mice (20 electron microscopic images analyzed for each group). We then went on to show that the deficiency in autophagy in Goat−/− mice can be restored by infusion of growth hormone. It can also be restored by injections of lactate, a gluconeogenic precursor, or octanoate, a fatty acid that spares the usage of glucose. Protein expression of p- STAT 5, a downstream target of growth hormone action, was significantly lower in livers of calorie-restricted Goat−/− mice, and was restored by infusion of growth hormone and by injections of lactate or octanoate. Protein expression levels of LC3-II and p-STAT 5 showed a strong correlation (r2=0.87, p<10-6) through the time course of calorie-restriction. Considered together, these data suggest that the onset of autophagy during calorie restriction is strongly correlated with the ghrelin-growth hormone axis, and that autophagy plays an important role in maintaining blood glucose homeostasis during chronic starvation.

Advisors/Committee Members: Repa, Joyce J., Horton, Jay D., Chen, Zhijian J., Goldstein, Joseph L., Brown, Michael S..

Subjects/Keywords: Autophagy; Blood Glucose; Caloric Restriction; Ghrelin; Hypoglycemia; Liver

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Zhang, Y. (2016). From Feast to Famine: A Tale of Satiety and Hunger Hormones. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/7082

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Zhang, Yuanyuan. “From Feast to Famine: A Tale of Satiety and Hunger Hormones.” 2016. Thesis, University of Texas Southwestern Medical Center. Accessed January 18, 2021. http://hdl.handle.net/2152.5/7082.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Zhang, Yuanyuan. “From Feast to Famine: A Tale of Satiety and Hunger Hormones.” 2016. Web. 18 Jan 2021.

Vancouver:

Zhang Y. From Feast to Famine: A Tale of Satiety and Hunger Hormones. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2016. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/2152.5/7082.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Zhang Y. From Feast to Famine: A Tale of Satiety and Hunger Hormones. [Thesis]. University of Texas Southwestern Medical Center; 2016. Available from: http://hdl.handle.net/2152.5/7082

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Freie Universität Berlin

15. Szela, Anna-Maria. Effects of caloric restriction upon memory performance of older, healthy, obese females.

Degree: 2018, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-4408

► Introduction: Degenerative agerelated processes, including dementia conditions, often cause a negative impact on a human’s memory and are still neither stoppable nor curable. Epidemiological studies… (more)

▼ Introduction: Degenerative agerelated processes, including dementia conditions, often cause a negative impact on a human’s memory and are still neither stoppable nor curable. Epidemiological studies have shown that adiposity in middle age is a modifiable risk factor for dementia. Interventional studies on rodents and primates have reported beneficial effects of caloric restriction on memory and overall health. Although there have been indications of similar effects in humans, supporting evidence is scarce and further investigation is needed to uncover the underlying mechanism of the relationship between decreased adiposity and memory. The aim of this study was to further examine the relationship between caloric restriction and memory performance in older, healthy, obese women. Specifically, the study investigated whether the beneficial effect could be attributed to either having a lower BMI or to the process of losing weight and a catabolic metabolic state. Methods: A randomized interventional study was undertaken with healthy, postmenopausal, obese women (n=42) in order to investigate the link between caloric restriction and memory. The intervention consisted of a twelve-week caloric restriction period leading to a minimal 10% reduction of the participants’ BMI, followed by a four-week period of stable weight management. Neuropsychological tests and medical exams were per- formed at three points: at the beginning (baseline, BL), after the twelve-week caloric restriction period (follow up 1, FU1) and after four weeks of stable weight (follow up 2, FU2). Results: Repeated-measures design ANOVA with post-hoc analysis was able to demonstrate significant improvement of the intervention group in three of four measured memory parameters in comparison to the control group at FU1, as well as an approximation of this performance at the end of the stable weight period (FU2). Discussion: These results sustain the theory of a positive influence of the catabolic metabolic state secondary to caloric restriction on the memory of humans rather than the resulting lower body weight itself. These results open up the possibility of ameliorating the effects of age-induced cognitive decline through repeated short-term caloric- restrictions; a hypothesis that should be investigated in future research. Advisors/Committee Members: w (gender), N.N. (firstReferee), N.N. (furtherReferee).

Subjects/Keywords: caloric restriction; caloric formula; diet cognition; memory diet; obese; overweight; elder; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Szela, A. (2018). Effects of caloric restriction upon memory performance of older, healthy, obese females. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-4408

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Szela, Anna-Maria. “Effects of caloric restriction upon memory performance of older, healthy, obese females.” 2018. Thesis, Freie Universität Berlin. Accessed January 18, 2021. http://dx.doi.org/10.17169/refubium-4408.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Szela, Anna-Maria. “Effects of caloric restriction upon memory performance of older, healthy, obese females.” 2018. Web. 18 Jan 2021.

Vancouver:

Szela A. Effects of caloric restriction upon memory performance of older, healthy, obese females. [Internet] [Thesis]. Freie Universität Berlin; 2018. [cited 2021 Jan 18]. Available from: http://dx.doi.org/10.17169/refubium-4408.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Szela A. Effects of caloric restriction upon memory performance of older, healthy, obese females. [Thesis]. Freie Universität Berlin; 2018. Available from: http://dx.doi.org/10.17169/refubium-4408

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Université de Bordeaux I

16. Georgeon Chartier, Carole. Evaluation des effets du vieillissement sur la signalisation calcique des cellules musculaires lisses des artères cérébrales dans les modèles murins C57BL6/J, SAMR1 et SAMP8 dans des conditions normales et sous restriction calorique : Effect of ageing on calcium signaling in smooth muscle cell in cerebral arteries of C57Bl6/J, SAMR1 and SAMP8 mice under control condition and caloric restriction.

Degree: Docteur es, Neurosciences, 2012, Université de Bordeaux I

URL: http://www.theses.fr/2012BOR14692

►

Au cours du vieillissement, les artères cérébrales subissent des modifications structurelles et fonctionnelles, notamment au niveau des cellules musculaires lisses (CML). La CML a pour… (more)

▼

Au cours du vieillissement, les artères cérébrales subissent des modifications structurelles et fonctionnelles, notamment au niveau des cellules musculaires lisses (CML). La CML a pour rôle de maintenir la réactivité vasculaire via une signalisation calcique qui fait intervenir différents acteurs pouvant ainsi réguler deux phénomènes : la contraction et la relaxation. Ces acteurs rassemblent, au sein d’une même cellule, des canaux (CCVD, RYR, IP3R), des pompes calciques (SERCA, PMCA, NCX, STIM/ORAI) et leurs régulateurs (PLB, FKBP12.6, TRPP2, SARAF, TRIC). La restriction calorique (RC), apparaît comme étant un facteur retardant le vieillissement et ses pathologies. Notre travail s’est donc fortement impliqué dans l’étude de la signalisation calcique de la CML, en se focalisant sur les altérations génomiques et fonctionnelles au cours du vieillissement des artères cérébrales chez la souris C57Bl6/j. Nous avons ainsi pu mettre en évidence une altération de la signalisation calcique qui passe en partie par une modulation des niveaux d’expressions génique et protéique des canaux et pompes calciques impliqués dans ce phénomène, et par une modification fonctionnelle en termes de signaux calciques et de contraction. Après 5 mois de régime RC, il a été mis en évidence un ralentissement des altérations de la signalisation calcique liées au vieillissement et une diminution de l’oxydation des CML.

During aging, cerebral arteries undergo structural and functional changes, particularly in smooth muscle cells (SMC). SMC is responsible for maintaining vascular reactivity via calcium signaling involving different actors and can regulate two phenomena: contraction and relaxation. These actors regroup channels (CCVD, RYR, IP3R) calcium pumps (SERCA, PMCA, NCX, STIM / ORAI) and their regulators (PLB, FKBP12.6, TRPP2, SARAF, TRIC). Caloric restriction (CR) appears as a factor in delaying aging and its pathologies. Our work is strongly involved in the study of calcium signaling in SMC, focusing on genomic and functional alterations during aging of cerebral arteries in mice C57BL6/J. We were able to demonstrate an altered calcium signaling, which is partly through modulation of gene and protein expression levels of calcium channels and pumps involved in this phenomenon, and a functional change in terms of calcium signals and contraction. After 5 months under RC, it was highlighted a slow calcium signaling alterations associated with aging and a decrease of SMC oxidation by SAMP8.

Advisors/Committee Members: Morel, Jean-Luc (thesis director).

Subjects/Keywords: Vieillissement; Artères cérébrales; Calcium; Ip3r; Ryr; Serca; Restriction calorique; Samp8; Aging; Cerebral arteries; Calcium; Ip3r; Ryr; Serca; Caloric restriction; Samp8

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Georgeon Chartier, C. (2012). Evaluation des effets du vieillissement sur la signalisation calcique des cellules musculaires lisses des artères cérébrales dans les modèles murins C57BL6/J, SAMR1 et SAMP8 dans des conditions normales et sous restriction calorique : Effect of ageing on calcium signaling in smooth muscle cell in cerebral arteries of C57Bl6/J, SAMR1 and SAMP8 mice under control condition and caloric restriction. (Doctoral Dissertation). Université de Bordeaux I. Retrieved from http://www.theses.fr/2012BOR14692

Chicago Manual of Style (16^th Edition):

Georgeon Chartier, Carole. “Evaluation des effets du vieillissement sur la signalisation calcique des cellules musculaires lisses des artères cérébrales dans les modèles murins C57BL6/J, SAMR1 et SAMP8 dans des conditions normales et sous restriction calorique : Effect of ageing on calcium signaling in smooth muscle cell in cerebral arteries of C57Bl6/J, SAMR1 and SAMP8 mice under control condition and caloric restriction.” 2012. Doctoral Dissertation, Université de Bordeaux I. Accessed January 18, 2021. http://www.theses.fr/2012BOR14692.

MLA Handbook (7^th Edition):

Georgeon Chartier, Carole. “Evaluation des effets du vieillissement sur la signalisation calcique des cellules musculaires lisses des artères cérébrales dans les modèles murins C57BL6/J, SAMR1 et SAMP8 dans des conditions normales et sous restriction calorique : Effect of ageing on calcium signaling in smooth muscle cell in cerebral arteries of C57Bl6/J, SAMR1 and SAMP8 mice under control condition and caloric restriction.” 2012. Web. 18 Jan 2021.

Vancouver:

Georgeon Chartier C. Evaluation des effets du vieillissement sur la signalisation calcique des cellules musculaires lisses des artères cérébrales dans les modèles murins C57BL6/J, SAMR1 et SAMP8 dans des conditions normales et sous restriction calorique : Effect of ageing on calcium signaling in smooth muscle cell in cerebral arteries of C57Bl6/J, SAMR1 and SAMP8 mice under control condition and caloric restriction. [Internet] [Doctoral dissertation]. Université de Bordeaux I; 2012. [cited 2021 Jan 18]. Available from: http://www.theses.fr/2012BOR14692.

Council of Science Editors:

Georgeon Chartier C. Evaluation des effets du vieillissement sur la signalisation calcique des cellules musculaires lisses des artères cérébrales dans les modèles murins C57BL6/J, SAMR1 et SAMP8 dans des conditions normales et sous restriction calorique : Effect of ageing on calcium signaling in smooth muscle cell in cerebral arteries of C57Bl6/J, SAMR1 and SAMP8 mice under control condition and caloric restriction. [Doctoral Dissertation]. Université de Bordeaux I; 2012. Available from: http://www.theses.fr/2012BOR14692

Université Paris-Sud – Paris XI

17. Pietrocola, Federico. Regulation of Autophagy by Acetyl Coenzime A : From the Mechanisms to a Revised Definition of Caloric Restriction Mimetics : Régulation de l’autophagie par l’Acétyl Coenzyme A : des mécanismes à une nouvelle définition des mimétiques de la restriction calorique.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2015, Université Paris-Sud – Paris XI

URL: http://www.theses.fr/2015PA11T039

►

L’autophagie est un processus d’autodigestion dans lequel la cellule dégrade ses propres composants dans le but de maintenir l’homéostasie dans ses conditions basales. En absence… (more)

▼

L’autophagie est un processus d’autodigestion dans lequel la cellule dégrade ses propres composants dans le but de maintenir l’homéostasie dans ses conditions basales. En absence de nutriments, l’autophagie est activée et favorise la survie cellulaire en fournissant des substrats énergétiques résistant aux conditions de stress. Autophagie et métabolisme communiquent à différents niveaux; une baisse en métabolites richement énergétiques, tels qu’en ATP et en NADH, est détectée par des senseurs cellulaires (AMPK et SIRT1 respectivement) et mène à l’activation de l’autophagie. Ici, nous définissons un niveau supplémentaire de régulation de l’autophagie induite par le jeûne. Dans ce travail, nous montrons que cette privation en nutriments est caractérisée par une diminution rapide de l’Acétyl CoA, intégrateur majeur de l’état nutritionnel au carrefour du catabolisme des graisses, des sucres et des protéines. La baisse en AcCoA s’accompagne de la réduction proportionnelle des niveaux généraux d’acétylation des protéines ainsi que par l’induction de l’autophagie. Les manipulations destinées à augmenter ou diminuer les niveaux cytosoliques d’AcCoA, ciblant soit la synthèse mitochondriale soit son transport dans le cytoplasme, résultent en la suppression ou l’induction de l’autophagie aussi bien dans les cultures cellulaires que dans les tissus de souris. La déplétion en AcCoA impacte directement l’activité des KATs utilisant l’AcCoA comme substrat pour l’acétylation protéique. Nous avont montré que cette baisse en AcCoA réduit spécifiquement l’activité de EP300; cette KAT est en effet nécessaire à la suppression de l’autophagie à des niveaux élevés d’AcCoA, se comportant ainsi comme le senseur des niveaux cytosoliques d’AcCoA. A son tour, EP300 contrôle l’autophagie en inhibant les protéines autophagiques clés. Dans l’ensemble, nos résultats illustrent les fonctions de l’AcCoA cytosolique comme régulateur métabolique central de l’autophagie, délimitant ainsi des stratégies pharmacologiques centrées sur l’AcCoA qui permettent la manipulation thérapeutique de l’autophagie. En effet, la privation en nutriments et la restriction calorique sont connues pour jouer un rôle positif sur la santé et la longévité en promouvant leurs effets. Néanmoins, les stratégies basées sur la restriction calorique sont difficilement applicables en clinique. Ici, nous proposons une nouvelle définition biochimique des Mimétiques de la Restriction Calorique, composés imitant l’effet positif du jeûne. Dans notre contexte, un MRC est un composé capable de réduire l’acétylation protéique par des mécanismes distincts mais convergents: premièrement, par diminution des niveaux d’AcCoA, deuxièmement par inhibition directe des KATs, et enfin, par activation des protéines déacétylases. Ces résultats de l’exécution d’un programme cellulaire conduisent finalement à des effets pro-santé liés à la restriction calorique incluant mais non limités à l’autophagie.

Autophagy is a self-digestion process in which cell degrades its own components in order to maintain…

Advisors/Committee Members: Kroemer, Guido (thesis director).

Subjects/Keywords: Acétylation; Restriction calorique; Café; Macroautophagie; Métabolisme; Polyphénoles; Spermidine; Jeun; Acetylation; Caloric restriction; Coffee; Macroautophagy; Metabolism; Polyphenols; Spermidine; Starvation

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Pietrocola, F. (2015). Regulation of Autophagy by Acetyl Coenzime A : From the Mechanisms to a Revised Definition of Caloric Restriction Mimetics : Régulation de l’autophagie par l’Acétyl Coenzyme A : des mécanismes à une nouvelle définition des mimétiques de la restriction calorique. (Doctoral Dissertation). Université Paris-Sud – Paris XI. Retrieved from http://www.theses.fr/2015PA11T039

Chicago Manual of Style (16^th Edition):

Pietrocola, Federico. “Regulation of Autophagy by Acetyl Coenzime A : From the Mechanisms to a Revised Definition of Caloric Restriction Mimetics : Régulation de l’autophagie par l’Acétyl Coenzyme A : des mécanismes à une nouvelle définition des mimétiques de la restriction calorique.” 2015. Doctoral Dissertation, Université Paris-Sud – Paris XI. Accessed January 18, 2021. http://www.theses.fr/2015PA11T039.

MLA Handbook (7^th Edition):

Pietrocola, Federico. “Regulation of Autophagy by Acetyl Coenzime A : From the Mechanisms to a Revised Definition of Caloric Restriction Mimetics : Régulation de l’autophagie par l’Acétyl Coenzyme A : des mécanismes à une nouvelle définition des mimétiques de la restriction calorique.” 2015. Web. 18 Jan 2021.

Vancouver:

Pietrocola F. Regulation of Autophagy by Acetyl Coenzime A : From the Mechanisms to a Revised Definition of Caloric Restriction Mimetics : Régulation de l’autophagie par l’Acétyl Coenzyme A : des mécanismes à une nouvelle définition des mimétiques de la restriction calorique. [Internet] [Doctoral dissertation]. Université Paris-Sud – Paris XI; 2015. [cited 2021 Jan 18]. Available from: http://www.theses.fr/2015PA11T039.

Council of Science Editors:

Pietrocola F. Regulation of Autophagy by Acetyl Coenzime A : From the Mechanisms to a Revised Definition of Caloric Restriction Mimetics : Régulation de l’autophagie par l’Acétyl Coenzyme A : des mécanismes à une nouvelle définition des mimétiques de la restriction calorique. [Doctoral Dissertation]. Université Paris-Sud – Paris XI; 2015. Available from: http://www.theses.fr/2015PA11T039

Universidade Federal de Mato Grosso do Sul

18. Oliveira, Ana Priscila Cayres de. Influência do exercício físico sobre a via da miostatina e o fenótipo muscular em ratos submetidos a alimentação intermitente .

Degree: 2016, Universidade Federal de Mato Grosso do Sul

URL: http://repositorio.cbc.ufms.br:8080/jspui/handle/123456789/2803

► A alimentação intermitente (AI), alternativa à tradicional restrição calórica (RC), consiste em intervenção dietética envolvendo ciclos de jejum e alimentação. O principal efeito da RC… (more)

▼ A alimentação intermitente (AI), alternativa à tradicional restrição calórica (RC), consiste em intervenção dietética envolvendo ciclos de jejum e alimentação. O principal efeito da RC tradicional sobre a musculatura esquelética é a redução do tamanho da fibra, a qual pode ser atenuada pelo exercício físico. Entretanto, pouco se sabe sobre a influência da AI sobre o fenótipo muscular e os mecanismos moleculares envolvidos. Neste sentido, a miostatina é um fator de crescimento que regula negativamente o crescimento de músculos esqueléticos. O objetivo deste trabalho foi avaliar a influência do exercício físico sobre a via da miostatina e o fenótipo muscular de ratos submetidos a alimentação intermitente. Ratos Wistar machos (n=40) foram distribuídos em 4 grupos: Controle Sedentário (C-S), Alimentação Intermitente Sedentário (AI-S), Controle Exercício Físico (C-EF) e Alimentação Intermitente e Exercício Físico (AI-EF). Os grupos C-S e C-EF receberam ração normocalórica ad libitum diariamente; AI-S e AI-EF receberam a mesma ração, administrada ad libitum em dias alternados com dias de jejum total. Os grupos C-EF e AI-EF foram submetidos a protocolo de exercício em esteira rolante por 90 dias. A expressão proteica de miostatina e de sua antagonista folistatina foi avaliada por Western blot nos músculos sóleo e gastrocnêmio (porção branca). Exercício físico melhorou à tolerância ao esforço, avaliada por teste incremental em esteira. Em relação à musculatura esquelética, a massa do músculo sóleo foi menor no grupo AI-S que no C-S. A massa do músculo gastrocnêmio foi menor nos grupos AI-S e AI-EF em comparação ao C-S e C-EF, respectivamente, porém maior no grupo AI-EF que no AI-S. A área seccional transversa das fibras do músculo gastrocnêmio foi significativamente menor no grupo AI-S quando comparado ao grupo C-S e menor no grupo AI-EF em relação ao C-EF. No músculo sóleo, a área seccional transversa das fibras musculares foi significativamente menor no grupo AI-S quando comparado ao grupo C-S e maior no grupo AI-EF em relação ao AI-S. O fator exercício físico teve influência sobre a expressão proteica de miostatina no músculo gastrocnêmio; adicionalmente, a expressão de miostatina foi significativamente menor no grupo C-EF que no C-S. Não houve diferença significativa para a expressão de miostatina no músculo sóleo e de folistatina em ambos os músculos avaliados. Em conclusão, a alimentação intermitente promove redução da massa dos músculos sóleo e gastrocnêmio em ratos, a qual é prevenida pelo exercício físico em esteira rolante. A via da miostatina, apesar de ser modulada pelo exercício físico, não parece estar envolvida no processo de atrofia muscular associada à alimentação intermitente. Advisors/Committee Members: Martinez, Paula Felippe (advisor).

Subjects/Keywords: Alimentação; Exercícios Físicos; Músculo Esquelético; Miostatina; Restrição Calórica; Feeding; Exercise; Muscle, Skeletal; Myostatin; Caloric Restriction

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Oliveira, A. P. C. d. (2016). Influência do exercício físico sobre a via da miostatina e o fenótipo muscular em ratos submetidos a alimentação intermitente . (Thesis). Universidade Federal de Mato Grosso do Sul. Retrieved from http://repositorio.cbc.ufms.br:8080/jspui/handle/123456789/2803

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Oliveira, Ana Priscila Cayres de. “Influência do exercício físico sobre a via da miostatina e o fenótipo muscular em ratos submetidos a alimentação intermitente .” 2016. Thesis, Universidade Federal de Mato Grosso do Sul. Accessed January 18, 2021. http://repositorio.cbc.ufms.br:8080/jspui/handle/123456789/2803.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Oliveira, Ana Priscila Cayres de. “Influência do exercício físico sobre a via da miostatina e o fenótipo muscular em ratos submetidos a alimentação intermitente .” 2016. Web. 18 Jan 2021.

Vancouver:

Oliveira APCd. Influência do exercício físico sobre a via da miostatina e o fenótipo muscular em ratos submetidos a alimentação intermitente . [Internet] [Thesis]. Universidade Federal de Mato Grosso do Sul; 2016. [cited 2021 Jan 18]. Available from: http://repositorio.cbc.ufms.br:8080/jspui/handle/123456789/2803.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Oliveira APCd. Influência do exercício físico sobre a via da miostatina e o fenótipo muscular em ratos submetidos a alimentação intermitente . [Thesis]. Universidade Federal de Mato Grosso do Sul; 2016. Available from: http://repositorio.cbc.ufms.br:8080/jspui/handle/123456789/2803

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

19. Pedroso, João Alfredo Bolivar. Efeito da restrição calórica sobre marcadores de inflamação, homeostase glicêmica e proteínas envolvidas na sinalização da insulina de ratos destreinados.

Degree: Mestrado, Nutrição Experimental, 2013, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/9/9132/tde-13112013-153819/ ;

►

Diversos estudos demonstram que os benefícios induzidos pelo exercício físico são revertidos após a interrupção do mesmo. Essa interrupção, também conhecida como destreinamento físico, leva… (more)

▼

Diversos estudos demonstram que os benefícios induzidos pelo exercício físico são revertidos após a interrupção do mesmo. Essa interrupção, também conhecida como destreinamento físico, leva ao aumento da massa corporal, ganho de massa adiposa e resistência à insulina. Apesar dessas evidências, pouca atenção é destinada para investigação de estratégias que possam atenuar esse quadro. Portanto, o objetivo deste trabalho foi investigar os efeitos da restrição calórica sobre sensibilidade à insulina e os marcadores de inflamação no tecido adiposo epididimal de ratos destreinados. A amostra foi composta por 32 ratos Sprague-Dawley, machos e adultos. Inicialmente, os animais foram distribuídos em 2 grupos: Controle (CON) e Treinamento (TREIN), animais que foram submetidos ao treinamento em esteira ergométrica durante 8 semanas. Em seguida os animais TREIN foram redistribuídos em três grupos: Um grupo foi constituído por animais que continuaram o programa de treinamento físico (TF) por 6 semanas e mantidos ao acesso de ração ad libitum (TREIN). Os outros dois grupos tiveram o TF interrompido e foram mantidos ao acesso de ração ad libitum (DT) ou a restrição calórica de 30% (DTRC) por 6 semanas. Os animais do grupo CON continuaram o experimento, por mais 6 semanas, sem realizar qualquer tipo de exercício físico. A mensuração da massa corporal e o teste oral de tolerância à glicose foram realizados na oitava e na décima terceira semana de experimento. A partir disso, foi calculado o delta percentual da massa corporal (Δ%MC) e da área sob a curva glicêmica (Δ%ASC). Após 14 semanas de experimento, os animais foram eutanasiados para determinação da composição corporal. Também, foram analisadas proteínas envolvidas na via de sinalização da insulina (PKB), proteínas e adipocinas envolvidas no proceso inflamatório (PKC; IKK-beta; JNK; TNF-α; leptina; adiponectina)O grupo DTRC apresentou valores significativamente menores para Δ%MC ,Δ%ASC e gordura relativa comparado ao DT Além disso, os valores encontrados no grupo DT foram estatisticamente maiores em comparação ao TREIN. Por outro lado, a massa livre de gordura relativa foi estatisticamente menor no grupo DT em contraste aos grupos DTRC e TREIN. Baseados nesses resultados, conclui-se que a restrição calórica foi capaz de atenuar o ganho de peso corporal e massa adiposa, além de evitar a diminuição da sensibilidade à insulina e da massa livre de gordura após 6 semanas de destreinamento físico.

Several studies show that the benefits induced by exercise are reversed after cessation it. This interrupt, also known as physical detraining leads to increased body weight, body mass gain and insulin resistance. Despite this evidence, little attention is directed to investigate strategies to increase this situation. Therefore, the aim of this study was to investigate the effects of calorie restriction on insulin sensitivity and inflammation markers in epididymal adipose tissue of rats untrained. The sample consisted of 32 male Sprague-Dawley male and adult.…

Advisors/Committee Members: Tirapegui, Julio.

Subjects/Keywords: Adipose tissue; Caloric restriction; Destreinamento físico; Physical detraining; Restrição calórica; Tecido adiposo

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Pedroso, J. A. B. (2013). Efeito da restrição calórica sobre marcadores de inflamação, homeostase glicêmica e proteínas envolvidas na sinalização da insulina de ratos destreinados. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/9/9132/tde-13112013-153819/ ;

Chicago Manual of Style (16^th Edition):

Pedroso, João Alfredo Bolivar. “Efeito da restrição calórica sobre marcadores de inflamação, homeostase glicêmica e proteínas envolvidas na sinalização da insulina de ratos destreinados.” 2013. Masters Thesis, University of São Paulo. Accessed January 18, 2021. http://www.teses.usp.br/teses/disponiveis/9/9132/tde-13112013-153819/ ;.

MLA Handbook (7^th Edition):

Pedroso, João Alfredo Bolivar. “Efeito da restrição calórica sobre marcadores de inflamação, homeostase glicêmica e proteínas envolvidas na sinalização da insulina de ratos destreinados.” 2013. Web. 18 Jan 2021.

Vancouver:

Pedroso JAB. Efeito da restrição calórica sobre marcadores de inflamação, homeostase glicêmica e proteínas envolvidas na sinalização da insulina de ratos destreinados. [Internet] [Masters thesis]. University of São Paulo; 2013. [cited 2021 Jan 18]. Available from: http://www.teses.usp.br/teses/disponiveis/9/9132/tde-13112013-153819/ ;.

Council of Science Editors:

Pedroso JAB. Efeito da restrição calórica sobre marcadores de inflamação, homeostase glicêmica e proteínas envolvidas na sinalização da insulina de ratos destreinados. [Masters Thesis]. University of São Paulo; 2013. Available from: http://www.teses.usp.br/teses/disponiveis/9/9132/tde-13112013-153819/ ;

20. Fontinele, Renata Gabriel. Estudo morfoquantitativo e imunohistoquímico da cartilagem articular do joelho de ratos Wistar submetidos à restrição calórica no envelhecimento.

Degree: PhD, Anatomia dos Animais Domésticos e Silvestres, 2012, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/10/10132/tde-01112013-115832/ ;

► A doença degenerativa da cartilagem articular, ou osteoartrose, pode ser causada por diversos fatores, dentre eles o envelhecimento. Com o aumento da longevidade no Brasil,… (more)

▼ A doença degenerativa da cartilagem articular, ou osteoartrose, pode ser causada por diversos fatores, dentre eles o envelhecimento. Com o aumento da longevidade no Brasil, a prevalência da osteoartrose vai aumentar com o aumento progressivo da idade média da população nas próximas décadas. O estresse do dia a dia, com o avanço da vida moderna, são acompanhados pela má alimentação, sendo essa caracterizada por uma subnutrição ou até uma nutrição excessiva. Utilizando ratos Wistar, como modelo experimental, o objetivo deste trabalho é verificar se a alimentação com baixo nível calórico ameniza ou acelera as alterações na estrutura da cartilagem articular das epífises distal do fêmur e proximal da tíbia, causadas pelo envelhecimento. Para tanto foram utilizadas 15 ratos, separados em três grupos, com 5 animais cada: C- animais de 06 meses alimentados com dieta normal (A); SR- animais de 18 meses alimentados dieta normal (A); RC- animais de 18 meses submetidos à restrição calórica de 31% alimentados com dieta B. A avaliação foi realizada pela microscopia de luz em cortes histológicos corados pela Hematoxilina-Eosina, Picrossírius e por imunohistoquímica com marcação do colágeno tipo II. Foram feitas medidas da espessura das zonas da cartilagem articular, contado o número de condrócitos por área, determinados os volumes dos núcleos dos condrócitos, a morfometria do colágeno, a identificação dos tipos de colágeno e a análise imunohistoquímica. Os resultados mostram que os animais do grupo RC ganharam massa corpórea de maneira significativamente mais lenta que os do SR a partir dos 8 meses. Os animais do SR apresentaram na tíbia, aumento da espessura total bicondilar provocado pelo aumento da zona profunda, aumento do número de condrócitos no côndilo lateral, manutenção do volume dos núcleos e da proporção volumétrica de colágeno, marcação mais heterogenea do colágeno tipo II no côndilo lateral, predominância desse tipo de fibras na zona média do côndilo medial. No fêmur os animais do SR mostraram diminuição da espessura total bicondilar provocada pela diminuição da zona profunda, sendo menor no côndilo medial, diminuição do número de condrócitos causado por diminuição da zona profunda, sendo menor no côndilo medial, diminuição do volume total dos núcleos dos condrócitos no côndilo medial, diminuição da proporção volumétrica do colágeno bicondilar, marcação heterogênea do colágeno tipo II, predomínio desse tipo de fibras nas zonas média e profunda bicondilar. Os animais do RC apresentaram na tíbia, manutenção da espessura, aumento do número de condrócitos bicondilar, manutenção do volume nuclear, aumento da densidade de colágeno, marcação menos heterogênea do colágeno tipo II no côndilo lateral, predominância desse tipo de fibras nas zonas média e profunda do côndilo lateral. No fêmur, os animais do RC mostraram aumento da espessura total pelo aumento da zona profunda no côndilo medial, aumento do número de condrócitos pelo aumento da zona profunda, sendo maior no côndilo medial, aumento do volume total dos núcleos dos… Advisors/Committee Members: Kfoury Junior, José Roberto.

Subjects/Keywords: Aging; Articular cartilage; Caloric restriction; Cartilagem articular; Envelhecimento; Osteoarthritis; Osteoartrose; Rat; Ratos; Restrição calórica

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fontinele, R. G. (2012). Estudo morfoquantitativo e imunohistoquímico da cartilagem articular do joelho de ratos Wistar submetidos à restrição calórica no envelhecimento. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/10/10132/tde-01112013-115832/ ;

Chicago Manual of Style (16^th Edition):

Fontinele, Renata Gabriel. “Estudo morfoquantitativo e imunohistoquímico da cartilagem articular do joelho de ratos Wistar submetidos à restrição calórica no envelhecimento.” 2012. Doctoral Dissertation, University of São Paulo. Accessed January 18, 2021. http://www.teses.usp.br/teses/disponiveis/10/10132/tde-01112013-115832/ ;.

MLA Handbook (7^th Edition):

Fontinele, Renata Gabriel. “Estudo morfoquantitativo e imunohistoquímico da cartilagem articular do joelho de ratos Wistar submetidos à restrição calórica no envelhecimento.” 2012. Web. 18 Jan 2021.

Vancouver:

Fontinele RG. Estudo morfoquantitativo e imunohistoquímico da cartilagem articular do joelho de ratos Wistar submetidos à restrição calórica no envelhecimento. [Internet] [Doctoral dissertation]. University of São Paulo; 2012. [cited 2021 Jan 18]. Available from: http://www.teses.usp.br/teses/disponiveis/10/10132/tde-01112013-115832/ ;.

Council of Science Editors:

Fontinele RG. Estudo morfoquantitativo e imunohistoquímico da cartilagem articular do joelho de ratos Wistar submetidos à restrição calórica no envelhecimento. [Doctoral Dissertation]. University of São Paulo; 2012. Available from: http://www.teses.usp.br/teses/disponiveis/10/10132/tde-01112013-115832/ ;

Temple University

21. Butler, Tiffiny A. THE EFFECTS OF POST PUBERTAL FOOD RESTRICTION ON BONE ARCHITECTURE, STRENGTH, AND MEDULLARY ADIPOSE COMPOSITION.

Degree: PhD, 2013, Temple University

URL: http://digital.library.temple.edu/u?/p245801coll10,244901

►

Kinesiology

The purpose of this investigation was to determine the effects of post pubertal caloric restriction on bone architecture, strength, and medullary adipose quantity. A… (more)

▼

Kinesiology

The purpose of this investigation was to determine the effects of post pubertal caloric restriction on bone architecture, strength, and medullary adipose quantity. A randomized control comparison design was utilized and the study was conducted in a laboratory setting. All procedures were approved by the Institutional Animal Care and Use Committee (IACUC) at Temple University (protocol number 3396). Female Sprague Dawley rats (23days-of-age, n=120) were randomly assigned into seven groups, baseline (BL) (n=18), control (C) (n=17), caloric restriction (FR) (n=17), control recovery (RC) (n=17), caloric restriction recovery (RFR) (n=17), control ovariectomy (COVX) (n=17) and food restricted ovariectomy (FROVX) (n=17). On day 65, a 6 week 30% caloric restriction protocol was administered. Following food restriction, a subset of the control and food restricted groups were sacrificed (n=34) and the remaining animals (n=68) control recovery (RC) and food restricted recovery (RFR) groups had a 10 week recovery with ad lib food. Recovery groups, RC and RFR: were sacrificed after the 10 week recovery period at 183 days of age (n=34). The remaining animals were ovariectomized (OVX) and grouped into control ovariectomy (COVX) and food restricted ovariectomy (FROVX). Six weeks post OVX the animals were sacrificed at 270 days of age. After sacrifice blood was taken by cardiac puncture, bones were harvested, cleaned of soft tissue, fixed and prepared for analysis. Anthropometric measurements were taken including retroperitineal and gonadal fat pad weights as well as adrenal glands, ovaries, uteri, and tricep surae muscle group weights. Main Outcome Measures: The outcome variables for this study were bone mechanical competence, trabecular and cortical bone mass and architecture, marrow adipocyte number as well as serum markers of bone formation and resorption. Insulin - like growth factor - 1 (IGF-1) and C- terminal telopeptide (CTX) was measured to determine bone formation and resorption. Statistical Analysis: One-way Analysis of Variance (ANOVA) was performed to determine differences between all groups. Tukey's honestly significant difference (HSD) post hoc analysis was conducted to determine differences between groups. Student's t - tests were used to detect differences between age groups (acute, recovery, post-OVX) A p value was set at less than or equal to 0.05 for all statistical tests. All statistical analysis was performed using (GraphPad Prism version 5.00 for Windows, GraphPad Software, San Diego California USA). Variables were normalized with a linear regression-based correction using body weight. All variables with an R2 level greater than 0 were normalized to avoid choosing an arbitrary R2 value as a cut-off for normalization. Results: Body weight was 18% lower than control animals following caloric restriction. Weight loss was due to fat mass predominately; muscle mass was maintained relative to body weight. Bone length and growth rates were diminished however no differences were found following…

Advisors/Committee Members: Yingling, Vanessa;, Barbe, Mary F., Shapses, Sue, Park, Joon Young, Ph. D..

Subjects/Keywords: Kinesiology; Biomechanics;

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Butler, T. A. (2013). THE EFFECTS OF POST PUBERTAL FOOD RESTRICTION ON BONE ARCHITECTURE, STRENGTH, AND MEDULLARY ADIPOSE COMPOSITION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,244901

Chicago Manual of Style (16^th Edition):

Butler, Tiffiny A. “THE EFFECTS OF POST PUBERTAL FOOD RESTRICTION ON BONE ARCHITECTURE, STRENGTH, AND MEDULLARY ADIPOSE COMPOSITION.” 2013. Doctoral Dissertation, Temple University. Accessed January 18, 2021. http://digital.library.temple.edu/u?/p245801coll10,244901.

MLA Handbook (7^th Edition):

Butler, Tiffiny A. “THE EFFECTS OF POST PUBERTAL FOOD RESTRICTION ON BONE ARCHITECTURE, STRENGTH, AND MEDULLARY ADIPOSE COMPOSITION.” 2013. Web. 18 Jan 2021.

Vancouver:

Butler TA. THE EFFECTS OF POST PUBERTAL FOOD RESTRICTION ON BONE ARCHITECTURE, STRENGTH, AND MEDULLARY ADIPOSE COMPOSITION. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2021 Jan 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,244901.

Council of Science Editors:

Butler TA. THE EFFECTS OF POST PUBERTAL FOOD RESTRICTION ON BONE ARCHITECTURE, STRENGTH, AND MEDULLARY ADIPOSE COMPOSITION. [Doctoral Dissertation]. Temple University; 2013. Available from: http://digital.library.temple.edu/u?/p245801coll10,244901

22. Hanzén, Sarah. Proteostasis and Aging in Saccharomyces cerevisiae - The role of a Peroxiredoxin.

Degree: 2017, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/52316

► Aging is characterized by a progressive decline in physiological functions that limits biological processes, increases the risk of disease, and ultimately leads to death. At… (more)

▼ Aging is characterized by a progressive decline in physiological functions that limits biological processes, increases the risk of disease, and ultimately leads to death. At the cellular level, aging is associated with accumulation of damaged components, including proteins, indicating that protein homeostasis (or proteostasis) fails to maintain the integrity and functionality of the proteome as cells age. Reduced caloric intake elevates proteostasis, counteracts the accumulation of damage during cellular aging, and prolongs lifespan in organisms ranging from yeast to primates. Caloric restriction is intimately linked to reduced signaling through nutrient sensing pathways, including the Target-Of-Rapamycin (TOR) and Protein Kinase A (PKA) pathways but which downstream targets of these nutrient-signaling pathways are most important for lifespan control is not known. In this thesis, using the yeast Saccharomyces cerevisiae as a model organism, I found that the peroxiredoxin Tsa1, which belongs to a family of peroxide scavengers, is a downstream target of the PKA pathway and acts as a major modulator of aging. I found that Tsa1 is required for the resistance to hydrogen peroxide and lifespan extension induced by caloric restriction. Further, I traced the beneficial role of Tsa1 in longevity assurance to its involvement in proteostasis; an involvement linked to the hyperoxidized chaperone-like form of Tsa1. This function of Tsa1 in proteostasis entails recruitment of other molecular chaperones to misfolded and damaged proteins under hydrogen peroxide stress and in aged cells, as well as assistance in the clearance of protein aggregates. Our findings suggest that the cell utilizes distinct strategies for managing protein aggregates under different stress conditions, as Tsa1 is important for the management of protein aggregates under hydrogen peroxide stress but not upon elevated temperatures. The data also point to hydrogen peroxide and reduced proteasomal-dependent degradation as contributing factors for the accumulation of protein aggregates in aged cells.

Subjects/Keywords: Aging; Caloric restriction; Oxidative stress; Peroxiredoxins; Proteostasis; Protein aggregates; Ubiquitin-proteasome system

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hanzén, S. (2017). Proteostasis and Aging in Saccharomyces cerevisiae - The role of a Peroxiredoxin. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/52316

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hanzén, Sarah. “Proteostasis and Aging in Saccharomyces cerevisiae - The role of a Peroxiredoxin.” 2017. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed January 18, 2021. http://hdl.handle.net/2077/52316.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hanzén, Sarah. “Proteostasis and Aging in Saccharomyces cerevisiae - The role of a Peroxiredoxin.” 2017. Web. 18 Jan 2021.

Vancouver:

Hanzén S. Proteostasis and Aging in Saccharomyces cerevisiae - The role of a Peroxiredoxin. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2017. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/2077/52316.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hanzén S. Proteostasis and Aging in Saccharomyces cerevisiae - The role of a Peroxiredoxin. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2017. Available from: http://hdl.handle.net/2077/52316

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Southern California

23. Yin, Fei. The mitochondrial energy – redox axis in aging and caloric restriction: role of nicotinamide nucleotide transhydrogenase.

Degree: PhD, Pharmaceutical Sciences, 2013, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/14579/rec/6996

► The mitochondrial energy-transducing capacity is essential for the maintenance of neuronal function: impairment of energy metabolism and redox homeostasis –integrated in the mitochondrial energy-redox axis–… (more)

▼ The mitochondrial energy-transducing capacity is essential for the maintenance of neuronal function: impairment of energy metabolism and redox homeostasis –integrated in the mitochondrial energy-redox axis– is a hallmark of brain aging and is accentuated in the early stages of neurodegenerative diseases. The energy component of the axis entails the formation of reducing equivalents (NADH) and their flow through the respiratory chain with consequent electron leak to generate O₂.⁻ and H₂O₂. The redox component of the axis entails the removal of H₂O₂ by NADPH-dependent, thiol-based systems. Mitochondrial NADPH generation is largely dependent on nicotinamide nucleotide transhydrogenase (NNT) that catalyzes the reduction of NADP⁺ to NADPH utilizing the proton gradient as the driving force and NADH as the electron donor, thereby linking the energy- and redox components of the axis. ❧ The hypothesis to be tested is that NNT activity is critical for the maintenance of the mitochondrial energy-redox axis and is compromised during aging leading to mitochondrial dysfunction and loss of cellular redox homeostasis. This hypothesis was tested by three specific aims that encompassed three different experimental models. ❧ I have shown that NNT dysfunction impairs cellular redox homeostasis and energy metabolism in PC12 cells. Knockdown of NNT results in decreased cellular NADPH supply, increased H₂O₂ levels, and increased redox potential. Altered redox status further leads to the impairment of mitochondrial bioenergetic function through the activation of redox-sensitive c-Jun N-terminal kinase (JNK) signaling and concomitant inhibition of pyruvate dehydrogenase. Active JNK also initiates mitochondrion-dependent intrinsic apoptosis after NNT suppression. ❧ The role of NNT in linking the mitochondrial energy status to the redox environment was further investigated in brain and liver of C57BL/6J mice –essentially NNT knockout mice– that show impaired glucose tolerance independent of obesity. The results showed that NNT regulates mitochondrial NADPH levels in an energy-sensitive manner in both tissues but with the NADP pool in the liver more affected. In primary hepatocytes of C57BL/6J mice, loss of NNT also leads to impaired mitochondrial energy-transducing capacity, a process related by the co-regulation of redox-sensitive signaling pathways. The diminished impact of NNT in brain was ascribed to the upregulation of another mitochondrial NADPH-generating enzyme, isocitrate dehydrogenase-2. ❧ The functional changes of the mitochondrial energy-redox axis in brain were further characterized in an aging model and the effects of short-term caloric restriction (CR) were assessed. It was shown that the substrate supply (pyruvate and ketone bodies) and mitochondrial energy-transducing capacity are enhanced in 26 month-old rats following short-term CR; likewise, short-term CR increases the expression and activity of mitochondrial redox systems which is associated with a more reduced redox environment in old animals. Short-term CR also rescued… Advisors/Committee Members: Cadenas, Enrique (Committee Chair), Alkana, Ronald L. (Committee Member), Davies, Kelvin J. A. (Committee Member).

Subjects/Keywords: brain aging; mitochondria; nicotinamide nucleotide transhydrogenase; caloric restriction; energy metabolism; redox signaling; hydrogen peroxide

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Yin, F. (2013). The mitochondrial energy – redox axis in aging and caloric restriction: role of nicotinamide nucleotide transhydrogenase. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/14579/rec/6996

Chicago Manual of Style (16^th Edition):

Yin, Fei. “The mitochondrial energy – redox axis in aging and caloric restriction: role of nicotinamide nucleotide transhydrogenase.” 2013. Doctoral Dissertation, University of Southern California. Accessed January 18, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/14579/rec/6996.

MLA Handbook (7^th Edition):

Yin, Fei. “The mitochondrial energy – redox axis in aging and caloric restriction: role of nicotinamide nucleotide transhydrogenase.” 2013. Web. 18 Jan 2021.

Vancouver:

Yin F. The mitochondrial energy – redox axis in aging and caloric restriction: role of nicotinamide nucleotide transhydrogenase. [Internet] [Doctoral dissertation]. University of Southern California; 2013. [cited 2021 Jan 18]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/14579/rec/6996.

Council of Science Editors:

Yin F. The mitochondrial energy – redox axis in aging and caloric restriction: role of nicotinamide nucleotide transhydrogenase. [Doctoral Dissertation]. University of Southern California; 2013. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/14579/rec/6996

University of Southern California

24. Hu, Jia. Studies of Sir2 and caloric restriction mimetic pathways in aging.

Degree: PhD, Molecular Biology, 2013, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/221121/rec/6170

► Increased dosage of Sir2, a conserved histone deacetylase, extends replicative life span in yeast, and possibly worms, and flies and protects mammals against certain diseases.… (more)

▼ Increased dosage of Sir2, a conserved histone deacetylase, extends replicative life span in yeast, and possibly worms, and flies and protects mammals against certain diseases. Previous work in our lab has shown that it is the lack of Sir2 and not its overexpression that promotes resistance to different stresses and extends chronological lifespan when combined with calorie restriction (CR) and/or mutations in the Tor/Sch9 or Ras pathways in yeast. To identify genes and pathways that mimic the effects of CR on aging and cellular protection we explored the role of Sir2 in regulating stress response and examined the genetic interaction between Sir2 and stress resistance transcription factors, Msn2/4 and Gis1. Our results suggest that Msn2/4 and Gis1 are required for the enhanced stress resistance of sir2Δ mutant and the further extension of chronological lifespan of sir2Δ mutant under caloric restriction. In agreement with this result, the serine/theronine kinase Rim15, a positive regulator of Msn2/4 and Gis1, was implicated in Sir2 mediated cellular sensitization to stress. We also examined the role of Sir2 in genomic stability during chronological aging and proposed a potential mechanism for its action. Further study of Sir2 implicated its involvement in regulating Ras2 expression. These studies shed light on the investigation of Sir2's function in higher eukaryotes. ❧ The Sir2 homolog SIRT1 deacetylase, one of the best-characterized sirtuins in mammals, has been shown to mediate some of the beneficial effects of calorie restriction (CR). However, its role in CR-dependent lifespan extension still remains unknown and highly controversial. We previously found that mice lacking both copies of SIRT1 displayed a shorter median lifespan than wild type mice on an ad libitum or a caloric resitriction diet. Here we demonstrated that the median lifespan of SIRT1+/- heterozygote mice in CR was identical to that observed in wild type mice but a higher frequency of pathologies was displayed in SIRT1+/- mice. Microarray gene expression analysis further revealed the possible relations between SIRT1 and CR. Our results suggest that some SIRT1 expression but not its high expression is required for the beneficial effect of CR in longevity and health. ❧ In mammals, several days of food deprivation lead to the accumulation of ketone bodies including acetoacetic acid in the blood. Here we show that as external glucose becomes depleted, S. cerevisiae convert leucine to the ketone body-like acetic acid, analogously to the conversion of leucine to acetoacetate in fasting mammals. Acetic acid promoted the activation of pro-aging pathways similarly to glucose and ethanol. Whereas wild type and ras2 mutant cells accumulated acetic acid, tor1 and sch9 mutants depleted it rapidly by a mechanism that required acetate CoA-transferase and that was essential for lifespan extension. In sch9mutants acetic acid was partly depleted by a mechanism that required oxidative phosphorylation and was utilized to promote the stress resistance carbon source… Advisors/Committee Members: Longo, Valter D. (Committee Chair), Tower, John G. (Committee Member), Zhang, Chao (Committee Member).

Subjects/Keywords: Sir2; stress resistance; genomic instability; SIRT1; caloric restriction; acetic ccid; ketone bodies

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hu, J. (2013). Studies of Sir2 and caloric restriction mimetic pathways in aging. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/221121/rec/6170

Chicago Manual of Style (16^th Edition):

Hu, Jia. “Studies of Sir2 and caloric restriction mimetic pathways in aging.” 2013. Doctoral Dissertation, University of Southern California. Accessed January 18, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/221121/rec/6170.

MLA Handbook (7^th Edition):

Hu, Jia. “Studies of Sir2 and caloric restriction mimetic pathways in aging.” 2013. Web. 18 Jan 2021.

Vancouver:

Hu J. Studies of Sir2 and caloric restriction mimetic pathways in aging. [Internet] [Doctoral dissertation]. University of Southern California; 2013. [cited 2021 Jan 18]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/221121/rec/6170.

Council of Science Editors:

Hu J. Studies of Sir2 and caloric restriction mimetic pathways in aging. [Doctoral Dissertation]. University of Southern California; 2013. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/221121/rec/6170

25. Paulino, Ellena Christina. Efeito do treinamento físico e da restrição alimentar na função cardíaca e resistência à insulina em ratos obesos.

Degree: PhD, Cardiologia, 2009, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5131/tde-08032010-154558/ ;

► INTRODUÇÃO: A obesidade está associada com alterações na função cardíaca e no metabolismo hepático de gordura. Por outro lado, o treinamento físico e a restrição… (more)

▼ INTRODUÇÃO: A obesidade está associada com alterações na função cardíaca e no metabolismo hepático de gordura. Por outro lado, o treinamento físico e a restrição alimentar são conhecidos por reverter às alterações metabólicas decorrentes da obesidade e melhorar o prognóstico em pacientes obesos. No entanto, se estas intervenções melhoram a função cardíaca e os seus mecanismos moleculares associados ao transiente de Ca2+ e a concentração hepática de gordura ainda são pouco conhecidos. Os objetivos deste estudo foram avaliar os efeitos do treinamento físico e da restrição alimentar: 1) na função cardíaca e no perfil molecular das proteínas responsáveis pelo transiente de Ca2+em ratos obesos; 2) na esteatose em ratos obesos. Além disso, se essas duas intervenções associadas tinham um efeito sinérgico nessas respostas. MÉTODOS: Ratos Wistar machos foram alimentados com dieta normocalórica ou dieta hipercalórica durante 25 semanas. Após este período, os ratos com dieta de cafeteria foram randomizados em 4 grupos e acompanhados por 10 semanas: 1) dieta hipercalórica (GO); 2) dieta hipercalórica e treinamento físico (60 % do VO2pico, GOTF); 3) restrição alimentar (-20% da ingestão diária, GORA); 4) treinamento físico e restrição alimentar (GOTFRA). Os ratos do grupo controle continuaram recebendo a dieta normocalórica (GM). O controle hepático glicêmico foi determinado pelo índice HOMA-IR (avaliação do modelo de homeostasia), a esteatose pela concentração hepática de triglicérides, a função cardíaca foi determinada pela ecocardiografia, Modo M e Doppler tecidual e a expressão das proteínas responsáveis pelo transiente de Ca2+ por Western blotting. RESULTADOS: Os ratos do GO apresentaram maior peso corporal, índice de adiposidade, HOMA-IR, concentração de glicose, leptina, adrenalina e noradrenalina e menor fração de encurtamento (39±1 vs 44±1%, P<0,05), fosforilação do receptor de rianodina (P-RyR-Ser2808/RyR , 52±7 vs 100±16%, P<0,01) e da fosfolambam (PPLB- Tre17/PLB, 76±6 vs 100±6%, P<0,05), concentração de nitrato e razão glutationa reduzida e oxidada quando comparados com os ratos do GM. Treinamento físico, restrição alimentar e a associação das dua intervenções diminuiram o índice de adiposidade, a concentração de leptina, adrenalina e noradrenalina e aumentaram a fração de encurtamento (41±1, 42±1 e 43±1%, respectivamente), a fosforilação do receptor de rianodina (80±9, 79±7 e 66±12 %, respectivamente) a da fosfolambam (107±9, 109±4 e 122±11 %, respectivamente), concentração de nitrato e razão glutationa reduzida e oxidada. Apenas o treinamento físico aumentou o consumo de oxigênio de pico. As intervenções envolvendo a restrição alimentar diminuíram o peso corporal e o conteúdo de triglicerídeo hepático (GORA= -52 e GORATF= - 63%). Nenhuma das intervenções normalizou o HOMA-IR e a concentração de glicose. CONCLUSÕES: A perda de peso por treinamento físico ou restrição alimentar por 10 semanas previne a alteração na função sistólica do ventrículo esquerdo relacionada ao perfil molecular das proteínas responsáveis pelo… Advisors/Committee Members: Negrão, Carlos Eduardo.

Subjects/Keywords: Caloric restriction; Cardiac function; Exercício; Exercise; Fatty liver; Fígado gorduroso; Função cardíaca; Obesidade; Obesity; Restrição calórica

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Paulino, E. C. (2009). Efeito do treinamento físico e da restrição alimentar na função cardíaca e resistência à insulina em ratos obesos. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5131/tde-08032010-154558/ ;

Chicago Manual of Style (16^th Edition):

Paulino, Ellena Christina. “Efeito do treinamento físico e da restrição alimentar na função cardíaca e resistência à insulina em ratos obesos.” 2009. Doctoral Dissertation, University of São Paulo. Accessed January 18, 2021. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-08032010-154558/ ;.

MLA Handbook (7^th Edition):

Paulino, Ellena Christina. “Efeito do treinamento físico e da restrição alimentar na função cardíaca e resistência à insulina em ratos obesos.” 2009. Web. 18 Jan 2021.

Vancouver:

Paulino EC. Efeito do treinamento físico e da restrição alimentar na função cardíaca e resistência à insulina em ratos obesos. [Internet] [Doctoral dissertation]. University of São Paulo; 2009. [cited 2021 Jan 18]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5131/tde-08032010-154558/ ;.

Council of Science Editors:

Paulino EC. Efeito do treinamento físico e da restrição alimentar na função cardíaca e resistência à insulina em ratos obesos. [Doctoral Dissertation]. University of São Paulo; 2009. Available from: http://www.teses.usp.br/teses/disponiveis/5/5131/tde-08032010-154558/ ;

26. Cerqueira, Fernanda Menezes. Efeitos da restrição calórica nas vias de sinalização por insulina e óxido nítrico: implicações para biogênese, morfologia e função mitocondriais.

Degree: PhD, Bioquímica, 2012, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/46/46131/tde-24022013-151501/ ;

► A restrição calórica (RC) estende a expectativa de vida de muitos organismos por mecanismos ainda em estudo. Entre os vários efeitos fisiológicos da RC encontra-se… (more)

▼ A restrição calórica (RC) estende a expectativa de vida de muitos organismos por mecanismos ainda em estudo. Entre os vários efeitos fisiológicos da RC encontra-se o aumento na biogênese mitocondrial, dependente de óxido nítrico (NO•), sintetizado pela enzima óxido nítrico sintase endotelial (eNOS). Um dos indutores fisiológicos mais potentes da eNOS é a insulina, cujos níveis plasmáticos são consideravelmente reduzidos nos organismos em RC. O objetivo deste trabalho foi investigar os mecanismos associados ao aumento da sinalização por NO• durante a RC in vivo e in vitro, e as conseqüências celulares do aumento de massa mitocondrial no que diz respeito à longevidade e capacidade respiratória celulares. Submetemos camundongos Swiss fêmeas à RC de 40% e observamos um considerável aumento tecido-específico na fosforilação basal de Akt e eNOS em músculo esquelético, tecido adiposo visceral e cérebro, os quais também apresentaram maior massa mitocondrial. A associação entre a sinalização por insulina, NO• e biogênese mitocondrial foi adicionalmente confirmada em um grupo de camundongos tratados com o desacoplador mitocondrial dinitrofenol (DNP), que também reduz a insulinemia e aumenta a longevidade em camundongos. Para o estudo mecanístico deste fenômeno, usamos soros de ratos Sprague-Dawley submetidos à RC de 40% ou alimentados ad libitum (AL) em cultura celular de células vasculares da musculatura lisa (VSMC), reproduzindo um protocolo descrito para RC in vitro. O uso do soro RC aumentou a fosforilação do receptor de insulina e Akt, a expressão de eNOS e nNOS (forma neural da NOS) e a fosforilação de eNOS, o que se refletiu em maior liberação de nitrito (NO2) no meio de cultura. Inibindo-se a Akt, todos os efeitos promovidos pela RC na sinalização por NO• foram revertidos. Ao se imunoprecipitar do soro a adiponectina, citocina conhecida por aumentar a sensibilidade à insulina, aumentada durante a RC, os efeitos do soro RC na via de sinalização de insulina foram abolidos e, conseqüentemente, os efeitos na sinalização por •NO foram prevenidos. Neurônios de células granulosas de cerebelo, que não expressam eNOS, apenas nNOS, foram cultivados com os soros AL ou RC, e também apresentaram considerável aumento na sinalização por •NO. Estas alterações induziram a biogênese mitocondrial e capacidade respiratória, e foram associadas à maior longevidade celular. Os mesmos efeitos mitocondriais foram observados em células secretoras de insulina, INS1, entretanto a secreção de insulina em resposta à glicose tornou-se inibida, por um mecanismo desconhecido, porém associado a reduzidos níveis intracelulares de espécies oxidantes, moléculas-chave para a secreção de insulina; e à alteração da morfologia mitocondrial, provavelmente devido à maior expressão de mitofusina-2 (Mfn-2). Ao se nocautear a Mfn-2, houve um aumento na geração de EROs e as células em RC passaram a secretar insulina a níveis comparáveis aos das células controle. Concluímos que durante a RC a maior sensibilidade à insulina… Advisors/Committee Members: Kowaltowski, Alicia Juliana.

Subjects/Keywords: Adiponectin; Adiponectina; Biogênese mitocondrial; Caloric restriction; Insulin signaling; Mitochondrial biogenesis; Mitofusin; Mitofusina; Nitric oxide; Óxido nítrico; Restrição calórica; Sinalização por insulina

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cerqueira, F. M. (2012). Efeitos da restrição calórica nas vias de sinalização por insulina e óxido nítrico: implicações para biogênese, morfologia e função mitocondriais. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/46/46131/tde-24022013-151501/ ;

Chicago Manual of Style (16^th Edition):

Cerqueira, Fernanda Menezes. “Efeitos da restrição calórica nas vias de sinalização por insulina e óxido nítrico: implicações para biogênese, morfologia e função mitocondriais.” 2012. Doctoral Dissertation, University of São Paulo. Accessed January 18, 2021. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-24022013-151501/ ;.

MLA Handbook (7^th Edition):

Cerqueira, Fernanda Menezes. “Efeitos da restrição calórica nas vias de sinalização por insulina e óxido nítrico: implicações para biogênese, morfologia e função mitocondriais.” 2012. Web. 18 Jan 2021.

Vancouver:

Cerqueira FM. Efeitos da restrição calórica nas vias de sinalização por insulina e óxido nítrico: implicações para biogênese, morfologia e função mitocondriais. [Internet] [Doctoral dissertation]. University of São Paulo; 2012. [cited 2021 Jan 18]. Available from: http://www.teses.usp.br/teses/disponiveis/46/46131/tde-24022013-151501/ ;.

Council of Science Editors:

Cerqueira FM. Efeitos da restrição calórica nas vias de sinalização por insulina e óxido nítrico: implicações para biogênese, morfologia e função mitocondriais. [Doctoral Dissertation]. University of São Paulo; 2012. Available from: http://www.teses.usp.br/teses/disponiveis/46/46131/tde-24022013-151501/ ;

27. Mari, Renata de Britto. Efeitos da alimentação com diferentes níveis calóricos nos neurônios mioentéricos do cólon de ratos Wistar durante o processo de envelhecimento.

Degree: PhD, Anatomia dos Animais Domésticos e Silvestres, 2009, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/10/10132/tde-10082010-160611/ ;

►

Os últimos anos se caracterizaram pelo aumento significativo da população idosa mundial. Por esta razão, a preocupação com o idoso está se tornando uma constante… (more)

▼

Os últimos anos se caracterizaram pelo aumento significativo da população idosa mundial. Por esta razão, a preocupação com o idoso está se tornando uma constante em nossa sociedade, uma vez que o envelhecimento resulta em comprometimento das funções fisiológicas, acompanhado ou não de alterações estruturais. No trato gastrointestinal (TGI), o processo de envelhecimento pode provocar alterações morfofuncionais significativas. A regulação da motilidade do TGI é controlada principalmente pelos neurônios mioentéricos do sistema nervoso entérico. A diminuição na densidade destes neurônios no cólon pode levar à redução na frequência e na amplitude da contração colônica manifestada como constipação. As ações que visam diminuir os efeitos do envelhecimento no TGI incluem aquelas relacionadas à dieta alimentar, entre as quais se destaca a restrição calórica. A restrição calórica, além de apresentar efeito protetor nos neurônios mioentéricos durante o envelhecimento, também é responsável pela diminuição da morte neuronal por apoptose, processo este acentuado com o envelhecimento. Assim sendo, este trabalho teve por objetivo avaliar os efeitos de diferentes níveis de restrição calórica sobre a plasticidade dos neurônios mioentéricos NADPH e acetilcolinesterase positivos do cólon de ratos Wistar durante o processo de envelhecimento por meio das análises ultraestrutural (microscopia eletrônica de transmissão) e morfoquantitativa. Para tanto foram utilizados 40 ratos machos (Rattus norvegicus), da linhagem Wistar, distribuídos em quatro grupos (n= 10/grupo): CI- animais de seis meses; SR- animais de 18 meses alimentados com dieta normal; RCI- animais de 18 meses alimentados com dieta com 12% de restrição calórica; RCII- animais de 18 meses submetidos à restrição calórica de 30%. Aos seis meses de idade, os animais foram transferidos para o biotério setorial, onde permaneceram até aos 18 meses sob condições ambientais controladas de temperatura e de iluminação e água ad libitum. Foi possível observar que a RC em nível de 30% minimizou de forma eficaz os efeitos deletérios do envelhecimento nos neurônios mioentéricos, podendo ser adotada como alternativa contra os distúrbios gastrointestinais comuns em indivíduos idosos.

The last years were characterized by a significant increase in the elderly population. For this reason, concern for the elderly is becoming a constant in our society, since the aging results in impairment of bodily function, or not accompanied by structural changes. In the gastrointestinal tract (GI), the aging process can cause significant morphological changes. The regulation of motility of the gut is controlled mainly by myenteric neurons of the enteric nervous system. The decrease in the density of neurons in the colon can lead to a reduction in the frequency and amplitude of contraction expressed as colonic constipation. The actions aimed at reducing the effects of aging on the GI system include those related to diet, among which stands out caloric restriction. Caloric restriction, and have a protective…

Advisors/Committee Members: Souza, Romeu Rodrigues de.

Subjects/Keywords: Aging; Caloric restriction; Envelhecimento; Intestine; Intestino grosso; Myenteric plexus; Neuronal plasticity; Plasticidade neuronal; Plexo mioentérico; Restrição calórica

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mari, R. d. B. (2009). Efeitos da alimentação com diferentes níveis calóricos nos neurônios mioentéricos do cólon de ratos Wistar durante o processo de envelhecimento. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/10/10132/tde-10082010-160611/ ;

Chicago Manual of Style (16^th Edition):

Mari, Renata de Britto. “Efeitos da alimentação com diferentes níveis calóricos nos neurônios mioentéricos do cólon de ratos Wistar durante o processo de envelhecimento.” 2009. Doctoral Dissertation, University of São Paulo. Accessed January 18, 2021. http://www.teses.usp.br/teses/disponiveis/10/10132/tde-10082010-160611/ ;.

MLA Handbook (7^th Edition):

Mari, Renata de Britto. “Efeitos da alimentação com diferentes níveis calóricos nos neurônios mioentéricos do cólon de ratos Wistar durante o processo de envelhecimento.” 2009. Web. 18 Jan 2021.

Vancouver:

Mari RdB. Efeitos da alimentação com diferentes níveis calóricos nos neurônios mioentéricos do cólon de ratos Wistar durante o processo de envelhecimento. [Internet] [Doctoral dissertation]. University of São Paulo; 2009. [cited 2021 Jan 18]. Available from: http://www.teses.usp.br/teses/disponiveis/10/10132/tde-10082010-160611/ ;.

Council of Science Editors:

Mari RdB. Efeitos da alimentação com diferentes níveis calóricos nos neurônios mioentéricos do cólon de ratos Wistar durante o processo de envelhecimento. [Doctoral Dissertation]. University of São Paulo; 2009. Available from: http://www.teses.usp.br/teses/disponiveis/10/10132/tde-10082010-160611/ ;

Penn State University

28. Matzko, Michelle Elizabeth. Ghrelin as a Metabolic Regulator During Caloric Restriction .

Degree: 2010, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/11474

► The actions of caloric restriction (CR) on lifespan are long-known and well-described. Many mechanisms for this relationship have been postulated and studied, however none has… (more)

Subjects/Keywords: ghrelin; single nucleotide polymorphism; gastric bypass surgery; caloric restriction

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Matzko, M. E. (2010). Ghrelin as a Metabolic Regulator During Caloric Restriction . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/11474

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Matzko, Michelle Elizabeth. “Ghrelin as a Metabolic Regulator During Caloric Restriction .” 2010. Thesis, Penn State University. Accessed January 18, 2021. https://submit-etda.libraries.psu.edu/catalog/11474.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Matzko, Michelle Elizabeth. “Ghrelin as a Metabolic Regulator During Caloric Restriction .” 2010. Web. 18 Jan 2021.

Vancouver:

Matzko ME. Ghrelin as a Metabolic Regulator During Caloric Restriction . [Internet] [Thesis]. Penn State University; 2010. [cited 2021 Jan 18]. Available from: https://submit-etda.libraries.psu.edu/catalog/11474.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Matzko ME. Ghrelin as a Metabolic Regulator During Caloric Restriction . [Thesis]. Penn State University; 2010. Available from: https://submit-etda.libraries.psu.edu/catalog/11474

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Freie Universität Berlin

29. Hermannstädter, Henrike. Effects of caloric restriction on cognitive function.

Degree: 2013, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-13428

► Background: Because of growing numbers of dementia and the lack of curative therapeutic options, there is the need for preventive measures against loss of cognitive… (more)

▼ Background: Because of growing numbers of dementia and the lack of curative therapeutic options, there is the need for preventive measures against loss of cognitive function. In animal studies, 30-50% caloric restriction (CR) was associated with improvements in cognitive tests. The underlying mechanisms could be associated with glucose-/insulin- as well as inflammatory metabolism. Methods: In a prospective clinical study we tested the influence of caloric restriction on cognitive function in healthy elderly subjects. The subjects were 50-80 years old; their BMI was 24-31. For the duration of six months the goal was to reduce the caloric intake of the subjects in the CR-Group by 30% and not to chance the caloric intake of the subjects in the control group. Neuropsychological testing included the VLMT for verbal episodic memory, Trail making Test B and Stroop for executive function and digit span backwards for working memory. The neuropsychological testing was carried out along with a clinical exam, blood work, bio impedance analysis and questionnaires at the beginning and at the end of the six month study duration. Statistical analysis was carried in an intention-to-treat approach comparing the CR-group with the control group. Unfortunately the CR group did not lose significantly more weight than the control group. Therefore, in an exploratory approach, the subjects were newly classified into one “weight loss” group and one “weight gain” group and all statistical analyses were additionally carried out for this classification. Results: The results show that weight gain in associated with improvements in verbal memory. There was a correlation between weight loss and improvement in consolidation (p=0,034). These improvements were associated with favorable changes in glucose metabolism (p=0,008). Also executive function was positively influenced by CR and weight loss. In group comparisons the CR group improved significantly in the Stroop test (p=0,017), while the “weight loss” group improved significantly in the Trail making test B. Those changes coincided with favorable changes in inflammatory markers. In the area of working memory statistical trends can be seen: the “weight loss” group tends to improve when compared to the “weight gain” group and both glucose-/insulin- as well as inflammatory markers show potential associations with these improvements. Conclusion: The results indicate that a moderate weight loss in healthy, elderly patients might be a cost effective and low- risk preventive strategy against cognitive decline. Moderate weight loss could play a more significant role as a preventive measure against dementia in medical guidelines. As these conclusions were drawn from an exploratory approach, more studies should be performed to validate the results. Advisors/Committee Members: w (gender), Prof. Dr. med. A. Flöel (firstReferee), Prof. Dr. med. M. Nitsche (furtherReferee), Prof. Dr. med. A. Pfeiffer (furtherReferee).

Subjects/Keywords: caloric restriction; cognition; diet; memory; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit::610 Medizin und Gesundheit

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hermannstädter, H. (2013). Effects of caloric restriction on cognitive function. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-13428

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hermannstädter, Henrike. “Effects of caloric restriction on cognitive function.” 2013. Thesis, Freie Universität Berlin. Accessed January 18, 2021. http://dx.doi.org/10.17169/refubium-13428.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hermannstädter, Henrike. “Effects of caloric restriction on cognitive function.” 2013. Web. 18 Jan 2021.

Vancouver:

Hermannstädter H. Effects of caloric restriction on cognitive function. [Internet] [Thesis]. Freie Universität Berlin; 2013. [cited 2021 Jan 18]. Available from: http://dx.doi.org/10.17169/refubium-13428.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hermannstädter H. Effects of caloric restriction on cognitive function. [Thesis]. Freie Universität Berlin; 2013. Available from: http://dx.doi.org/10.17169/refubium-13428

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Helsinki

30. Björkstén, Sofie. Hypertension, kardiotoxicitet och njursvikt i samband med tyrosinkinashämmaren sunitinib.

Degree: Farmaceutiska fakulteten, 2011, University of Helsinki

URL: http://hdl.handle.net/10138/28723

► Nybildning av blodkärl från tidigare existerande kärl, angiogenes, är ett väsentligt skede vid tumörtillväxt. Denna process regleras av bland annat tillväxtfaktorer, var av den vaskulära… (more)

▼ Nybildning av blodkärl från tidigare existerande kärl, angiogenes, är ett väsentligt skede vid tumörtillväxt. Denna process regleras av bland annat tillväxtfaktorer, var av den vaskulära endoteliala tillväxtfaktorn har en central roll. Hämning av angiogenes kan ske antingen extracellulärt med hjälp av humaniserade monoklonala antikroppar eller intracellulärt med hjälp av småmolekylära hämmaren. Sunitinib är en småmolekylär multikinashämmare och inhiberar flera tyrosinkinasreceptorer som påverkar tumörtillväxten och metastasutvecklingen vid cancer. Sunitinibs främsta indikationer är gastrointestinala stromacellstumörer, metastaserad njurcellscancer och neuroendokrina tumörer i bukspottskörteln. Behandling med tyrosinkinashämmare orsakar biverkningar som hypertension, kardiotoxicitet och njursvikt, vilka antas bero på de hämmande effekterna på mål som inte är väsentliga för anti-cancer-aktiviteten ("off-target" biverkningar). Bland annat AMP-aktiverat proteinkinas (AMPK), ett kinas som upprätthåller metabolisk homeostas i hjärtat, inhiberas av sunitinib och antas framkalla kardiovaskulära biverkningar. För att reducera "off-target" biverkningar strävar man till att hitta alternativ som minskar de skadliga effekterna utan att den terapeutiska aktiviteten försvagas. Bland annat ett begränsat kaloriintag har uppvisat skyddande effekt på hjärtat via mekanismer sammankopplade till ökad resistens mot oxidativ stress, inflammation och mitokondriell dysfunktion, samt avtagande apoptos och autofagi. Detta sker delvis genom aktivering av enzymet Sirt1. Syftet med den här studien var att undersöka ifall kaloribegränsning skyddar mot kardiovaskulära och renala biverkningar inducerade av sunitinib hos råttor. Dessutom studerades vilka signalkedjor i cellen som medverkar. I studien användes 40 spontant hypertensiva råttor samt 10 normotensiva Wistar-Kyoto råttor. Försöksdjuren delades in i fem grupper beroende på behandling; I WKY kontroll, II SHR kontroll, III SHR + kaloribegränsning 70 %, IV SHR + sunitinib 3 mg/kg och V SHR + sunitinib 3 mg/kg + kaloribegränsning 70 %. Behandlingsperioden var åtta veckor. Blodtrycket mättes varje vecka med svansmanchett, urinutsöndringen undersöktes vecka 4 och vecka 8 med metabolismburar, ultraljudsundersökning av hjärtat utfördes sista veckan och blodkärlens respons till acetylkolin och natriumnitroprussid studerades i samband med avlivning. Proteinerna Sirt1 och AMPK analyserades i hjärtat med Western blotting samt förekomsten av makrofagmarkören ED1 i njurarna med immunhistokemi. Studien visade att sunitinibdosen 3 mg/kg är mycket väl tolererbar hos råttor eftersom sunitinib inte orsakade högre blodtryck, kraftigare hypertrofi eller mer omfattande njurskada jämfört med obehandlade SHR- grupper. Utgående från resultaten kan man också konstatera att kaloribegränsningen har positiva kardiovaskulära effekter.

Subjects/Keywords: VEGF; tyrosinkinas; tyrosinkinashämmare; sunitinib; kaloribegränsning; tyrosine kinase; tyrosine kinase inhibitor; sunitinib; caloric restriction; Farmakologi; Pharmacology; Farmakologia

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Björkstén, S. (2011). Hypertension, kardiotoxicitet och njursvikt i samband med tyrosinkinashämmaren sunitinib. (Masters Thesis). University of Helsinki. Retrieved from http://hdl.handle.net/10138/28723

Chicago Manual of Style (16^th Edition):

Björkstén, Sofie. “Hypertension, kardiotoxicitet och njursvikt i samband med tyrosinkinashämmaren sunitinib.” 2011. Masters Thesis, University of Helsinki. Accessed January 18, 2021. http://hdl.handle.net/10138/28723.

MLA Handbook (7^th Edition):

Björkstén, Sofie. “Hypertension, kardiotoxicitet och njursvikt i samband med tyrosinkinashämmaren sunitinib.” 2011. Web. 18 Jan 2021.

Vancouver:

Björkstén S. Hypertension, kardiotoxicitet och njursvikt i samband med tyrosinkinashämmaren sunitinib. [Internet] [Masters thesis]. University of Helsinki; 2011. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10138/28723.

Council of Science Editors:

Björkstén S. Hypertension, kardiotoxicitet och njursvikt i samband med tyrosinkinashämmaren sunitinib. [Masters Thesis]. University of Helsinki; 2011. Available from: http://hdl.handle.net/10138/28723

		in
And / Or
		in
And / Or
		in
And / Or
		in

Open Access Theses and Dissertations