+publisher:"Universidade Estadual de Campinas" +contributor:("Oliveira, Helena Coutinho Franco de, 1958-")

Universidade Estadual de Campinas

1. Zago, Vanessa Helena de Souza, 1984-. Estudo molecular dos genes ABCA1, ABCG1, ABCG5, ABCG8 e SCARB1 em amostra populacional brasileira assintomática: Molecular study of ABCA1, ABCG1, ABCG5, ABCG8 and SCARB1 genes in an asymptomatic brazilian population sample.

Degree: 2015, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/312594

► Abstract: Given the important role played by ATP binding cassete transporters A1 (ABCA1), G1 (ABCG1), G5 (ABCG5), G8 (ABCG8) and by scavenger receptor class B… (more)

▼ Abstract: Given the important role played by ATP binding cassete transporters A1 (ABCA1), G1 (ABCG1), G5 (ABCG5), G8 (ABCG8) and by scavenger receptor class B type I (SR-BI) on body cholesterol homeostasis and atherosclerosis development, this study proposes to: (i) investigate the relationship of polymorphisms rs2275543 (ABCA1), rs1893590 (ABCG1), rs6720173 (ABCG5), rs6544718 (ABCG8) e rs5888 (SCARB1) with gender, age and body mass index (BMI) and its interactions with clinical and biochemical variables (n=654); (ii) determine the effects of these polymorphisms on the studied parameters in the total population and in a gender-specific manner (n=590) and (iii) evaluate if miRNAs hsa-miR-33a e hsa-miR-128a are differentially expressed in a subgroup of the population (n=51) and verify its association with plasma levels of high-density lipoprotein cholesterol (HDL-C), subclinical atherosclerosis plus ABCA1, ABCG1 and SCARB1 expression. Thus, normolipidemic and asymptomatic volunteers from both genders, with ages ranging from 20 to 75 years were selected. Clinical and anthropometric data were obtained, as well as peripheral venous blood for biochemical determinations plus DNA and RNA extraction. The subgroup of 51 individuals was classified according HDL-C (mg/dL) in hypoalphalipoproteinemics (hypo, HDL-C?39), hyperalphalipoproteinemics (hyper, HDL-C?68) and controls (CTL, HDL-C?40<68); then, were determinated the carotid intima-media thickness and proteins related to HDL metabolism. The polymorphism rs1893590 interacts with age and BMI, modulating HDL-C levels as well as the particle size and volume, suggesting its role on HDL metabolism and composition. Comparative analysis demonstrated that rs2275543 has different, but beneficial repercussions in both genders; furthermore, rs6720173 determines a pro-atherogenic lipoprotein profile in males, while the variants rs5888 and rs6544718 affect positively adiposity markers in females. The analyses of the five studied polymorphism in this population provide evidences of its role in several pathways of lipoproteins metabolism, in most cases in a gender-specific manner. Moreover, the ABCA1, ABCG1, SCARB1, hsa-miR-33a and hsa-miR-128a expression analysis revealed that hyper group presents a significant increase of ABCA1 and ABCG1 expression in relation to the control group; additionally, hsa-miR-33a decreased by 72%. Together, these results indicate a potential regulatory role of this miRNA in asymptomatic individuals, probably contributing to increased cholesterol efflux and reverse cholesterol transport Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Faria, Eliana Cotta de, 1950- (advisor), Oliveira, Helena Coutinho Franco de, 1958- (coadvisor), Scherrer, Daniel Zanetti (coadvisor), Universidade Estadual de Campinas. Faculdade de Ciências Médicas (institution), Programa de Pós-Graduação em Ciências Médicas (nameofprogram), Nunes, Valeria Sutti (committee member), Cazita, Patricia Miralda (committee member), Sposito, Andrei Carvalho (committee member), Vieira, Tarsis Antonio Paiva (committee member).

Subjects/Keywords: Lipoproteinas; Polimorfismo de nucleotídeo único; MicroRNAs; Lipoproteins; Polymorphism, Single nucleotide; MicroRNAs

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APA (6^th Edition):

Zago, Vanessa Helena de Souza, 1. (2015). Estudo molecular dos genes ABCA1, ABCG1, ABCG5, ABCG8 e SCARB1 em amostra populacional brasileira assintomática: Molecular study of ABCA1, ABCG1, ABCG5, ABCG8 and SCARB1 genes in an asymptomatic brazilian population sample. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/312594

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):

Zago, Vanessa Helena de Souza, 1984-. “Estudo molecular dos genes ABCA1, ABCG1, ABCG5, ABCG8 e SCARB1 em amostra populacional brasileira assintomática: Molecular study of ABCA1, ABCG1, ABCG5, ABCG8 and SCARB1 genes in an asymptomatic brazilian population sample.” 2015. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312594.

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

MLA Handbook (7^th Edition):

Zago, Vanessa Helena de Souza, 1984-. “Estudo molecular dos genes ABCA1, ABCG1, ABCG5, ABCG8 e SCARB1 em amostra populacional brasileira assintomática: Molecular study of ABCA1, ABCG1, ABCG5, ABCG8 and SCARB1 genes in an asymptomatic brazilian population sample.” 2015. Web. 23 Jan 2021.

Vancouver:

Zago, Vanessa Helena de Souza 1. Estudo molecular dos genes ABCA1, ABCG1, ABCG5, ABCG8 e SCARB1 em amostra populacional brasileira assintomática: Molecular study of ABCA1, ABCG1, ABCG5, ABCG8 and SCARB1 genes in an asymptomatic brazilian population sample. [Internet] [Thesis]. Universidade Estadual de Campinas; 2015. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/312594.

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

Council of Science Editors:

Zago, Vanessa Helena de Souza 1. Estudo molecular dos genes ABCA1, ABCG1, ABCG5, ABCG8 e SCARB1 em amostra populacional brasileira assintomática: Molecular study of ABCA1, ABCG1, ABCG5, ABCG8 and SCARB1 genes in an asymptomatic brazilian population sample. [Thesis]. Universidade Estadual de Campinas; 2015. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/312594

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

Universidade Estadual de Campinas

2. Paiva, Adriene Alexandra, 1985-. Severidade da esteatose hepática não alcoólica induzida por super expressão da apolipoproteína CIII é associada à inflamação e morte celular = Severity of nonalcoholic fatty liver disease induced by apolipoprotein CIII overexpression is associated with inflammation and cell death: Severity of nonalcoholic fatty liver disease induced by apolipoprotein CIII overexpression is associated with inflammation and cell death.

Degree: 2015, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314291

► Abstract: Nonalcoholic fatty liver disease (NAFLD) is the principal liver manifestation in obesity and metabolic syndrome. The natural history of the disease involves steatosis, oxidative… (more)

▼ Abstract: Nonalcoholic fatty liver disease (NAFLD) is the principal liver manifestation in obesity and metabolic syndrome. The natural history of the disease involves steatosis, oxidative stress, inflammation, fibrosis and cell death. Elevated plasma levels of triglyceride-rich remnant lipoproteins are independent cardiovascular disease risk factors. Clinical and experimental studies show strong correlation and causal links between plasma triglycerides (TG) and apolipoprotein CIII levels. Apolipoprotein CIII is also increased in the plasma of diabetic patients. By comparing apolipoprotein (apo) CIII transgenic mice with control non-transgenic (NTg) littermates, we show here that the overexpression of apoCIII, independently of high fat diet (HFD), results in NAFLD features, namely, increased liver lipid content, decreased antioxidant power, increased expression of TNF'alfa', TNF'alfa' receptor, cleaved caspase-1 and interleukin-1'beta', decreased adiponectin receptor-2 and increased cell death. In addition, systemic indicators of inflammation TNF? and C-reactive protein are also elevated in apoCIII mice. This picture is aggravated and additional NAFLD features are differentially induced by HFD in apoCIII mice. HFD induced glucose intolerance together with increased gluconeogenesis, evidencing hepatic insulin resistance. Marked increases in plasma TNF'alfa' (8-fold) and IL-6 (60%) were induced by HFD in apoCIII mice compared to NTg mice. The other inflammatory indicators (plasma C reactive protein, liver TNF'alfa', TNFr, caspase-1 and IL1 'beta') remained higher in HFD apoCIII mice. Cell death signaling (Bax/Bcl2), effector (caspase-3) and apoptosis were augmented in both low and HFD apoCIII mice. As expected, fenofibrate treatment reversed several of the diet and apoCIII effects. However, fibrate did not normalize apoCIII inflammatory traits, such as increased TNF'alfa1, TNFr, IL1'beta' and reduced adiponectin-R2, even under fully corrected liver lipid content. These results indicate that apoCIII overexpression play a major role in liver inflammation and cell death increasing susceptibility to and the severity of diet induced NAFLD 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), Latorraca, Marcia Queiroz (committee member), Chaves, Valéria Ernestânia (committee member), Milanski, Marciane (committee member), Sampaio, Helena Cristina de Lima Barbosa (committee member).

Subjects/Keywords: Fígado gorduroso; Inflamação; Morte celular; Fatty liver; Inflammation; Cell death

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

APA (6^th Edition):

Paiva, Adriene Alexandra, 1. (2015). Severidade da esteatose hepática não alcoólica induzida por super expressão da apolipoproteína CIII é associada à inflamação e morte celular = Severity of nonalcoholic fatty liver disease induced by apolipoprotein CIII overexpression is associated with inflammation and cell death: Severity of nonalcoholic fatty liver disease induced by apolipoprotein CIII overexpression is associated with inflammation and cell death. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/314291

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):

Paiva, Adriene Alexandra, 1985-. “Severidade da esteatose hepática não alcoólica induzida por super expressão da apolipoproteína CIII é associada à inflamação e morte celular = Severity of nonalcoholic fatty liver disease induced by apolipoprotein CIII overexpression is associated with inflammation and cell death: Severity of nonalcoholic fatty liver disease induced by apolipoprotein CIII overexpression is associated with inflammation and cell death.” 2015. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314291.

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

MLA Handbook (7^th Edition):

Paiva, Adriene Alexandra, 1985-. “Severidade da esteatose hepática não alcoólica induzida por super expressão da apolipoproteína CIII é associada à inflamação e morte celular = Severity of nonalcoholic fatty liver disease induced by apolipoprotein CIII overexpression is associated with inflammation and cell death: Severity of nonalcoholic fatty liver disease induced by apolipoprotein CIII overexpression is associated with inflammation and cell death.” 2015. Web. 23 Jan 2021.

Vancouver:

Paiva, Adriene Alexandra 1. Severidade da esteatose hepática não alcoólica induzida por super expressão da apolipoproteína CIII é associada à inflamação e morte celular = Severity of nonalcoholic fatty liver disease induced by apolipoprotein CIII overexpression is associated with inflammation and cell death: Severity of nonalcoholic fatty liver disease induced by apolipoprotein CIII overexpression is associated with inflammation and cell death. [Internet] [Thesis]. Universidade Estadual de Campinas; 2015. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314291.

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

Council of Science Editors:

Paiva, Adriene Alexandra 1. Severidade da esteatose hepática não alcoólica induzida por super expressão da apolipoproteína CIII é associada à inflamação e morte celular = Severity of nonalcoholic fatty liver disease induced by apolipoprotein CIII overexpression is associated with inflammation and cell death: Severity of nonalcoholic fatty liver disease induced by apolipoprotein CIII overexpression is associated with inflammation and cell death. [Thesis]. Universidade Estadual de Campinas; 2015. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314291

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

3. Lorza-Gil, Estela, 1988-. Efeito da inibição da 3-hidroxi-3-metilglutaril coenzima A (HMG-CoA) redutase por pravastatina sobre a homeostase glicêmica e função da célula beta : estudos em camundongos hipercolesterolêmicos e in vitro = Effect of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition by pravastatin on glucose homeostasis and beta cell function: studies in hypercholesterolemic mice and in vitro : Effect of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition by pravastatin on glucose homeostasis and beta cell function : studies in hypercholesterolemic mice and in vitro .

Degree: 2017, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/332745

► Abstract: We have previously demonstrated that genetic hypercholesterolemia by LDL receptor deficiency show an impairment of insulin secretion. LDL receptor knockout (LDLr-/-) mice, a model… (more)

▼ Abstract: We have previously demonstrated that genetic hypercholesterolemia by LDL receptor deficiency show an impairment of insulin secretion. LDL receptor knockout (LDLr-/-) mice, a model of human familial hypercholesterolemia secretes less insulin than wild type mice. By removing cholesterol from LDLr-/- islets ex vivo using methyl-?-cyclodextrin reversed this defect. Thereby, we hypothesized that in vivo treatment of LDLr-/- mice with the cholesterol inhibitor (pravastatin) would normalize glucose-stimulated insulin secretion. Contrary to our hypothesis, female LDLr-/- mice treated for two or three months with pravastatin exhibit increased glycemia and reducted glucose-stimulated insulin secretion by isolated pancreatic islets. These effects were associated with reductions in the levels of SNARE proteins, increased beta cell death and lipid peroxidation in LDLr-/- mice islets treated with pravastatin. Cell culture studies of insulin secreting cells (INS1E) treated with pravastatin showed an increase of cell death and oxidative stress (indicated by H2O2 production). By inhibiting HMG-CoA reductase, statins also inhibit the production of other intermediaries of cholesterol synthesis pathway, such as coenzyme Q10 (CoQ10). Thus, we hypothesized that the islet toxic effects of pravastatin could be caused by the decrease in CoQ10 biosynthesis. For this reason, LDLr-/- mice treated with pravastatin were supplemented with CoQ10. Diet CoQ10 supplementation reversed fasting hyperglycemia observed in pravastatin treated LDLr-/- mice, as well as, improved their glucose tolerance and restored the glucose stimulated insulin secretion. INS1E cells treated with CoQ10 were protected from cell death and oxidative stress induced by pravastatin. After that, we investigated the long term effects of pravastatin treatment and the possible development of diabetes. LDLr-/- mice became glucose intolerant and insulin resistant after 10 months of pravastatin treatment. Experiments in vitro with C2C12 myotubes treated with pravastatin showed a decrease in insulin signaling, oxidative stress and cell death by apoptosis. In conclusion, these results indicate that inhibition of cholesterol synthesis by chronic treatment with statins causes CoQ10 deficit, which impairs beta cell viability and insulin secretion. The stains diabetogenic effects are also related to myotoxicity and reduction of insulin sensitivity, thus increasing the risk of developing type II diabetes mellitus 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), Ortis, Fernanda (committee member), Silva, Silvana Auxiliadora Bordin da (committee member), Sampaio, Helena Cristina de Lima Barbosa (committee member), Abdulkader, Fernando Rodrigues de Moraes (committee member).

Subjects/Keywords: Diabetes Mellitus; Colesterol; Insulina; Pravastatina; Diabetes mellitus; Cholesterol; Insulin; Pravastatin

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

APA (6^th Edition):

Lorza-Gil, Estela, 1. (2017). Efeito da inibição da 3-hidroxi-3-metilglutaril coenzima A (HMG-CoA) redutase por pravastatina sobre a homeostase glicêmica e função da célula beta : estudos em camundongos hipercolesterolêmicos e in vitro = Effect of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition by pravastatin on glucose homeostasis and beta cell function: studies in hypercholesterolemic mice and in vitro : Effect of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition by pravastatin on glucose homeostasis and beta cell function : studies in hypercholesterolemic mice and in vitro . (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/332745

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):

Lorza-Gil, Estela, 1988-. “Efeito da inibição da 3-hidroxi-3-metilglutaril coenzima A (HMG-CoA) redutase por pravastatina sobre a homeostase glicêmica e função da célula beta : estudos em camundongos hipercolesterolêmicos e in vitro = Effect of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition by pravastatin on glucose homeostasis and beta cell function: studies in hypercholesterolemic mice and in vitro : Effect of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition by pravastatin on glucose homeostasis and beta cell function : studies in hypercholesterolemic mice and in vitro .” 2017. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/332745.

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

MLA Handbook (7^th Edition):

Lorza-Gil, Estela, 1988-. “Efeito da inibição da 3-hidroxi-3-metilglutaril coenzima A (HMG-CoA) redutase por pravastatina sobre a homeostase glicêmica e função da célula beta : estudos em camundongos hipercolesterolêmicos e in vitro = Effect of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition by pravastatin on glucose homeostasis and beta cell function: studies in hypercholesterolemic mice and in vitro : Effect of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition by pravastatin on glucose homeostasis and beta cell function : studies in hypercholesterolemic mice and in vitro .” 2017. Web. 23 Jan 2021.

Vancouver:

Lorza-Gil, Estela 1. Efeito da inibição da 3-hidroxi-3-metilglutaril coenzima A (HMG-CoA) redutase por pravastatina sobre a homeostase glicêmica e função da célula beta : estudos em camundongos hipercolesterolêmicos e in vitro = Effect of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition by pravastatin on glucose homeostasis and beta cell function: studies in hypercholesterolemic mice and in vitro : Effect of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition by pravastatin on glucose homeostasis and beta cell function : studies in hypercholesterolemic mice and in vitro . [Internet] [Thesis]. Universidade Estadual de Campinas; 2017. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/332745.

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

Council of Science Editors:

Lorza-Gil, Estela 1. Efeito da inibição da 3-hidroxi-3-metilglutaril coenzima A (HMG-CoA) redutase por pravastatina sobre a homeostase glicêmica e função da célula beta : estudos em camundongos hipercolesterolêmicos e in vitro = Effect of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition by pravastatin on glucose homeostasis and beta cell function: studies in hypercholesterolemic mice and in vitro : Effect of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition by pravastatin on glucose homeostasis and beta cell function : studies in hypercholesterolemic mice and in vitro . [Thesis]. Universidade Estadual de Campinas; 2017. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/332745

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

Universidade Estadual de Campinas

4. Souza, Jane Cristina de, 1981-. Secreção e ação da insulina em camundongos knockout para o receptor de LDL (LDLR -/-) alimentados com dieta padrão ou hiperlipídica: Secretion and action of the insulin on LDL receptor knockout mice (LDLR -/-) fed with chow or hyperlipidic diet.

Degree: 2012, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/313951

► Abstract: Changes in cellular cholesterol levels may contribute to beta cell dysfunction. Islets from LDL receptor knockout (LDLR-/-) possess higher cholesterol content and secrete less… (more)

▼ Abstract: Changes in cellular cholesterol levels may contribute to beta cell dysfunction. Islets from LDL receptor knockout (LDLR-/-) possess higher cholesterol content and secrete less insulin than wild type (WT) mice. Here, we investigated the association between cholesterol content, insulin secretion and Ca2+ handling in these islets. In addition, we analyzed the effects of highfat- diet (HFD) on glucose homeostasis, insulin secretion and action in these mice. Both first and second phase of glucose-stimulated insulin secretion (GSIS) were lower in LDLR-/- compared with WT islets. This lower secretion was paralleled by impairment in Ca2+ handling in these islets. The contents of SNAP-25 and VAMP-2 proteins, which participate in the extrusion of the insulin containing granules, were reduced in LDLR-/- compared with WT islets. Removal of the excess of cholesterol from LDLR-/- islets (Methyl-?-cyclodextrine, M?CD) normalized glucose- and tolbutamide-induced insulin release. Glucose-stimulated Ca2+ handling was also normalized in cholesterol-depleted LDLR-/- islets. Cholesterol removal from WT islets by 0.1 and 1.0 mmol/L M?CD impaired both GSIS and Ca2+ handling. However, 10 mmol/L M?CD markedly increased insulin secretion induced by glucose or tolbutamide in WT islets, despite a significant reduction in Ca2+ handling. The HFD promoted higher body weight gain and visceral fat pad depot in LDLR-/-H than in WTH. LDLR-/-H mice showed fasted and fed glucose levels significantly higher whereas no changes in fasted plasma insulin levels were observed. WTH mice also showed an increase in fasted and fed glucose levels, but a higher fasted plasma insulin level (p<0.05) was noticed. The area under the curve of the oGTT in LDLR-/-H, but not in WTH, was increased (30%) by HFD. GSIS was not significantly altered by HFD in both groups. LDLR-/- mice showed higher IR? and AKT phosphorylation in liver and skeletal muscle. Insulin degrading enzyme (IDE) protein content was lower in liver of LDLR-/-. The HFD reduced insulin signaling in liver, skeletal muscle and adipose tissue in LDLR-/-H. In WTH the HFD reduced only the IR? phosphorylation in muscle. In conclusion, our results indicate that abnormal high (LDLR-/- islets) or low (WT islets treated with M?CD) cholesterol contents alter both GSIS and Ca2+ handling. Normalization of islet cholesterol content improved Ca2+ handling and insulin secretion in LDLR-/- islets, despite the lower expression of SNAP-25 and VAMP-2. LDLR-/- mice, fed a chow diet, are more sensitive to insulin probably due adaptive mechanisms that compensate the low insulin secretion. However, these changes are not sufficient to promote glucose homeostasis since these mice were glucose intolerants. When fed a high-fat diet, they became also insulin resistant probably due to an increase in the mass of the visceral adipose tissue Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Boschiero, Antonio Carlos, 1943- (advisor), Oliveira, Helena Coutinho Franco de, 1958- (coadvisor), Universidade Estadual de Campinas. Instituto de Biologia (institution), Programa de Pós-Graduação em Biologia Funcional e Molecular (nameofprogram), Carpinelli, Angelo Rafael (committee member), Torsoni, Marcio Alberto (committee member), Bonfleur, Maria Lúcia (committee member), Silva, Silvana Auxiliadora Bordin da (committee member).

Subjects/Keywords: Insulina - Secreção; Colesterol; Movimentação de cálcio; Dieta hiperlipídica; Resistência à insulina; Receptores LDL; Insulin - Secretion; Cholesterol; Calcium handling; High-fast diet; Insulin resistance; LDL receptors

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

APA (6^th Edition):

Souza, Jane Cristina de, 1. (2012). Secreção e ação da insulina em camundongos knockout para o receptor de LDL (LDLR -/-) alimentados com dieta padrão ou hiperlipídica: Secretion and action of the insulin on LDL receptor knockout mice (LDLR -/-) fed with chow or hyperlipidic diet. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/313951

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):

Souza, Jane Cristina de, 1981-. “Secreção e ação da insulina em camundongos knockout para o receptor de LDL (LDLR -/-) alimentados com dieta padrão ou hiperlipídica: Secretion and action of the insulin on LDL receptor knockout mice (LDLR -/-) fed with chow or hyperlipidic diet.” 2012. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/313951.

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

MLA Handbook (7^th Edition):

Souza, Jane Cristina de, 1981-. “Secreção e ação da insulina em camundongos knockout para o receptor de LDL (LDLR -/-) alimentados com dieta padrão ou hiperlipídica: Secretion and action of the insulin on LDL receptor knockout mice (LDLR -/-) fed with chow or hyperlipidic diet.” 2012. Web. 23 Jan 2021.

Vancouver:

Souza, Jane Cristina de 1. Secreção e ação da insulina em camundongos knockout para o receptor de LDL (LDLR -/-) alimentados com dieta padrão ou hiperlipídica: Secretion and action of the insulin on LDL receptor knockout mice (LDLR -/-) fed with chow or hyperlipidic diet. [Internet] [Thesis]. Universidade Estadual de Campinas; 2012. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/313951.

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

Council of Science Editors:

Souza, Jane Cristina de 1. Secreção e ação da insulina em camundongos knockout para o receptor de LDL (LDLR -/-) alimentados com dieta padrão ou hiperlipídica: Secretion and action of the insulin on LDL receptor knockout mice (LDLR -/-) fed with chow or hyperlipidic diet. [Thesis]. Universidade Estadual de Campinas; 2012. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/313951

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

Universidade Estadual de Campinas

5. Malaguti, Carina, 1981-. Estresse oxidativo e susceptibilidade à transição de permeabilidade mitocondrial precedem o apareceimento do diabetes autoimune em camundongos nod: Oxidative stress susceptibility to permeability transition precede the onset of autoimmune diabetes in nod mice.

Degree: 2012, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/311455

► Abstract: Reactive oxygen species (ROS) have been extensively associated with a large variety of human metabolic diseases including type 1 diabetes auto-immune (T1D A). The… (more)

▼ Abstract: Reactive oxygen species (ROS) have been extensively associated with a large variety of human metabolic diseases including type 1 diabetes auto-immune (T1D A). The destruction of islet beta cells in T1DA is associated with cellular oxidative stress and with the mitochondrial pathway of cell death. The aim of this study was to determine whether oxidative stress and mitochondrial dysfunction are present in T1DA experimental model NOD (non obese diabetic mouse) and if they are related to the stages of the development of the disease. The experiments were done in liver and soleus muscles biopsies, isolated liver mitochondria, spleen and circulating lymphocytes, bone marrow stem cells and isolated pancreatic islets from NOD and control Balb/c mice. NOD mice were studied at 3 stages: non-diabetic (glycemia < 100 mg/dL, 4-6 weeks of age), pre-diabetic (glycemia range 100-150 mg/dL, 7-10 weeks of age) and diabetic (glycemia > 250 mg/dL, 14-25 weeks of age) and compared to age matched Balb/c mice. Mitochondria respiration rates (oxygen consumption) measured at phosphorylating and resting states in liver and soleus biopsies and in isolated liver mitochondria were similar in NOD at the three stages of the disease as compared to age matched Balb/c mice. However, NOD isolated liver mitochondrial were shown to be more susceptible to calcium induced mitochondrial permeability transition (MPT), as determined by calcium induced cyclosporine A sensitive swelling and by decreased calcium retention capacity. This higher MPT susceptibility was observed in all 3 stages of the development of diabetes. Hydrogen peroxide production (Amplex red) was higher in isolated liver mitochondria from non-diabetic NOD, but unaltered in pre-diabetic and diabetic NOD mice. The oxidation of H2DCF by intact cells was significantly increased in NOD lymphocytes and stem cells in non-, pre- and diabetic stages as compared to controls. In addition, we observed higher rates of H2DCF oxidation in pancreatic islets from non-diabetic NOD mice. These results suggest that the oxidative stress precedes the establishment of diabetes and may be the cause of mitochondrial dysfunction that is involved in beta cell death. We propose that oxidative stress is a key event in the pathogenesis of T1DA and may be a potential target for interventions Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Vercesi, Anibal Eugenio, 1946- (advisor), Oliveira, Helena Coutinho Franco de, 1958- (coadvisor), Universidade Estadual de Campinas. Faculdade de Ciências Médicas (institution), Programa de Pós-Graduação em Fisiopatologia Médica (nameofprogram), Passarelli, Marisa (committee member), Silveira, Leonardo dos Reis (committee member), Boschiero, Antonio Carlos (committee member), Pavin, Elizabeth João (committee member).

Subjects/Keywords: Diabetes mellitus tipo 1; Mitocôndria; Consumo de oxigênio; Espécies de oxigênio reativas; Type 1 diabetes; Mitochondria; Oxygen consumption; Reactive oxygen species

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

APA (6^th Edition):

Malaguti, Carina, 1. (2012). Estresse oxidativo e susceptibilidade à transição de permeabilidade mitocondrial precedem o apareceimento do diabetes autoimune em camundongos nod: Oxidative stress susceptibility to permeability transition precede the onset of autoimmune diabetes in nod mice. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/311455

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):

Malaguti, Carina, 1981-. “Estresse oxidativo e susceptibilidade à transição de permeabilidade mitocondrial precedem o apareceimento do diabetes autoimune em camundongos nod: Oxidative stress susceptibility to permeability transition precede the onset of autoimmune diabetes in nod mice.” 2012. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311455.

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

MLA Handbook (7^th Edition):

Malaguti, Carina, 1981-. “Estresse oxidativo e susceptibilidade à transição de permeabilidade mitocondrial precedem o apareceimento do diabetes autoimune em camundongos nod: Oxidative stress susceptibility to permeability transition precede the onset of autoimmune diabetes in nod mice.” 2012. Web. 23 Jan 2021.

Vancouver:

Malaguti, Carina 1. Estresse oxidativo e susceptibilidade à transição de permeabilidade mitocondrial precedem o apareceimento do diabetes autoimune em camundongos nod: Oxidative stress susceptibility to permeability transition precede the onset of autoimmune diabetes in nod mice. [Internet] [Thesis]. Universidade Estadual de Campinas; 2012. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/311455.

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

Council of Science Editors:

Malaguti, Carina 1. Estresse oxidativo e susceptibilidade à transição de permeabilidade mitocondrial precedem o apareceimento do diabetes autoimune em camundongos nod: Oxidative stress susceptibility to permeability transition precede the onset of autoimmune diabetes in nod mice. [Thesis]. Universidade Estadual de Campinas; 2012. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/311455

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

Universidade Estadual de Campinas

6. Raposo, Helena Fonseca, 1981-. Estudo dos mecanismos envolvidos na redução de adiposidade de camundongos que super-expressam a proteína de transferência de colesteril éster (CETP): Effects of n-3 and n-6 fatty acids on the cholesteryl ester transfer protein (CETP) expression and activity in transgenic mice.

Degree: 2013, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314295

► Abstract: Cholesteryl ester transfer protein (CETP) is a plasma protein that mediates the exchange of triglycerides for esterified cholesterol from HDL to the apoB containing… (more)

▼ Abstract: Cholesteryl ester transfer protein (CETP) is a plasma protein that mediates the exchange of triglycerides for esterified cholesterol from HDL to the apoB containing lipoproteins. In this way, CETP promotes reduction of plasma HDLcholesterol and, thus, increases the risk of atherosclerosis. Recently, we found that CETP expressing mice (CETP-Tg) presented less adipose tissue mass than nonexpressing controls. In this work we investigated possible mechanisms to explain these findings. CETP-Tg and non-transgenic (NTg) control mice (C57/BL6 background) were fed with chow diet from weaning to 5 month of age. CETP-Tg mice had reduced visceral and subcutaneous fat depots (~30%) that was not compensated by lipid ectopic deposition and could not be explained by differences in fat intake and excretion. Lipogenesis rates in vivo and in isolated adipocytes (estimated using 3H2O and 14C-acetate) were similar in both CETP-Tg and control mice. Lipid retention and glucose uptake by liver, muscle and adipose tissues (estimated after an oral dose of 3H-triolein and IP injection of 3H-deoxiglucose) showed no significant differences between groups. In the fed state, CETP group showed higher (~50%) basal lipolysis rates in vivo and in isoproterenol stimulated lipolysis rates in isolated adipocytes. In accordance, visceral adipose hormone sensitive lipase (HSL) and adipose triglyceride lipase (ATGL) mRNA expression were elevated, as well as fatty acid transport protein (FATP1). In brown adipose tissue, ATGL, FATP1 and uncoupling protein 1 (UCP1) were increased. Furthermore, beta 3 adrenergic receptor proteins mass were upregulated in visceral and brown adipose tissues membrane extracts. In addition, whole body energy expenditure (measured by respirometry) was found to be elevated in CETP-Tg mice (10%). In conclusion, CETP change expression and function of proteins related to lipolysis and thermogeneis, thus, increasing whole body energy expenditure and resulting in less body fat content. These findings disclose a novel anti-adipogenic role for CETP 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), Nakandakare, Edna Regina (committee member), Vale, Maria Isabel Cardoso Alonso (committee member), Torsoni, Marcio Alberto (committee member), Navegantes, Luiz Carlos Carvalho (committee member).

Subjects/Keywords: Proteínas de transferência de ésteres de colesterol; Lipolise; Adiposidade; Cholesterol ester transfer proteins; Lipolyse; Adiposity

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

APA (6^th Edition):

Raposo, Helena Fonseca, 1. (2013). Estudo dos mecanismos envolvidos na redução de adiposidade de camundongos que super-expressam a proteína de transferência de colesteril éster (CETP): Effects of n-3 and n-6 fatty acids on the cholesteryl ester transfer protein (CETP) expression and activity in transgenic mice. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/314295

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):

Raposo, Helena Fonseca, 1981-. “Estudo dos mecanismos envolvidos na redução de adiposidade de camundongos que super-expressam a proteína de transferência de colesteril éster (CETP): Effects of n-3 and n-6 fatty acids on the cholesteryl ester transfer protein (CETP) expression and activity in transgenic mice.” 2013. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314295.

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

MLA Handbook (7^th Edition):

Raposo, Helena Fonseca, 1981-. “Estudo dos mecanismos envolvidos na redução de adiposidade de camundongos que super-expressam a proteína de transferência de colesteril éster (CETP): Effects of n-3 and n-6 fatty acids on the cholesteryl ester transfer protein (CETP) expression and activity in transgenic mice.” 2013. Web. 23 Jan 2021.

Vancouver:

Raposo, Helena Fonseca 1. Estudo dos mecanismos envolvidos na redução de adiposidade de camundongos que super-expressam a proteína de transferência de colesteril éster (CETP): Effects of n-3 and n-6 fatty acids on the cholesteryl ester transfer protein (CETP) expression and activity in transgenic mice. [Internet] [Thesis]. Universidade Estadual de Campinas; 2013. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314295.

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

Council of Science Editors:

Raposo, Helena Fonseca 1. Estudo dos mecanismos envolvidos na redução de adiposidade de camundongos que super-expressam a proteína de transferência de colesteril éster (CETP): Effects of n-3 and n-6 fatty acids on the cholesteryl ester transfer protein (CETP) expression and activity in transgenic mice. [Thesis]. Universidade Estadual de Campinas; 2013. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314295

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

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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 23, 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. 23 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 23]. 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

Universidade Estadual de Campinas

8. Rentz, Thiago, 1990-. Modulação da aterogênese pela expressão da transidrogenase de nucleotídeo de nicotinamida (Nnt) e da proteína de transferência de colesterol esterificado (CETP) em macrófagos : Atherogenesis modulation by nicotinamide nucleotide transhydrogenase (Nnt) and cholesterol ester transfer protein (CETP) expression in macrophages: Atherogenesis modulation by nicotinamide nucleotide transhydrogenase (Nnt) and cholesterol ester transfer protein (CETP) expression in macrophages.

Degree: 2020, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/343574

► Abstract: Atherosclerosis leads to the development of cardiovascular diseases (CVD), which are the main causes of death worldwide. The events that characterize atherosclerosis are slow… (more)

▼ Abstract: Atherosclerosis leads to the development of cardiovascular diseases (CVD), which are the main causes of death worldwide. The events that characterize atherosclerosis are slow and progressive and involve lipid infiltration, inflammation and oxidative stress in the arterial wall. Macrophages are essential cells in all stages of atherosclerosis and appear as a therapeutic target. In this work, we investigated the impact of the expression of nicotinamide nucleotide transhydrogenase (Nnt) and cholesteryl ester transfer protein (CETP) on the formation of atherosclerotic lesions in LDL receptor deficient mice (Ldlr-/-). While CETP promotes reverse cholesterol transport in plasma, Nnt is an important mitochondrial enzyme for cellular redox homeostasis. Ldlr-/- mice express neither CETP nor Nnt. Thus, in the first study, we aimed at evaluating whether Nnt deficiency in macrophages contributes to oxidative stress and hence to atherosclerosis development. For this, we evaluated functional and biochemical processes in peritoneal macrophages from three different strains of C57BL/6J mice. Our observations demonstrate that peritoneal macrophages with absence of Nnt showed an increase in the production of oxidants, in the inflammatory response and in mitochondrial biogenesis. When exposed to modified LDL, increased foam cell formation was observed in the Nnt deficient background, what could be explained by decreased ABCA1 and increased CD36 expression. When Ldlr-/- were transplanted with Nnt expressing bone marrow, they showed smaller lesions, with less lipid, macrophage and nitrotyrosine content. Thus, we conclude that Nnt has an important role in the maintenance of redox, inflammatory and cholesterol homeostasis. In the second study, we investigated whether the expression of CETP in macrophages would modulate atherogenesis in a well defined background: in the presence of Ldlr and Nnt. For this purpose Ldlr-/- mice, that express neither Nnt nor CETP genes, were transplanted with bone marrow from four donor mice lines: itself (autologous control), and lines expressing Ldlr, Ldlr + Nnt and Ldlr + Nnt + CETP. We observed that the expression of Ldlr reduced the content of lipid, macrophages, indicators of nitroxidative stress and nucleic acid oxidative damage in the aorta of transplanted mice. Nnt and CETP expression had no significant additional effects. The expression of Nnt + Ldlr reduced significantly the amount of neutrophils infiltration in the aorta of transplanted mice. CETP expression further decreased neutrophils infiltration,TNF- content and E-selectin mRNA in aorta. Both Nnt and CETP expression also reduced the circulating levels of pro-inflammatory cytokines, IL-6 e IL-1. In bone marrow derived macrophages, CETP and Nnt reduced proinflammatory and increased anti-inflammatory mRNA levels. In addition, CETP expression reduced a migration (CDC42) related gene expression in bone marrow derived macrophages. In conclusion, CETP expression in bone marrow derived cells reduces inflammatory features of early… 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), Vicente, Cristina Pontes (committee member), Davel, Ana Paula (committee member), Quintão, Eder Carlos Rocha (committee member), Cazita, Patricia Miralda (committee member).

Subjects/Keywords: Aterosclerose; Macrofagos; Estresse oxidativo; Inflamação; Atherosclerosis; Macrophages; Oxidative stress; Inflammation

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

APA (6^th Edition):

Rentz, Thiago, 1. (2020). Modulação da aterogênese pela expressão da transidrogenase de nucleotídeo de nicotinamida (Nnt) e da proteína de transferência de colesterol esterificado (CETP) em macrófagos : Atherogenesis modulation by nicotinamide nucleotide transhydrogenase (Nnt) and cholesterol ester transfer protein (CETP) expression in macrophages: Atherogenesis modulation by nicotinamide nucleotide transhydrogenase (Nnt) and cholesterol ester transfer protein (CETP) expression in macrophages. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/343574

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):

Rentz, Thiago, 1990-. “Modulação da aterogênese pela expressão da transidrogenase de nucleotídeo de nicotinamida (Nnt) e da proteína de transferência de colesterol esterificado (CETP) em macrófagos : Atherogenesis modulation by nicotinamide nucleotide transhydrogenase (Nnt) and cholesterol ester transfer protein (CETP) expression in macrophages: Atherogenesis modulation by nicotinamide nucleotide transhydrogenase (Nnt) and cholesterol ester transfer protein (CETP) expression in macrophages.” 2020. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/343574.

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

MLA Handbook (7^th Edition):

Rentz, Thiago, 1990-. “Modulação da aterogênese pela expressão da transidrogenase de nucleotídeo de nicotinamida (Nnt) e da proteína de transferência de colesterol esterificado (CETP) em macrófagos : Atherogenesis modulation by nicotinamide nucleotide transhydrogenase (Nnt) and cholesterol ester transfer protein (CETP) expression in macrophages: Atherogenesis modulation by nicotinamide nucleotide transhydrogenase (Nnt) and cholesterol ester transfer protein (CETP) expression in macrophages.” 2020. Web. 23 Jan 2021.

Vancouver:

Rentz, Thiago 1. Modulação da aterogênese pela expressão da transidrogenase de nucleotídeo de nicotinamida (Nnt) e da proteína de transferência de colesterol esterificado (CETP) em macrófagos : Atherogenesis modulation by nicotinamide nucleotide transhydrogenase (Nnt) and cholesterol ester transfer protein (CETP) expression in macrophages: Atherogenesis modulation by nicotinamide nucleotide transhydrogenase (Nnt) and cholesterol ester transfer protein (CETP) expression in macrophages. [Internet] [Thesis]. Universidade Estadual de Campinas; 2020. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/343574.

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

Council of Science Editors:

Rentz, Thiago 1. Modulação da aterogênese pela expressão da transidrogenase de nucleotídeo de nicotinamida (Nnt) e da proteína de transferência de colesterol esterificado (CETP) em macrófagos : Atherogenesis modulation by nicotinamide nucleotide transhydrogenase (Nnt) and cholesterol ester transfer protein (CETP) expression in macrophages: Atherogenesis modulation by nicotinamide nucleotide transhydrogenase (Nnt) and cholesterol ester transfer protein (CETP) expression in macrophages. [Thesis]. Universidade Estadual de Campinas; 2020. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/343574

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

Universidade Estadual de Campinas

9. Rovani, Juliana Cristine, 1988-. Papel da transidrogenase de nucleotídeo de nicotinamida mitocondrial (NNT) no metabolismo glicídico e no metabolismo lipídico: Role of mitochondrial nicotinamide nucleotide transhydrogenase in glucose and lipids metabolism.

Degree: 2018, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/333238

► Abstract: Mitochondrial nicotinamide nucleotide transhydrogenase (NNT) is the main source of NA(D)PH in mitochondria, which is used for detoxification of mitochondrial hydrogen peroxide. Previous studies… (more)

▼ Abstract: Mitochondrial nicotinamide nucleotide transhydrogenase (NNT) is the main source of NA(D)PH in mitochondria, which is used for detoxification of mitochondrial hydrogen peroxide. Previous studies have shown that the mutation in this enzyme is associated with changes in the redox state of mitochondria, reduction of insulin secretion and increase of diet-induced obesity in C57BL/6J mice from the Jackson Laboratory (B6-J) when compared to strains without this mutation (e.g., C57BL/6JUnib). In this work, we investigate the glucose and lipid metabolism in order to understand the role of NNT in the susceptibility to diabetes and obesity. For this, we studied independent isogenic C57BL6 sub line, with and without mutation of NNT, B6-J and B6-UNI, respectively, as well as congenic lineages (with >99% genetic background homogeneity) with and without the NNT mutation (NNT-/- vs. NNT+/+). These studies were performed with either normal (standard) diet or high fat (HF, 20 weeks) diet. In the first study we evaluated the effect of NNT on glycemic homeostasis. We observed that in relation to the non-mutants (B6-UNI), NNT deficient animals (B6-J) presented glucose intolerance due to both insulin secretion deficiency and peripheral resistance to the hormone. In the pancreatic islets, in addition to the reduction of insulin secretion stimulated by glucose, there was a reduction of autofluorescence of NAD(P)H and increase of H2O2 production. NNT-deficient animals had hepatic insulin resistance as determined by the pyruvate-to-glucose test and reduced hepatic insulin signaling (pAKT). All these findings were observed in both normal and HF diet fed mice. However, in congenic strains, we demonstrated that NNT deficient animals (NNT-/-) were also glucose intolerant, but with secretory insulin function preserved, both in normal and HF diet. Glucose intolerance in NNT-/- animals is explained by increased peripheral insulin resistance, overall (insulin tolerance test) and in liver (conversion of pyruvate to glucose and phosphorylation of AKT). Based on previous studies showing redox abnormalities in hepatic mitochondria with NNT deficiency, our hypothesis is that these abnormalities are responsible for hepatic insulin resistance. Thus, we treated the animals for a month with the antioxidant TEMPOL, which in fact reversed the glucose intolerance caused by NNT deficiency. Thus, we conclude that NNT is important for hepatic insulin signaling, but does not alter insulin secretion. Probably other genetic differences between the B6-J and B6-UNI strains besides NNT mutation are responsible for the impairment of glucose-stimulated insulin secretion in C57BL/6J animals. In the second study we evaluated the role of NNT on lipid metabolism. We observed that NNT-deficient B6-J mice present increased body adiposity and hepatic triglycerides (TG), increased leptinemia and reduced body metabolism (respirometry). These findings were obtained both in the normal diet and in the HF diet. Increased liver fat can be explained by increased dietary lipid… 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), Figueira, Tiago Rezende (committee member), Sampaio, Helena Cristina de Lima Barbosa (committee member), Silveira, Leonardo dos Reis (committee member), Nunes, Valeria Sutti (committee member).

Subjects/Keywords: NADP trans-hidrogenases; Insulina - Secreção; Resistência à insulina; Obesidade; NADP transhydrogenases; Insulin - Secretion; Insulin resistance; Obesity

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

APA (6^th Edition):

Rovani, Juliana Cristine, 1. (2018). Papel da transidrogenase de nucleotídeo de nicotinamida mitocondrial (NNT) no metabolismo glicídico e no metabolismo lipídico: Role of mitochondrial nicotinamide nucleotide transhydrogenase in glucose and lipids metabolism. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/333238

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):

Rovani, Juliana Cristine, 1988-. “Papel da transidrogenase de nucleotídeo de nicotinamida mitocondrial (NNT) no metabolismo glicídico e no metabolismo lipídico: Role of mitochondrial nicotinamide nucleotide transhydrogenase in glucose and lipids metabolism.” 2018. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/333238.

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

MLA Handbook (7^th Edition):

Rovani, Juliana Cristine, 1988-. “Papel da transidrogenase de nucleotídeo de nicotinamida mitocondrial (NNT) no metabolismo glicídico e no metabolismo lipídico: Role of mitochondrial nicotinamide nucleotide transhydrogenase in glucose and lipids metabolism.” 2018. Web. 23 Jan 2021.

Vancouver:

Rovani, Juliana Cristine 1. Papel da transidrogenase de nucleotídeo de nicotinamida mitocondrial (NNT) no metabolismo glicídico e no metabolismo lipídico: Role of mitochondrial nicotinamide nucleotide transhydrogenase in glucose and lipids metabolism. [Internet] [Thesis]. Universidade Estadual de Campinas; 2018. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/333238.

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

Council of Science Editors:

Rovani, Juliana Cristine 1. Papel da transidrogenase de nucleotídeo de nicotinamida mitocondrial (NNT) no metabolismo glicídico e no metabolismo lipídico: Role of mitochondrial nicotinamide nucleotide transhydrogenase in glucose and lipids metabolism. [Thesis]. Universidade Estadual de Campinas; 2018. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/333238

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

10. Marques, Ana Carolina, 1988-. Coenzima Q10 ou creatina protegem contra alterações redox hepáticas induzidas por pravastatina em camundongos hipercolesterolêmicos : Coenzyme Q10 or creatine counteract pravastatin-induced liver redox changes in hypercholesterolemic mice : Coenzyme Q10 or creatine counteract pravastatin-induced liver redox changes in hypercholesterolemic mice .

Degree: 2018, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/335088

► Abstract: Statins are the preferred therapy to treat hypercholesterolemia. Their main action consists of inhibiting the cholesterol biosynthesis pathway. Previous studies report mitochondrial oxidative stress… (more)

▼ Abstract: Statins are the preferred therapy to treat hypercholesterolemia. Their main action consists of inhibiting the cholesterol biosynthesis pathway. Previous studies report mitochondrial oxidative stress and membrane permeability transition (MPT) of several experimental models submitted to diverse statins treatments. The aim of the present study was to investigate whether chronic treatment with the hydrophilic pravastatin induces hepatotoxicity in LDL receptor knockout mice (LDLr-/-), a model for human familial hypercholesterolemia. We evaluated respiration and reactive oxygen production rates, cyclosporine-A sensitive mitochondrial calcium release, antioxidant enzyme activities in liver mitochondria or homogenates obtained from LDLr-/- mice treated with pravastatin for three months. We observed that pravastatin induced higher H2O2 production rate (40%), decreased activity of aconitase (28%), a superoxide-sensitive Krebs cycle enzyme, and increased susceptibility to Ca2+-induced MPT (32%) in liver mitochondria. Among several antioxidant enzymes, only glucose-6-phosphate dehydrogenase (G6PD) activity was increased (44%) in the liver of treated mice. Total glutathione content and reduced to oxidized glutathione ratio were increased in livers of pravastatin treated mice (1.5- and 2-fold, respectively). The presence of oxidized lipid species were detected in pravastatin group but protein oxidation markers (carbonyl and SH-groups) were not altered. Diet supplementation with the antioxidants CoQ10 or creatine fully reversed all pravastatin effects (reduced H2O2 generation, susceptibility to MPT and normalized aconitase and G6PD activity). Taken together, these results suggest that 1- pravastatin induces liver mitochondrial redox imbalance that may explain the hepatic side effects reported in a small number of patients, and 2- the co-treatment with safe antioxidants neutralize these side effects Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Vercesi, Anibal Eugenio, 1946- (advisor), Oliveira, Helena Coutinho Franco de, 1958- (coadvisor), Universidade Estadual de Campinas. Faculdade de Ciências Médicas (institution), Programa de Pós-Graduação em Fisiopatologia Médica (nameofprogram), Reis, Sérgio Furtado dos (committee member), Silveira, Leonardo dos Reis (committee member), Uyemura, Sergio Akira (committee member), Graminha, Marcia Aparecida Silva (committee member).

Subjects/Keywords: Mitocôndrias hepáticas; Pravastatina; Espécies reativas de oxigênio (ERO); Creatina; Coenzima Q10; Mitochondria, Liver; Pravastatin; Reactive oxygen species; Creatine; Coenzyme Q10

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

APA (6^th Edition):

Marques, Ana Carolina, 1. (2018). Coenzima Q10 ou creatina protegem contra alterações redox hepáticas induzidas por pravastatina em camundongos hipercolesterolêmicos : Coenzyme Q10 or creatine counteract pravastatin-induced liver redox changes in hypercholesterolemic mice : Coenzyme Q10 or creatine counteract pravastatin-induced liver redox changes in hypercholesterolemic mice . (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/335088

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):

Marques, Ana Carolina, 1988-. “Coenzima Q10 ou creatina protegem contra alterações redox hepáticas induzidas por pravastatina em camundongos hipercolesterolêmicos : Coenzyme Q10 or creatine counteract pravastatin-induced liver redox changes in hypercholesterolemic mice : Coenzyme Q10 or creatine counteract pravastatin-induced liver redox changes in hypercholesterolemic mice .” 2018. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/335088.

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

MLA Handbook (7^th Edition):

Marques, Ana Carolina, 1988-. “Coenzima Q10 ou creatina protegem contra alterações redox hepáticas induzidas por pravastatina em camundongos hipercolesterolêmicos : Coenzyme Q10 or creatine counteract pravastatin-induced liver redox changes in hypercholesterolemic mice : Coenzyme Q10 or creatine counteract pravastatin-induced liver redox changes in hypercholesterolemic mice .” 2018. Web. 23 Jan 2021.

Vancouver:

Marques, Ana Carolina 1. Coenzima Q10 ou creatina protegem contra alterações redox hepáticas induzidas por pravastatina em camundongos hipercolesterolêmicos : Coenzyme Q10 or creatine counteract pravastatin-induced liver redox changes in hypercholesterolemic mice : Coenzyme Q10 or creatine counteract pravastatin-induced liver redox changes in hypercholesterolemic mice . [Internet] [Thesis]. Universidade Estadual de Campinas; 2018. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/335088.

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

Council of Science Editors:

Marques, Ana Carolina 1. Coenzima Q10 ou creatina protegem contra alterações redox hepáticas induzidas por pravastatina em camundongos hipercolesterolêmicos : Coenzyme Q10 or creatine counteract pravastatin-induced liver redox changes in hypercholesterolemic mice : Coenzyme Q10 or creatine counteract pravastatin-induced liver redox changes in hypercholesterolemic mice . [Thesis]. Universidade Estadual de Campinas; 2018. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/335088

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

Universidade Estadual de Campinas

11. Bighetti, Eliete Janaina Bueno. Efeito do tratamento com agonista dos PPARalfa (Ciprofibrato), sobre a homeostase lipidica e glicemica em camundongos geneticamente modificados.

Degree: 2003, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314305

Subjects/Keywords: Lipoproteinas - Metabolismo; Tratamento; Animais transgênicos

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

APA (6^th Edition):

Bighetti, E. J. B. (2003). Efeito do tratamento com agonista dos PPARalfa (Ciprofibrato), sobre a homeostase lipidica e glicemica em camundongos geneticamente modificados. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/314305

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):

Bighetti, Eliete Janaina Bueno. “Efeito do tratamento com agonista dos PPARalfa (Ciprofibrato), sobre a homeostase lipidica e glicemica em camundongos geneticamente modificados.” 2003. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314305.

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

MLA Handbook (7^th Edition):

Bighetti, Eliete Janaina Bueno. “Efeito do tratamento com agonista dos PPARalfa (Ciprofibrato), sobre a homeostase lipidica e glicemica em camundongos geneticamente modificados.” 2003. Web. 23 Jan 2021.

Vancouver:

Bighetti EJB. Efeito do tratamento com agonista dos PPARalfa (Ciprofibrato), sobre a homeostase lipidica e glicemica em camundongos geneticamente modificados. [Internet] [Thesis]. Universidade Estadual de Campinas; 2003. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314305.

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

Council of Science Editors:

Bighetti EJB. Efeito do tratamento com agonista dos PPARalfa (Ciprofibrato), sobre a homeostase lipidica e glicemica em camundongos geneticamente modificados. [Thesis]. Universidade Estadual de Campinas; 2003. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314305

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

Universidade Estadual de Campinas

12. Patrício, Patrícia Riva. A expressão da proteína de transferência de colesteril éster (CETP) modula a adiposidade e a expressão de genes envolvidos em lipólise e lipogênese: Cholesteryl ester transfer protein (CETP) expression modulates adiposity and expression of genes involved in lipolysis and lipogenesis.

Degree: 2010, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314297

► Abstract: CETP is a plasma protein that promotes lipid transfer among plasma lipoproteins causing reduction of HDL-cholesterol and, thus, increases the risk of atherosclerosis. In… (more)

▼ Abstract: CETP is a plasma protein that promotes lipid transfer among plasma lipoproteins causing reduction of HDL-cholesterol and, thus, increases the risk of atherosclerosis. In this work we investigated the effect of CETP expression on differential gene expression and adiposity in two animal models. Human CETP expressing transgenic (Tg) mice and control CETP non-expressing littermates were compared. CETP-Tg mice had reduced body weight, plasma leptin levels, perigonadal and subcutaneous fat depots and adipocyte area. We also observed that CETP mRNA levels were higher in subcutaneous than in perigonadal adipose tissue. As compared to controls, CETP-Tg had altered tissue mRNA levels in the perigonadal adipose tissue: reduction of SREBP2 and lipoprotein lipase and elevation in AMPK. Regarding subcutaneous depot, there was a decrease in PPAR_ and marked elevation of hormone sensitive lipase and AMPK. In addition, an elevation in liver PPAR_ was found in female and hepatic lipase in male CETP Tg mice. Naturally CETP expressing Golden Syrian hamsters were used to confirm whether the inhibition of CETP would affect adiposity. Treatment with a neutralizing CETP monoclonal antibody (TP2) during one month resulted in 70% reduction in plasma CETP activity and significant increases in weight gain, visceral adipose tissue mass and adipocyte area, as compared to the control group (irrelevant IgG treated). In conclusion, CETP induces differential lipolitic and lipogenic gene expression in adipose tissue, resulting in reduction of body fat content. These findings disclose a novel anti-adipogenic role for CETP. 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), Faria, Eliana Cotta de (committee member), Velloso, Licio Augusto (committee member), Seelaender, Marilia Cerqueira Leite (committee member), Carrilho, Alexandre Jose Faria (committee member).

Subjects/Keywords: Proteínas de transferência de ésteres de colesterol; Obesidade; Expressão gênica; Cholesteryl ester transfer proteins; Obesity; Gene expression

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

APA (6^th Edition):

Patrício, P. R. (2010). A expressão da proteína de transferência de colesteril éster (CETP) modula a adiposidade e a expressão de genes envolvidos em lipólise e lipogênese: Cholesteryl ester transfer protein (CETP) expression modulates adiposity and expression of genes involved in lipolysis and lipogenesis. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/314297

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):

Patrício, Patrícia Riva. “A expressão da proteína de transferência de colesteril éster (CETP) modula a adiposidade e a expressão de genes envolvidos em lipólise e lipogênese: Cholesteryl ester transfer protein (CETP) expression modulates adiposity and expression of genes involved in lipolysis and lipogenesis.” 2010. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314297.

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

MLA Handbook (7^th Edition):

Patrício, Patrícia Riva. “A expressão da proteína de transferência de colesteril éster (CETP) modula a adiposidade e a expressão de genes envolvidos em lipólise e lipogênese: Cholesteryl ester transfer protein (CETP) expression modulates adiposity and expression of genes involved in lipolysis and lipogenesis.” 2010. Web. 23 Jan 2021.

Vancouver:

Patrício PR. A expressão da proteína de transferência de colesteril éster (CETP) modula a adiposidade e a expressão de genes envolvidos em lipólise e lipogênese: Cholesteryl ester transfer protein (CETP) expression modulates adiposity and expression of genes involved in lipolysis and lipogenesis. [Internet] [Thesis]. Universidade Estadual de Campinas; 2010. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314297.

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

Council of Science Editors:

Patrício PR. A expressão da proteína de transferência de colesteril éster (CETP) modula a adiposidade e a expressão de genes envolvidos em lipólise e lipogênese: Cholesteryl ester transfer protein (CETP) expression modulates adiposity and expression of genes involved in lipolysis and lipogenesis. [Thesis]. Universidade Estadual de Campinas; 2010. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314297

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

Universidade Estadual de Campinas

13. Salerno, Alessandro Gonzales. Efeito da expressão da proteina de transferencia de colesteril ester (CETP) sobre o metabolismo das lipoproteinas ricas em triglicerides e adiposidade em camundongos transgenicos: Effects of cholesteryl ester transfer protein (CETP) expression on triglyceride rich lipoprotein metabolism and adiposity in transgenic mice.

Degree: 2007, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314759

► Abstract: Cholesteryl ester transfer protein (CETP) promotes the exchange between cholesteryl ester (CE) from HDL and triglycerides (TG) from TG rich lipoproteins. The overexpression of… (more)

▼ Abstract: Cholesteryl ester transfer protein (CETP) promotes the exchange between cholesteryl ester (CE) from HDL and triglycerides (TG) from TG rich lipoproteins. The overexpression of apolipoprotein (apo) CIII in transgenic mice causes hypertriglyceridemia due to decreased TG rich lipoprotein plasma removal rate. In this work we investigated whether CETP expression and apo CIII expression affect the post-prandial TG levels and diet induced visceral adipose tissue formation in genetically modified mice. Results showed that the expression of CETP lead to augmented post-prandial TG levels, similar intestinal fat absorption and hepatic TG and cholesterol secretion rates, diminished TG rich lipoproteins plasma removal rates and reduced lipoprotein lipase activity. These findings indicate that the levels of circulating CETP modulate dietary fat tolerance. Under long-term high fat diet, the expression of CETP reduced the subcutaneous adipose depot, visceral adipocyte size and plasma leptin levels of hypertriglyceridemic mice overexpressing the apo CIII. On the other hand, under low fat diet, the apo CIII transgenic mice presented visceral and subcutaneous adipose depots similar to the wild type mice and increased body metabolic rate and mitochondrial resting respiration rates. However, under high fat diet, the apo CIII transgenic mice showed increased visceral and subcutaneous adipose tissue, visceral adipocyte size and plasma leptin levels and no differences in body energy dissipation (rectal temperature and mitochondrial resting respiration). In conclusion, the elevation of plasma apo CIII levels aggravates diet-induced obesity and the expression of physiological levels of circulating CETP reverses this adipogenic effect, indicating a novel role for CETP in modulating adiposity 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), Seelaender, Marilia Cerqueira Leite (committee member), Castilho, Lucia Nassi (committee member), Brito, Alba Regina Monteiro Souza (committee member), Areas, Miguel Arcanjo (committee member).

Subjects/Keywords: Proteínas de transferência de ésteres de colesterol; Adiposidade; Camundongos transgênicos; Triglicérides; Lipoproteinas; Cholesterol ester transfer proteins; Triglycerides; Transgenic mice; Adiposity; CETP; Lipoproteins

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

APA (6^th Edition):

Salerno, A. G. (2007). Efeito da expressão da proteina de transferencia de colesteril ester (CETP) sobre o metabolismo das lipoproteinas ricas em triglicerides e adiposidade em camundongos transgenicos: Effects of cholesteryl ester transfer protein (CETP) expression on triglyceride rich lipoprotein metabolism and adiposity in transgenic mice. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/314759

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):

Salerno, Alessandro Gonzales. “Efeito da expressão da proteina de transferencia de colesteril ester (CETP) sobre o metabolismo das lipoproteinas ricas em triglicerides e adiposidade em camundongos transgenicos: Effects of cholesteryl ester transfer protein (CETP) expression on triglyceride rich lipoprotein metabolism and adiposity in transgenic mice.” 2007. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314759.

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

MLA Handbook (7^th Edition):

Salerno, Alessandro Gonzales. “Efeito da expressão da proteina de transferencia de colesteril ester (CETP) sobre o metabolismo das lipoproteinas ricas em triglicerides e adiposidade em camundongos transgenicos: Effects of cholesteryl ester transfer protein (CETP) expression on triglyceride rich lipoprotein metabolism and adiposity in transgenic mice.” 2007. Web. 23 Jan 2021.

Vancouver:

Salerno AG. Efeito da expressão da proteina de transferencia de colesteril ester (CETP) sobre o metabolismo das lipoproteinas ricas em triglicerides e adiposidade em camundongos transgenicos: Effects of cholesteryl ester transfer protein (CETP) expression on triglyceride rich lipoprotein metabolism and adiposity in transgenic mice. [Internet] [Thesis]. Universidade Estadual de Campinas; 2007. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314759.

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

Council of Science Editors:

Salerno AG. Efeito da expressão da proteina de transferencia de colesteril ester (CETP) sobre o metabolismo das lipoproteinas ricas em triglicerides e adiposidade em camundongos transgenicos: Effects of cholesteryl ester transfer protein (CETP) expression on triglyceride rich lipoprotein metabolism and adiposity in transgenic mice. [Thesis]. Universidade Estadual de Campinas; 2007. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314759

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

Universidade Estadual de Campinas

14. Alberici, Luciane Carla. Camundongos hiperlipidemicos transgenicos para a apolipoproteina-III tem aumento de catabolismo corporal e atividade do canal mitocondrial de 'K POT.+' sensivel a ATP: Hyperlipidemic mice present enhance catabolism and higher mitochondrial ATP-sensitive K+ channel activity.

Degree: 2006, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/313574

► Abstract: Changes in mitochondrial energy metabolism promoted by uncoupling proteins (UCPs) are often found in metabolic disorders. We have recently shown that hypertriglyceridemic (HTG) mice… (more)

▼ Abstract: Changes in mitochondrial energy metabolism promoted by uncoupling proteins (UCPs) are often found in metabolic disorders. We have recently shown that hypertriglyceridemic (HTG) mice present higher mitochondrial resting respiration unrelated to UCPs. Here, we disclose the underlying mechanism and consequences, in tissue and whole body metabolism, of this mitochondrial response to hyperlipidemia. Results: As observed in HTG mice, liver mitochondria from animals submitted to the rich energy diets presented high resting respiration. Mitochondria isolated from the livers and spleen mononuclear cells of HTG mice presented enhanced respiratory rates compared to those from wild-type mice. Changes in oxygen consumption of liver mitochondria from HTG mice were sensitive to ATP, diazoxide and 5-hydroxydecanoate (5-HD), indicating they can be attributable to mitochondrial ATP-sensitive K+ channel (mitoKATP) activity. Indeed, mitochondria from HTG mice presented enhanced swelling in the presence of K+ ions, sensitive to mitoKATP agonists and antagonists. Furthermore, mitochondrial binding to fluorescent glibenclamide indicates that HTG mice expressed higher quantities of sulfonylurea receptors, a component of mitoKATP. An overall faster metabolic state was evidenced by increased liver oxygen consumption (sensitive to acute in vivo 5-HD administration), higher body CO2 release and temperature in these mice. In agreement with higher metabolic rates, food ingestion was significantly larger in HTG mice, without enhanced weight gain. Liver mitochondria isolated from rats fed glucose rich diet or from mice fed fat rich diet also presented higher resting respiration rates. Conclusions: These results demonstrate that primary hyperlipidemia leads to an elevation in liver mitoKATP activity, which may represent a regulated adaptation to oxidize excess fatty acids in HTG mice. Furthermore, our data indicate that mitoKATP, in addition to UCPs, may be involved in the control of energy metabolism and body weight Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Vercesi, Anibal Eugenio, 1946- (advisor), Oliveira, Helena Coutinho Franco de, 1958- (coadvisor), Universidade Estadual de Campinas. Faculdade de Ciências Médicas (institution), Programa de Pós-Graduação em Ciências Médicas (nameofprogram), Netto, Luis Eduardo Soares (committee member), Filho, Antonio Galina (committee member), Saad, Mario José Abdalla (committee member), Carvalheira, José Barreto Campello (committee member).

Subjects/Keywords: Mitocôndria; Metabolismo energético; Dislipidemias; Camundongos transgênicos; Mitochondria; Energy metabolism; Dyslipidemias; Mice transgenic

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

APA (6^th Edition):

Alberici, L. C. (2006). Camundongos hiperlipidemicos transgenicos para a apolipoproteina-III tem aumento de catabolismo corporal e atividade do canal mitocondrial de 'K POT.+' sensivel a ATP: Hyperlipidemic mice present enhance catabolism and higher mitochondrial ATP-sensitive K+ channel activity. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/313574

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):

Alberici, Luciane Carla. “Camundongos hiperlipidemicos transgenicos para a apolipoproteina-III tem aumento de catabolismo corporal e atividade do canal mitocondrial de 'K POT.+' sensivel a ATP: Hyperlipidemic mice present enhance catabolism and higher mitochondrial ATP-sensitive K+ channel activity.” 2006. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/313574.

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

MLA Handbook (7^th Edition):

Alberici, Luciane Carla. “Camundongos hiperlipidemicos transgenicos para a apolipoproteina-III tem aumento de catabolismo corporal e atividade do canal mitocondrial de 'K POT.+' sensivel a ATP: Hyperlipidemic mice present enhance catabolism and higher mitochondrial ATP-sensitive K+ channel activity.” 2006. Web. 23 Jan 2021.

Vancouver:

Alberici LC. Camundongos hiperlipidemicos transgenicos para a apolipoproteina-III tem aumento de catabolismo corporal e atividade do canal mitocondrial de 'K POT.+' sensivel a ATP: Hyperlipidemic mice present enhance catabolism and higher mitochondrial ATP-sensitive K+ channel activity. [Internet] [Thesis]. Universidade Estadual de Campinas; 2006. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/313574.

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

Council of Science Editors:

Alberici LC. Camundongos hiperlipidemicos transgenicos para a apolipoproteina-III tem aumento de catabolismo corporal e atividade do canal mitocondrial de 'K POT.+' sensivel a ATP: Hyperlipidemic mice present enhance catabolism and higher mitochondrial ATP-sensitive K+ channel activity. [Thesis]. Universidade Estadual de Campinas; 2006. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/313574

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

Universidade Estadual de Campinas

15. Bonfleur, Maria Lúcia. Efeito da hipercolesterolemia genetica sobre a homeostase glicemica e secreção de insulina em camundongos knockout para o recptor de LDL ('LDLR POT. -/-'): Effects ot genetic hypercholesterolemia on the glycemic homeostasis and insulin secretion in LDL recptor knockout mice ('LDLR POT. -/-').

Degree: 2007, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314760

► Abstract: In this work, we investigated whether primary hyperlipidemia per se, independently of a high-fat diet, affects glycemia and insulin secretion stimulated by several secretagogues… (more)

▼ Abstract: In this work, we investigated whether primary hyperlipidemia per se, independently of a high-fat diet, affects glycemia and insulin secretion stimulated by several secretagogues in hypercholesterolemic low-density lipoprotein receptor knockout mice (LDLR-/-). In addition, we investigated the possible mechanisms involved in the release of this hormone. We found that, besides higher total cholesterol and triglyceride plasma concentrations, glucose plasma levels were increased and insulin decreased in LDLR-/- compared to the wild type (WT) mice. LDLR-/- mice presented impaired glucose tolerance, but normal whole body insulin sensitivity. In addition, we also demonstrate that the main cause of the impaired glucose homeostasis is a reduced pancreatic islet insulin secretion ability following fuel secretagogue stimuli. LDLR-/- mice have impaired insulin secretion in response to glucose without alterations in the pancreatic total insulin and DNA contents. These findings support the idea that the decreased response to glucose cannot be explained by differences islet size or number of beta cells, but it is probably caused by a defect in the secretory process. Glucose oxidation was 30% lower and L-leucine oxidation 60% higher in LDLR-/- islets than in WT islets. At basal (2.8 mmol/l) and stimulatory (11.1 mmol/l) glucose concentrations, the insulin secretion rates induced by depolarizing agents such as KCl, L-arginine and tolbutamide were significantly reduced in LDLR-/- when compared with WT islets. Insulin secretion induced by the PKA activators, forskolin and IBMX, in the presence of 11.1 mmol/l glucose, was lower in LDLR-/- islets, and it was normalized in the presence of the PKC pathway activators, carbachol and PMA. Western blotting analysis showed that phospholipase C-b2 expression was increased and PKA-a decreased in LDLR-/- compared with WT islets. In conclusion, we demonstrate that genetic hypercholesterolemia, due to complete deficiency of LDLR, impairs the beta cell insulin secretion, leading to hyperglycemia without affecting body insulin sensitivity. The lower insulin secretion in LDLR-/- mice islets may be explained by reduced glucose metabolism and expression of PKA Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Oliveira, Helena Coutinho Franco de, 1958- (advisor), Boschiero, Antonio Carlos, 1943- (coadvisor), Universidade Estadual de Campinas. Instituto de Biologia (institution), Programa de Pós-Graduação em Biologia Funcional e Molecular (nameofprogram), Mathias, Paulo Cezar de Freitas (committee member), Carvalho, Carla Roberta de Oliveira (committee member), Torsoni, Marcio Alberto (committee member), Carvalheira, José Barreto Campello (committee member).

Subjects/Keywords: Insulina - Secreção; Hipercolesterolemia; Receptores LDL; Insulin - Secretion; Hypercholesterolemia; LDL receptors

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

APA (6^th Edition):

Bonfleur, M. L. (2007). Efeito da hipercolesterolemia genetica sobre a homeostase glicemica e secreção de insulina em camundongos knockout para o recptor de LDL ('LDLR POT. -/-'): Effects ot genetic hypercholesterolemia on the glycemic homeostasis and insulin secretion in LDL recptor knockout mice ('LDLR POT. -/-'). (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/314760

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):

Bonfleur, Maria Lúcia. “Efeito da hipercolesterolemia genetica sobre a homeostase glicemica e secreção de insulina em camundongos knockout para o recptor de LDL ('LDLR POT. -/-'): Effects ot genetic hypercholesterolemia on the glycemic homeostasis and insulin secretion in LDL recptor knockout mice ('LDLR POT. -/-').” 2007. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314760.

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

MLA Handbook (7^th Edition):

Bonfleur, Maria Lúcia. “Efeito da hipercolesterolemia genetica sobre a homeostase glicemica e secreção de insulina em camundongos knockout para o recptor de LDL ('LDLR POT. -/-'): Effects ot genetic hypercholesterolemia on the glycemic homeostasis and insulin secretion in LDL recptor knockout mice ('LDLR POT. -/-').” 2007. Web. 23 Jan 2021.

Vancouver:

Bonfleur ML. Efeito da hipercolesterolemia genetica sobre a homeostase glicemica e secreção de insulina em camundongos knockout para o recptor de LDL ('LDLR POT. -/-'): Effects ot genetic hypercholesterolemia on the glycemic homeostasis and insulin secretion in LDL recptor knockout mice ('LDLR POT. -/-'). [Internet] [Thesis]. Universidade Estadual de Campinas; 2007. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314760.

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

Council of Science Editors:

Bonfleur ML. Efeito da hipercolesterolemia genetica sobre a homeostase glicemica e secreção de insulina em camundongos knockout para o recptor de LDL ('LDLR POT. -/-'): Effects ot genetic hypercholesterolemia on the glycemic homeostasis and insulin secretion in LDL recptor knockout mice ('LDLR POT. -/-'). [Thesis]. Universidade Estadual de Campinas; 2007. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314760

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

Universidade Estadual de Campinas

16. Casquero, Andrea Camargo. Efeitos de hormonios sexuais masculinos sobre o metabolismo das lipoproteinas plasmaticas e expressão da CETP em camundongos geneticamente modificados sedentarios e exercitados: Effects of male sex hormone on the plasma lipoprotein metabolism and CETP expression in sedentary and trained genetically modified mice.

Degree: 2005, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314302

► Abstract: Gender differences in lipoprotein profile and atherosclerotic disease risk are generally attributed to an attenuating effect of estrogen and/or to a proatherogenic action of… (more)

▼ Abstract: Gender differences in lipoprotein profile and atherosclerotic disease risk are generally attributed to an attenuating effect of estrogen and/or to a proatherogenic action of androgens. In this work we studied the effects of dificiency and excess of testosterone on the lipoprotein metabolism and development of atherosclerosis in transgenic mice expressing CETP with or without partial deficiency of the LDL receptor. In the first study, we showed that testosterone deficiency increased the levels of plasma LDL-cholesterol, and the titers of auto-antibodies anti-oxidized LDL and doubled the size of atherosclerotic lesions in the aortic roots. CETP expression in this animal model led to a less pronounced elevation of LDL-cholesterol and reduced significantly the atherosclerotic lesion size. In the second study, we compared the effects of two types of testosterone supplementation, metabolizable or not. We showed that either type of testosterone induced significant elevations in LDL- and HDL- cholesterol. Howerver, only the metabolizable testosterone promoted an increase in the CETP and a reduction in the hepatic lipase expression. In the third work, we investigated the interaction between the effects of non metabolizable testosterone (mesterolone) and physical exercise. We observed that the physical exercise increased HDL, more potently in animals expressing CETP and without mesterolone treatment. Physical exercise also reduced the CETP activity, triglycerides and free fatty acids levels, independently of the mesterolone treatment. The treatment with mesterolone increased VLDL, independently of the genotype and physical active state, and reduced HDL in the exercised mice Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Oliveira, Helena Coutinho Franco de, 1958- (advisor), Universidade Estadual de Campinas. Instituto de Biologia (institution), Faria, Eliana Cotta de (committee member), Marcondes, Maria Cristina Cintra Gomes (committee member), Nakandakare, Edna Regina (committee member), Neto, Bruno Geloneze (committee member).

Subjects/Keywords: Testosterona; Aterosclerose; Animais transgênicos; Camundongo; Exercícios físicos; Testosterone; Atherosclerosis; Transgenic animals; Mice; Physical exercises

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

APA (6^th Edition):

Casquero, A. C. (2005). Efeitos de hormonios sexuais masculinos sobre o metabolismo das lipoproteinas plasmaticas e expressão da CETP em camundongos geneticamente modificados sedentarios e exercitados: Effects of male sex hormone on the plasma lipoprotein metabolism and CETP expression in sedentary and trained genetically modified mice. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/314302

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):

Casquero, Andrea Camargo. “Efeitos de hormonios sexuais masculinos sobre o metabolismo das lipoproteinas plasmaticas e expressão da CETP em camundongos geneticamente modificados sedentarios e exercitados: Effects of male sex hormone on the plasma lipoprotein metabolism and CETP expression in sedentary and trained genetically modified mice.” 2005. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314302.

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

MLA Handbook (7^th Edition):

Casquero, Andrea Camargo. “Efeitos de hormonios sexuais masculinos sobre o metabolismo das lipoproteinas plasmaticas e expressão da CETP em camundongos geneticamente modificados sedentarios e exercitados: Effects of male sex hormone on the plasma lipoprotein metabolism and CETP expression in sedentary and trained genetically modified mice.” 2005. Web. 23 Jan 2021.

Vancouver:

Casquero AC. Efeitos de hormonios sexuais masculinos sobre o metabolismo das lipoproteinas plasmaticas e expressão da CETP em camundongos geneticamente modificados sedentarios e exercitados: Effects of male sex hormone on the plasma lipoprotein metabolism and CETP expression in sedentary and trained genetically modified mice. [Internet] [Thesis]. Universidade Estadual de Campinas; 2005. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314302.

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

Council of Science Editors:

Casquero AC. Efeitos de hormonios sexuais masculinos sobre o metabolismo das lipoproteinas plasmaticas e expressão da CETP em camundongos geneticamente modificados sedentarios e exercitados: Effects of male sex hormone on the plasma lipoprotein metabolism and CETP expression in sedentary and trained genetically modified mice. [Thesis]. Universidade Estadual de Campinas; 2005. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314302

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

Universidade Estadual de Campinas

17. Cosso, Ricardo Guanaes. Transição de permeabilidade induzida quimicamente por oxigenio singlete em mitocondrias de figado de rato ou pelo estado oxidado de NADPH em mitocondrias isoladas de figado de camundongo hipercolesterolemico por inativação do gene do receptor de LDL.

Degree: 2003, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/310112

► Abstract: Pure singlet molecular oxygen (1O2) generated by thermal decomposition of the 3,3-(1,4-naphthylidene) dipropionate endoperoxide (NDPO2), inhibited respiration of isolated rat liver mitochondria supported by… (more)

Subjects/Keywords: Mitocôndria; Hipercolesterolemia; Oxigenio

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

APA (6^th Edition):

Cosso, R. G. (2003). Transição de permeabilidade induzida quimicamente por oxigenio singlete em mitocondrias de figado de rato ou pelo estado oxidado de NADPH em mitocondrias isoladas de figado de camundongo hipercolesterolemico por inativação do gene do receptor de LDL. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/310112

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):

Cosso, Ricardo Guanaes. “Transição de permeabilidade induzida quimicamente por oxigenio singlete em mitocondrias de figado de rato ou pelo estado oxidado de NADPH em mitocondrias isoladas de figado de camundongo hipercolesterolemico por inativação do gene do receptor de LDL.” 2003. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310112.

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

MLA Handbook (7^th Edition):

Cosso, Ricardo Guanaes. “Transição de permeabilidade induzida quimicamente por oxigenio singlete em mitocondrias de figado de rato ou pelo estado oxidado de NADPH em mitocondrias isoladas de figado de camundongo hipercolesterolemico por inativação do gene do receptor de LDL.” 2003. Web. 23 Jan 2021.

Vancouver:

Cosso RG. Transição de permeabilidade induzida quimicamente por oxigenio singlete em mitocondrias de figado de rato ou pelo estado oxidado de NADPH em mitocondrias isoladas de figado de camundongo hipercolesterolemico por inativação do gene do receptor de LDL. [Internet] [Thesis]. Universidade Estadual de Campinas; 2003. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/310112.

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

Council of Science Editors:

Cosso RG. Transição de permeabilidade induzida quimicamente por oxigenio singlete em mitocondrias de figado de rato ou pelo estado oxidado de NADPH em mitocondrias isoladas de figado de camundongo hipercolesterolemico por inativação do gene do receptor de LDL. [Thesis]. Universidade Estadual de Campinas; 2003. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/310112

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

Universidade Estadual de Campinas

18. Berti, Jairo Augusto. Estudo da relação entre a expressão da proteina de transferencia de colesteril ester, diabetes e aterosclerose em camundongos transgenicos.

Degree: 2003, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314304

► Abstract: Cholesteryl ester transfer protein (CETP) mediates cholesteryl ester and triglyceride redistribution among plasma lipoproteins. Contrasting effects of variations in CETP expression and presence of… (more)

▼ Abstract: Cholesteryl ester transfer protein (CETP) mediates cholesteryl ester and triglyceride redistribution among plasma lipoproteins. Contrasting effects of variations in CETP expression and presence of diabetes on the extension of atherosclerosis have been reported in distinct animal models and metabolic contexts. The CETP expression was studied in streptozotocin induced diabetic, in glucose fed, in glucose fed plus hyperinsulinemic and in control transgenic mice. The results showed that: 1- insulin deficiency and hyperglycemia increase CETP plasma levels and liver mRNA expression; 2- glucose supplementation increases CETP expression by post-transcriptional mechanisms; and 3- hyperinsulinemia downregulates the glucose-stimulated CETP expression by reducing its mRNA levels. In a second study, the effects of diabetes and CETP expression on the diet induced atherosclerosis in LDL receptor deficent mice were evaluated. The results showed that: 1CETP expression does not alter the responsiveness of lesion formation to diabetes, although it may be protective in euglycemic state, 2- triglyceride concentration is an independent risk factor in LDL receptor deficient mice but not in CETP expressing mice, 3- plasma cholesterollevels significantly increase the chances of developing large size atherosclerotic lesions, independently of genotype and presence of diabetes, and 4hyperglycemia contributes to the risk of atherosclerosis. In a third study, we investigated the effects of over-expressing three genes involved in the reverse cholesterol transport: apolipoprotein AI, lecithin-cholesterol acyl transferase (LCA T) and CETP on the development of diet induced atherosclerosis in aged mice. The results showed that: 1- LCA T and LCA T / AI expression impose a higher risk of developing atherosclerosis, 2- CETP expression on these backgrounds neutralizes this atherogenic scenario, and 3- isolated, apoAI overexpression reduces the chances of developing large size atherosclerotic lesions Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Oliveira, Helena Coutinho Franco de, 1958- (advisor), Universidade Estadual de Campinas. Instituto de Biologia (institution), Quintão, Eder Carlos Rocha (committee member), Hirata, Mario Hiroyuki (committee member), Castilho, Lucia Nassi (committee member), Bosqueiro, José Roberto (committee member), Areas, Miguel Arcanjo (committee member), Krieger, Marta Helena (committee member).

Subjects/Keywords: Lipoproteinas; Insulina; Aterosclerose

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

APA (6^th Edition):

Berti, J. A. (2003). Estudo da relação entre a expressão da proteina de transferencia de colesteril ester, diabetes e aterosclerose em camundongos transgenicos. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/314304

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):

Berti, Jairo Augusto. “Estudo da relação entre a expressão da proteina de transferencia de colesteril ester, diabetes e aterosclerose em camundongos transgenicos.” 2003. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314304.

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

MLA Handbook (7^th Edition):

Berti, Jairo Augusto. “Estudo da relação entre a expressão da proteina de transferencia de colesteril ester, diabetes e aterosclerose em camundongos transgenicos.” 2003. Web. 23 Jan 2021.

Vancouver:

Berti JA. Estudo da relação entre a expressão da proteina de transferencia de colesteril ester, diabetes e aterosclerose em camundongos transgenicos. [Internet] [Thesis]. Universidade Estadual de Campinas; 2003. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314304.

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

Council of Science Editors:

Berti JA. Estudo da relação entre a expressão da proteina de transferencia de colesteril ester, diabetes e aterosclerose em camundongos transgenicos. [Thesis]. Universidade Estadual de Campinas; 2003. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314304

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

Universidade Estadual de Campinas

19. Kaplan, Denise Beheregaray. Genetica da proteina de transferencia dos esteres de colesterol (CETP) na hiperalfalipoproteinemia e sua relação com a aterosclerose.

Degree: 2004, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/313572

► Abstract: There is an inverse association between the concentration of high density lipoprotein (HDL) and the risk of a coronary arterial disease (CAD). One ofthe… (more)

▼ Abstract: There is an inverse association between the concentration of high density lipoprotein (HDL) and the risk of a coronary arterial disease (CAD). One ofthe HDL anti-atherogenic properties is its participation in the reverse cholesterol transport (RCT). The cholesteryl ester transfer protein (CETP) facilitates the cholesteryl esters (CE) and triglycerides (TAG) exchange between HDL and others lipoproteins, increasing the cholesterol content of apoB lipoproteins. Mutations and polymorphisms of the CETP gene were detected in several populations, especially among Asiatic. In spite of a lower activity of the CETP and an increase of the HDL-C leveI in hyperalphalipoproteinemia (HALP), there are some doubts in regard to the prevalence ofthe cardiovascular disease (CVD) in these population groups. The aim of this work was to evaluate the prevalence of HALP and its relationship to the presence ofmutations and polymorphisms ofthe CETP gene, in a Brazilian population, and its relation with the arteriosclerosis.We determined lipid, lipoproteins, metabolic plasmatic parameters and markers of CVD, in a population of 291 to 294 HALP individuaIs (HDL-C 2: 68mg/dl) and 139 controls (HDL-C < 68mg/dl). The prevalence of the mutations Int14A and D442G, and the polymorphisms TaqIB and 1405V, was investigated by molecular methods. The presence of atherosclerosis in those patients with mutations and polymorphisms and in controls, was evaluated by clínical analyzes and measurements of the arterial intima-media thickness (IMT) by ultrasound method was performed. HDL-C was 1.5 higher in the HALP when compared to controls. A very low prevalence equal to 0.7% was found for D442G mutations, lower than in the Asiatic and Japanese population, and 4% for Int14A mutations, higher than the one described in the Caucasians. On HALP, the activities of lipoprotein lipase (LPL) and phospholipid transfer protein (PLTP) were higher and activities of CETP and hepatic lipase (HL) were lower than in controls. The seven mutants presented similar tendencies. The homozygous Int14A, showed indetectable activity of CETP and a reduction of HL, besides very high values of HDL-C. The BIB2 TaqIB genotype presented a :&equencyequal to 45%, and the IV I405V to 49%. Comparing all genotypes, B2B2 TaqIB presented higher IMT, lower autoantibodies against oxidized low density lipoprotein (LDLox) and lower CETP activity. The II I405V showed a highest CETP activity and a lowest HDL-C value. The lipoproteins, lipids and apolipoproteins were equal among all genotypes, as well as activities of LPL, HL and PLTP. The HALP phenotype was characterized by lower CETP and HL activities and higher LPL and PLTP activities when compared with controls but with no association with mutations or polymorphisms studied. It is possible that the low :&equencyof CETP mutations made impossible this statistic association. Perhaps other mutations, like in HL gene, could explain this phenotype. The HALP mutants did not show a difference in c1inical atherosc1erosis and IMT as compared with… Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Faria, Eliana Cotta de, 1950- (advisor), Oliveira, Helena Coutinho Franco de, 1958- (coadvisor), Universidade Estadual de Campinas. Faculdade de Ciências Médicas (institution), Programa de Pós-Graduação em Ciências Médicas (nameofprogram), Hirata, Mario (committee member), Passarelli, Marisa (committee member), Assumpção, Ligia Vera Montali da (committee member), Castilho, Lucia Nassi (committee member).

Subjects/Keywords: Proteinas de transporte; Genética; Aterosclerose

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

APA (6^th Edition):

Kaplan, D. B. (2004). Genetica da proteina de transferencia dos esteres de colesterol (CETP) na hiperalfalipoproteinemia e sua relação com a aterosclerose. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/313572

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):

Kaplan, Denise Beheregaray. “Genetica da proteina de transferencia dos esteres de colesterol (CETP) na hiperalfalipoproteinemia e sua relação com a aterosclerose.” 2004. Thesis, Universidade Estadual de Campinas. Accessed January 23, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/313572.

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

MLA Handbook (7^th Edition):

Kaplan, Denise Beheregaray. “Genetica da proteina de transferencia dos esteres de colesterol (CETP) na hiperalfalipoproteinemia e sua relação com a aterosclerose.” 2004. Web. 23 Jan 2021.

Vancouver:

Kaplan DB. Genetica da proteina de transferencia dos esteres de colesterol (CETP) na hiperalfalipoproteinemia e sua relação com a aterosclerose. [Internet] [Thesis]. Universidade Estadual de Campinas; 2004. [cited 2021 Jan 23]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/313572.

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

Council of Science Editors:

Kaplan DB. Genetica da proteina de transferencia dos esteres de colesterol (CETP) na hiperalfalipoproteinemia e sua relação com a aterosclerose. [Thesis]. Universidade Estadual de Campinas; 2004. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/313572

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

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