subject:(Steatosis)

University of Florida

1. Kim, Min Hyun. Regulation and Function of Zinc and Zinc Transporters during ER Stress.

Degree: PhD, Nutritional Sciences, 2017, University of Florida

► Extensive endoplasmic reticulum (ER) stress damages the liver causing apoptosis and steatosis, despite the activation of the unfolded protein response (UPR). Restriction of zinc from… (more)

▼ Extensive endoplasmic reticulum (ER) stress damages the liver causing apoptosis and steatosis, despite the activation of the unfolded protein response (UPR). Restriction of zinc from cells can induce ER stress, indicating zinc is essential to maintain normal ER function. Zinc transporter ZIP14 (SLC39A14) is abundantly expressed in liver. ZIP14 transports extracellular and organellar zinc into the cytosol of cells. We found ZIP14 expression was highly increased in mouse liver after administration with tunicamycin (TM), a potent ER stress inducer. However, the precise roles of zinc and/or ZIP14 in the UPR are unclear. This project has explored a role for ZIP14 during induced ER stress using Zip14-/- (KO) mice, which exhibit impaired hepatic zinc uptake. Major finding of the project is that ZIP14-mediated hepatic zinc uptake is critical for adaptation to ER stress by preventing sustained apoptosis and steatosis. Impaired hepatic zinc uptake in Zip14 KO mice during ER stress coincides with greater expression of pro-apoptotic proteins in the UPR pathway. In addition, ER stress-induced Zip14 KO mice show greater levels of hepatic steatosis due to higher expression of genes involved in de novo fatty acid synthesis, which are suppressed in ER stress-induced wild type (WT) mice. During ER stress, the UPR-activated transcription factors, activating transcription factor 4 (ATF4) and activating transcription factor 6 alpha (ATF6 alpha), transcriptionally up-regulate Zip14 expression. Mechanistically, ZIP14 mediates zinc transport into hepatocytes to inhibit protein-tyrosine phosphatase 1B (PTP1B) activity, which acts to suppress apoptosis and steatosis associated with hepatic ER stress. Zip14 KO mice show greater hepatic PTP1B activity during ER stress. Furthermore, WT mice were fed different levels of zinc to examine the importance of dietary zinc intake on the adaptation to TM-induced ER stress. Mice fed zinc deficient diet exhibit increased hepatic apoptosis and steatosis during TM-challenge, which coincides with greater PTP1B activity. These results show the importance of zinc trafficking and functional ZIP14 transporter activity for adaptation to ER stress. ( en ) Advisors/Committee Members: COUSINS,ROBERT J (committee chair), LEEUWENBURGH,CHRISTIAAN (committee member), DRIVER,JOHN P (committee member).

Subjects/Keywords: apoptosis – steatosis – upr – zinc – zip14

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APA (6^th Edition):

Kim, M. H. (2017). Regulation and Function of Zinc and Zinc Transporters during ER Stress. (Doctoral Dissertation). University of Florida. Retrieved from https://ufdc.ufl.edu/UFE0051263

Chicago Manual of Style (16^th Edition):

Kim, Min Hyun. “Regulation and Function of Zinc and Zinc Transporters during ER Stress.” 2017. Doctoral Dissertation, University of Florida. Accessed January 26, 2021. https://ufdc.ufl.edu/UFE0051263.

MLA Handbook (7^th Edition):

Kim, Min Hyun. “Regulation and Function of Zinc and Zinc Transporters during ER Stress.” 2017. Web. 26 Jan 2021.

Vancouver:

Kim MH. Regulation and Function of Zinc and Zinc Transporters during ER Stress. [Internet] [Doctoral dissertation]. University of Florida; 2017. [cited 2021 Jan 26]. Available from: https://ufdc.ufl.edu/UFE0051263.

Council of Science Editors:

Kim MH. Regulation and Function of Zinc and Zinc Transporters during ER Stress. [Doctoral Dissertation]. University of Florida; 2017. Available from: https://ufdc.ufl.edu/UFE0051263

2. Hendrikx, T. Intracellular traffic jam : cholesterol accumulation as cause for chronic inflammatory diseases.

Degree: 2015, Maastricht University

URL: https://cris.maastrichtuniversity.nl/en/publications/418fc04e-a720-4470-92a8-da5b284bd821 ; urn:nbn:nl:ui:27-418fc04e-a720-4470-92a8-da5b284bd821 ; 418fc04e-a720-4470-92a8-da5b284bd821 ; urn:isbn:9789462950603 ; urn:nbn:nl:ui:27-418fc04e-a720-4470-92a8-da5b284bd821 ; https://cris.maastrichtuniversity.nl/en/publications/418fc04e-a720-4470-92a8-da5b284bd821

► A rise in obesity has brought with it a rise in the incidences of fatty liver disease. Some people go on to develop liver inflammation,… (more)

Subjects/Keywords: hepatitis; steatosis; macrophages

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APA (6^th Edition):

Hendrikx, T. (2015). Intracellular traffic jam : cholesterol accumulation as cause for chronic inflammatory diseases. (Doctoral Dissertation). Maastricht University. Retrieved from https://cris.maastrichtuniversity.nl/en/publications/418fc04e-a720-4470-92a8-da5b284bd821 ; urn:nbn:nl:ui:27-418fc04e-a720-4470-92a8-da5b284bd821 ; 418fc04e-a720-4470-92a8-da5b284bd821 ; urn:isbn:9789462950603 ; urn:nbn:nl:ui:27-418fc04e-a720-4470-92a8-da5b284bd821 ; https://cris.maastrichtuniversity.nl/en/publications/418fc04e-a720-4470-92a8-da5b284bd821

Chicago Manual of Style (16^th Edition):

Hendrikx, T. “Intracellular traffic jam : cholesterol accumulation as cause for chronic inflammatory diseases.” 2015. Doctoral Dissertation, Maastricht University. Accessed January 26, 2021. https://cris.maastrichtuniversity.nl/en/publications/418fc04e-a720-4470-92a8-da5b284bd821 ; urn:nbn:nl:ui:27-418fc04e-a720-4470-92a8-da5b284bd821 ; 418fc04e-a720-4470-92a8-da5b284bd821 ; urn:isbn:9789462950603 ; urn:nbn:nl:ui:27-418fc04e-a720-4470-92a8-da5b284bd821 ; https://cris.maastrichtuniversity.nl/en/publications/418fc04e-a720-4470-92a8-da5b284bd821.

MLA Handbook (7^th Edition):

Hendrikx, T. “Intracellular traffic jam : cholesterol accumulation as cause for chronic inflammatory diseases.” 2015. Web. 26 Jan 2021.

Vancouver:

Hendrikx T. Intracellular traffic jam : cholesterol accumulation as cause for chronic inflammatory diseases. [Internet] [Doctoral dissertation]. Maastricht University; 2015. [cited 2021 Jan 26]. Available from: https://cris.maastrichtuniversity.nl/en/publications/418fc04e-a720-4470-92a8-da5b284bd821 ; urn:nbn:nl:ui:27-418fc04e-a720-4470-92a8-da5b284bd821 ; 418fc04e-a720-4470-92a8-da5b284bd821 ; urn:isbn:9789462950603 ; urn:nbn:nl:ui:27-418fc04e-a720-4470-92a8-da5b284bd821 ; https://cris.maastrichtuniversity.nl/en/publications/418fc04e-a720-4470-92a8-da5b284bd821.

Council of Science Editors:

Hendrikx T. Intracellular traffic jam : cholesterol accumulation as cause for chronic inflammatory diseases. [Doctoral Dissertation]. Maastricht University; 2015. Available from: https://cris.maastrichtuniversity.nl/en/publications/418fc04e-a720-4470-92a8-da5b284bd821 ; urn:nbn:nl:ui:27-418fc04e-a720-4470-92a8-da5b284bd821 ; 418fc04e-a720-4470-92a8-da5b284bd821 ; urn:isbn:9789462950603 ; urn:nbn:nl:ui:27-418fc04e-a720-4470-92a8-da5b284bd821 ; https://cris.maastrichtuniversity.nl/en/publications/418fc04e-a720-4470-92a8-da5b284bd821

Université Paris-Sud – Paris XI

3. Degli Esposti, Davide. Les mécanismes de réponse à l'inflammation chronique dans le foie stéatosique et les conséquences sur l'homéostasie cellulaire et la cancérogénèse : Response mechanisms to chronic inflammation in steatotic liver and consequences on cellular homeostasy and carcinogenesis.

Degree: Docteur es, Physiopathologie moléculaire et cellulaire, 2011, Université Paris-Sud – Paris XI

URL: http://www.theses.fr/2011PA114809

► Le foie est un organe essentiel à la vie chez tous les mammifères. C’est un organe central du métabolisme énergétique et de la détoxification des… (more)

▼ Le foie est un organe essentiel à la vie chez tous les mammifères. C’est un organe central du métabolisme énergétique et de la détoxification des substances xénobiotiques auxquelles l’individu est exposé. Le foie est la cible d’agressions diverses, telles que les virus, l’alcool, les substances chimiques présentes dans l’alimentation ou l’environnement. Il peut également subir destransformations pathologiques profondes, lors du diabète ou de l’obésité par exemple.La stéatose hépatique, caractérisée par une accumulation de triglycérides sous forme de vésiculesgénérant une réponse inflammatoire, est connue depuis de nombreuses années. Son étude a permisde définir un modèle en deux étapes (« two hits ») indispensables à la genèse d’une stéatohépatite ou NASH. La première est l’accumulation de lipides, la seconde consiste en la genèse d’un stress oxydant et la libération de cytokines. La NASH est une des conséquences pathologiques du syndrome métabolique au cours duquel une résistance des tissus à l’insuline se développe.Récemment, la composition des lipides accumulés dans la NASH a été décrite et montre la présence de cholestérol libre et de différents métabolites des acides gras dont la toxicité est grande mais variable. De façon surprenante, une nouvelle hypothèse tend à émerger quant aux rôles protecteurs de certaines catégories de lipides. En effet, le stockage des triglycérides sous forme de vésicules pourrait être un mécanisme de survie cellulaire (Neuschwander-Tetri, 2010). Il s’agirait principalement d’une tolérance à la mort cellulaire par nécrose ou apoptose. Dans ce contexte,l’activation de l’autophagie serait capitale et la nécrose ne serait plus un mécanisme non contrôlé,mais au contraire un système finement régulé.Des données expérimentales récentes suggèrent l’existence d’un réseau complexe d’interactions moléculaires qui lient, dans la NASH comme dans le cas de la cancérogenèse, le métabolisme énergétique, la réponse inflammatoire systémique et tissulaire et des altérations subcellulaires, telles que les lésions des mitochondries et du réticulum endoplasmique.Nous avons utilisé le cas particulier du préconditionnement ischémique, une technique chirurgicale qui consiste, grâce à de courtes périodes d’occlusion vasculaire avant l’ischémie, à conférer au tissu une protection contre les lésions d’ischémie/reperfusion (I/R), pour étudier les mécanismes de survie mis en place par les hépatocytes stéatosiques au cours d’un stress d’I/R. Dans deux contextes différents, celui d’une ischémie chaude au cours d’une hépatectomie partielle et celui d’une ischémie froide au cours de la transplantation hépatique, nous avons montré que l’autophagie peut jouer un rôle central dans la protection des hépatocytes stéatosiques. Cependant, il est envisageable qu’un dysfonctionnement de l’autophagie pourrait conduire à la genèse d’altérations cellulaires comme une instabilité génomique, caractéristique de la transformation cancéreuse. L’équilibre entre la survie et la mort cellulaire dépend donc de l’intégration de cette… Advisors/Committee Members: Poüs, Christian (thesis director), Lemoine, Antoinette (thesis director).

Subjects/Keywords: Autophagie; Steatosis; Autophagy; Hepatocellular carcinoma; Cancer; Liver

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APA (6^th Edition):

Degli Esposti, D. (2011). Les mécanismes de réponse à l'inflammation chronique dans le foie stéatosique et les conséquences sur l'homéostasie cellulaire et la cancérogénèse : Response mechanisms to chronic inflammation in steatotic liver and consequences on cellular homeostasy and carcinogenesis. (Doctoral Dissertation). Université Paris-Sud – Paris XI. Retrieved from http://www.theses.fr/2011PA114809

Chicago Manual of Style (16^th Edition):

Degli Esposti, Davide. “Les mécanismes de réponse à l'inflammation chronique dans le foie stéatosique et les conséquences sur l'homéostasie cellulaire et la cancérogénèse : Response mechanisms to chronic inflammation in steatotic liver and consequences on cellular homeostasy and carcinogenesis.” 2011. Doctoral Dissertation, Université Paris-Sud – Paris XI. Accessed January 26, 2021. http://www.theses.fr/2011PA114809.

MLA Handbook (7^th Edition):

Degli Esposti, Davide. “Les mécanismes de réponse à l'inflammation chronique dans le foie stéatosique et les conséquences sur l'homéostasie cellulaire et la cancérogénèse : Response mechanisms to chronic inflammation in steatotic liver and consequences on cellular homeostasy and carcinogenesis.” 2011. Web. 26 Jan 2021.

Vancouver:

Degli Esposti D. Les mécanismes de réponse à l'inflammation chronique dans le foie stéatosique et les conséquences sur l'homéostasie cellulaire et la cancérogénèse : Response mechanisms to chronic inflammation in steatotic liver and consequences on cellular homeostasy and carcinogenesis. [Internet] [Doctoral dissertation]. Université Paris-Sud – Paris XI; 2011. [cited 2021 Jan 26]. Available from: http://www.theses.fr/2011PA114809.

Council of Science Editors:

Degli Esposti D. Les mécanismes de réponse à l'inflammation chronique dans le foie stéatosique et les conséquences sur l'homéostasie cellulaire et la cancérogénèse : Response mechanisms to chronic inflammation in steatotic liver and consequences on cellular homeostasy and carcinogenesis. [Doctoral Dissertation]. Université Paris-Sud – Paris XI; 2011. Available from: http://www.theses.fr/2011PA114809

University of Adelaide

4. Tse, Edmund. Improving treatment predictors of HCV therapy and the impact of steatosis on the hepatocyte transcriptome and anti-HCV action of interferon.

Degree: 2015, University of Adelaide

URL: http://hdl.handle.net/2440/100718

► Hepatitis C Virus (HCV) is a significant global health issue that leads to the development of chronic liver inflammation, and subsequent establishment of cirrhosis and… (more)

▼ Hepatitis C Virus (HCV) is a significant global health issue that leads to the development of chronic liver inflammation, and subsequent establishment of cirrhosis and hepatocellular carcinoma (HCC). Previously the standard therapy of chronic hepatitis C (CHC) was pegylated interferon α (IFN-α) and ribavirin, which had poor treatment success rates and was associated with significant side effects. Risk factors that have been shown to be associated with treatment failure include excess alcohol consumption, advanced age, diabetes and obesity. Although these negative predictors of treatment outcome have been well established in clinical practice, little is known regarding the molecular mechanism(s) of treatment failure. Obesity is another major health issue which is associated with numerous deleterious health issues, one of which being steatosis, or non-alcoholic fatty liver disease (NAFLD). NAFLD can progress to necroinflammation of the liver or non-alcoholic steatohepatitis (NASH), leading to fibrosis and development of cirrhosis. Given how common obesity is, clinicians are commonly faced with managing patients with CHC and concurrent steatosis. Understanding the molecular mechanism(s) of interferonbased treatment failure in patients with CHC with concurrent steatosis, may allow adjuvant therapy to be targeted to those with negative predictors of treatment outcome, thus resulting in an improved virological response. In this thesis, an in vitro model of steatosis has been adopted to investigate the effect of lipid loading on gene expression, in particular, interferon-stimulated genes (ISGs). Two different free fatty acids, oleic acid and palmitic acid, were used to induce steatosis in the Huh-7 hepatoma cell line. In this thesis, it was shown that steatosis was associated with a marked alteration of gene expression, some of which interestingly were classical ISGs. This was likely due to TLR2 mediated pathways, leading to subsequent downstream NF-κβ activation and gene expression. Through induction of steatosis by oleic and palmitic acid, it was also shown that Huh- 7 cells can accentuate the effect of interferon stimulation, leading to an increased ISG expression, which is believed to be secondary to the increase in STAT1 phosphorylation. Finally the effect of steatosis-induced ISG expression on HCV replication, as well as the responsiveness to IFN-α treatment, was investigated. Surprisingly, it was found that steatosis alone led to a modest reduction of HCV replication, with reduced interferon sensitivity, leading to a reduction in HCV knockdown when IFN-α was used. It was shown that the combination of OA:PA, HCV replication and IFN-α stimulation resulted in a significant increase in CXCL8 protein production, a cytokine known to have anti-IFN modulating activity. Moreover, exogenous addition of CXCL8 to cultured cells abrogated the anti-HCV actions of IFN-α. This highlighted a potential mechanism for IFN failure in the HCV infected liver with concurrent steatosis. In summary, the in vitro model of steatosis has… Advisors/Committee Members: Beard, Michael Robert (advisor), School of Biological Sciences (school).

Subjects/Keywords: HCV; hepatitis C; steatosis; interferon; hepatocyte transcriptome

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APA (6^th Edition):

Tse, E. (2015). Improving treatment predictors of HCV therapy and the impact of steatosis on the hepatocyte transcriptome and anti-HCV action of interferon. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/100718

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):

Tse, Edmund. “Improving treatment predictors of HCV therapy and the impact of steatosis on the hepatocyte transcriptome and anti-HCV action of interferon.” 2015. Thesis, University of Adelaide. Accessed January 26, 2021. http://hdl.handle.net/2440/100718.

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

MLA Handbook (7^th Edition):

Tse, Edmund. “Improving treatment predictors of HCV therapy and the impact of steatosis on the hepatocyte transcriptome and anti-HCV action of interferon.” 2015. Web. 26 Jan 2021.

Vancouver:

Tse E. Improving treatment predictors of HCV therapy and the impact of steatosis on the hepatocyte transcriptome and anti-HCV action of interferon. [Internet] [Thesis]. University of Adelaide; 2015. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/2440/100718.

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

Council of Science Editors:

Tse E. Improving treatment predictors of HCV therapy and the impact of steatosis on the hepatocyte transcriptome and anti-HCV action of interferon. [Thesis]. University of Adelaide; 2015. Available from: http://hdl.handle.net/2440/100718

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

Univerzitet u Beogradu

5. Ivanović, Nevena Đ., 1983-. Uticaj oralne primene Lactobacillus rhamnosus LA68 i Lactobacillus plantarum WCFS1 na imunološke i metaboličke parametre miševa u uslovima eksperimentalno indukovane nealkoholne masne jetre.

Degree: Farmaceutski fakultet, 2016, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:13471/bdef:Content/get

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Farmacija - Hemija hrane i dijetetskih proizvoda / Pharmacy - Chemistry of food and dietary products

Prema definiciji Svetske Zdravstvene Organizacije, probiotici su živi mikroorganizmi… (more)

▼

Farmacija - Hemija hrane i dijetetskih proizvoda / Pharmacy - Chemistry of food and dietary products

Prema definiciji Svetske Zdravstvene Organizacije, probiotici su živi mikroorganizmi koji kada su konzumirani u adekvatnoj količini imaju povoljne efekte na zdravlje domaćina. Pod pojmom probiotskih bakterija misli se većinom na bakterije mlečne kiseline (BMK) koje obuhvataju uglavnom vrste iz rodova Lactobacillus i Bifidobacterium. Rastući je broj dokaza koji ukazuju da primena BMK može ispoljiti povoljne efekte u tretmanu komponenata metaboličkog sindroma, kao što su gojaznost, dijabetes tip 2, dislipidemije, nealkoholna masna bolest jetre (engl. Nonalcoholic Fatty Liver Disease, NAFLD). NAFLD obuhvata čitav spektar oboljenja, počev od hepatične steatoze preko nealkoholnog steatohepatitisa do hepatične fibroze. Predstavlja najčešći uzrok ozbiljnih i hroničnih oboljenja jetre kod odraslih i kod dece u zapadnim zemljama, sa prevalencom od 20-30% u opštoj odrasloj populaciji, pri čemu prevalenca korelira sa povećanom incidencom gojaznosti i metaboličkog sindroma. Nedavno objavljena istraživanja ukazuju na ulogu crevne mikrobiote u razvoju steatoze i progresiji NAFLD-a, a s obzirom da probiotici mogu delovati na više nivoa na patogenezu oboljenja, a uz to su još i bezbedni i pristupačni, nije iznenađujuće što LAB postaju sve privlačniji kao potencijalna dugoročna terapija NAFLDa. Kliničke i eksperimentalne studije sugerišu da se probiotici značajno razlikuju u efektima i mehanizmima dejstva a razlike postoje, ne samo između različitih vrsta, već i između različitih soje iste vrste. Zbog toga je najvažniji cilj ove studije bio da se razvije model NAFLD (stadijum steatoze) ishranom visokog sadržaja masti (VSM), a zatim da se ispita i izvrši poređenje dejstva oralne primene dva različita soja BMK, Lactobacillus rhamnosus LA68 i Lactobacillus plantarum WCFS1, na imunološke i metaboličke parametre, na razvoj steatoze, kao i na sastav masnih kiselina organa kod miševa soja C57BL/6 u uslovima VSM ishrane. Nakon 16 nedelja VSM ishrane, u kojoj je 41% energije poticao od masti, kod miševa soja C57BL/6 došlo je do značajnog porasta telesne mase, i razvoja steatoze koju je pratio poremećaj lipidnih parametara i porast nivoa leptina, što odgovara početnoj fazi NAFLD (stadijum steatoze)...

Advisors/Committee Members: Đorđević, Brižita, 1962-.

Subjects/Keywords: probiotics; Lactobacillus; high fat diet; NAFLD; steatosis

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APA (6^th Edition):

Ivanović, Nevena Đ., 1. (2016). Uticaj oralne primene Lactobacillus rhamnosus LA68 i Lactobacillus plantarum WCFS1 na imunološke i metaboličke parametre miševa u uslovima eksperimentalno indukovane nealkoholne masne jetre. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:13471/bdef:Content/get

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):

Ivanović, Nevena Đ., 1983-. “Uticaj oralne primene Lactobacillus rhamnosus LA68 i Lactobacillus plantarum WCFS1 na imunološke i metaboličke parametre miševa u uslovima eksperimentalno indukovane nealkoholne masne jetre.” 2016. Thesis, Univerzitet u Beogradu. Accessed January 26, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:13471/bdef:Content/get.

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

MLA Handbook (7^th Edition):

Ivanović, Nevena Đ., 1983-. “Uticaj oralne primene Lactobacillus rhamnosus LA68 i Lactobacillus plantarum WCFS1 na imunološke i metaboličke parametre miševa u uslovima eksperimentalno indukovane nealkoholne masne jetre.” 2016. Web. 26 Jan 2021.

Vancouver:

Ivanović, Nevena Đ. 1. Uticaj oralne primene Lactobacillus rhamnosus LA68 i Lactobacillus plantarum WCFS1 na imunološke i metaboličke parametre miševa u uslovima eksperimentalno indukovane nealkoholne masne jetre. [Internet] [Thesis]. Univerzitet u Beogradu; 2016. [cited 2021 Jan 26]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:13471/bdef:Content/get.

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

Council of Science Editors:

Ivanović, Nevena Đ. 1. Uticaj oralne primene Lactobacillus rhamnosus LA68 i Lactobacillus plantarum WCFS1 na imunološke i metaboličke parametre miševa u uslovima eksperimentalno indukovane nealkoholne masne jetre. [Thesis]. Univerzitet u Beogradu; 2016. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:13471/bdef:Content/get

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

University of Minnesota

6. Bagley, Bradford. The Effect of Perfluorooctane Sulfonate (PFOS) and Choline Supplementation on Hepatic Steatosis in Sprague Dawley Rats.

Degree: PhD, Toxicology, 2017, University of Minnesota

URL: http://hdl.handle.net/11299/198403

► Perfluorooctane sulfonate (PFOS) is bioaccumulative and prevalent in the human population. PFOS induces hepatic steatosis in male rats at dietary exposures of 100 ppm via… (more)

▼ Perfluorooctane sulfonate (PFOS) is bioaccumulative and prevalent in the human population. PFOS induces hepatic steatosis in male rats at dietary exposures of 100 ppm via an unknown mechanism. In vitro, PFOS creates a choline ion complex. Choline deficiency induces hepatic steatosis in rats by decreasing VLDL secretion. The primary hypothesis was that a hepatic PFOS:choline ion complex causes steatosis that could be prevented by dietary choline supplementation. PFOS activation of steatosis related nuclear receptors (i.e., LXR, PXR, CAR, and PPAR-gamma) was investigated as a secondary hypothesis. To identify a choline dietary concentration, Sprague Dawley rats (5-6/sex/group) were fed control diet or 5X, 10X, or 15X basal choline diets for four weeks. The 5X diet was selected based on decreased body weights and body weight gains in the 10X (females only) and 15X groups. Sprague Dawley rats (12/sex/group) were fed control, choline supplemented (CS), 100 ppm PFOS, or 100 ppm PFOS + CS diets for three weeks. The male PFOS (±CS) rats developed hepatic steatosis, decreased mean serum cholesterol, and increased liver choline concentrations; the supplemented diet did not prevent hepatic steatosis. Female rats did not have these findings, even though serum and liver PFOS concentrations were similar to the males. In vitro, 400 µM PFOS did not inhibit choline kinase activity, which does not support the primary hypothesis. Regarding the secondary hypothesis, there was no activation (LXR, PXR, and CAR) or very weak activation (PPAR-gamma) by PFOS in a luciferase-linked assay. Also, liver mRNA activated by these nuclear receptors were not upregulated in rats fed PFOS. There are no clear data from this project that support the primary or secondary hypothesis. However, increased hepatic choline concentrations in the male PFOS rats correlates with the primary hypothesis. This finding and the sex-related difference in PFOS-induced hepatic steatosis warrant further investigation.

Subjects/Keywords: Choline; Liver; Perfluorooctane sulfonate; PFOS; Steatosis

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APA (6^th Edition):

Bagley, B. (2017). The Effect of Perfluorooctane Sulfonate (PFOS) and Choline Supplementation on Hepatic Steatosis in Sprague Dawley Rats. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/198403

Chicago Manual of Style (16^th Edition):

Bagley, Bradford. “The Effect of Perfluorooctane Sulfonate (PFOS) and Choline Supplementation on Hepatic Steatosis in Sprague Dawley Rats.” 2017. Doctoral Dissertation, University of Minnesota. Accessed January 26, 2021. http://hdl.handle.net/11299/198403.

MLA Handbook (7^th Edition):

Bagley, Bradford. “The Effect of Perfluorooctane Sulfonate (PFOS) and Choline Supplementation on Hepatic Steatosis in Sprague Dawley Rats.” 2017. Web. 26 Jan 2021.

Vancouver:

Bagley B. The Effect of Perfluorooctane Sulfonate (PFOS) and Choline Supplementation on Hepatic Steatosis in Sprague Dawley Rats. [Internet] [Doctoral dissertation]. University of Minnesota; 2017. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/11299/198403.

Council of Science Editors:

Bagley B. The Effect of Perfluorooctane Sulfonate (PFOS) and Choline Supplementation on Hepatic Steatosis in Sprague Dawley Rats. [Doctoral Dissertation]. University of Minnesota; 2017. Available from: http://hdl.handle.net/11299/198403

University of Sydney

7. d'Avigdor, William Mark Henry. Differential gene expression in HCV liver injury .

Degree: 2015, University of Sydney

URL: http://hdl.handle.net/2123/13896

► Chronic hepatitis C virus (HCV) infection causes liver disease that can lead to cirrhosis and hepatocellular carcinoma (HCC). The predominant HCV genotypes in Australia (G1… (more)

▼ Chronic hepatitis C virus (HCV) infection causes liver disease that can lead to cirrhosis and hepatocellular carcinoma (HCC). The predominant HCV genotypes in Australia (G1 and G3) differ in the pathogenesis of liver injury and treatment response, but the molecular mechanisms are not well defined. The aim of this research is to determine specific HCV genotype differences in the global mRNA and miRNA expression associated with HCV induced liver injury. The mRNA transcriptome and miRNA expression of HCV induced liver injury (G1 or G3) was characterised in progressive liver injury, advanced cirrhosis from individuals with and without HCC compared with non diseased liver using Illumina Whole genome BeadChip Arrays and Taqman Low Density Arrays. Further, the mRNA expression of HCV genotype-specific core chimeric JFH1 infected Huh 7 cells following lipid loading was similarly characterised. In progressive liver injury, HCV genotype is associated with the greatest variation in gene expression between individuals. There is increased expression of interferon stimulated genes, inflammation and fibrosis genes in G3, and increased expression of fatty acid degradation and cholesterol transport associated genes in G1. In advanced cirrhosis, the cirrhotic gene signature masks the genotype specific gene expression patterns. No gene signature distinguishes cirrhotic liver injury from individuals with and without HCC. The miRNA expression is associated with the severity of disease with no HCV genotype specific differences identified. The mRNA transcriptome of a hepatic cell line infected with chimeric HCV specific for the HCV core protein is consistent with the in vivo analysis with increased expression of genes associated with fibrosis and proliferation in G3, but no differences were observed in fatty acid metabolism. In conclusion, the HCV genotype specific differences in gene expression are more defined in progressive liver injury compared with changes seen in advanced cirrhosis.

Subjects/Keywords: HCV; genotype; steatosis; HCC; gene expression; miRNA

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

APA (6^th Edition):

d'Avigdor, W. M. H. (2015). Differential gene expression in HCV liver injury . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/13896

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):

d'Avigdor, William Mark Henry. “Differential gene expression in HCV liver injury .” 2015. Thesis, University of Sydney. Accessed January 26, 2021. http://hdl.handle.net/2123/13896.

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

MLA Handbook (7^th Edition):

d'Avigdor, William Mark Henry. “Differential gene expression in HCV liver injury .” 2015. Web. 26 Jan 2021.

Vancouver:

d'Avigdor WMH. Differential gene expression in HCV liver injury . [Internet] [Thesis]. University of Sydney; 2015. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/2123/13896.

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

Council of Science Editors:

d'Avigdor WMH. Differential gene expression in HCV liver injury . [Thesis]. University of Sydney; 2015. Available from: http://hdl.handle.net/2123/13896

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

8. Borges, Nádia Juliana Beraldo Goulart. Efeitos da suplementação da colina e de frutooligossacarídeos na esteatose hepática em ratos wistar.

Degree: Mestrado, Clínica Médica, 2008, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/17/17138/tde-28032012-085320/ ;

►

A Doença Hepática Gordurosa Não Alcoólica (DHGNA) é uma condição clínicopatológica comum, caracterizada por depósito de lipídeos no hepatócito do parênquima hepático. A esteatose hepática… (more)

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A Doença Hepática Gordurosa Não Alcoólica (DHGNA) é uma condição clínicopatológica comum, caracterizada por depósito de lipídeos no hepatócito do parênquima hepático. A esteatose hepática (EH) é um dos componentes da DHGNA e caracteriza-se pela presença de vacúolos de lipídeos, principalmente triacilgliceróis (triglicerídeos), dentro dos hepatócitos. Alterações na oxidação das gorduras no fígado ou redução na exportação de lipoproteínas de muito baixa densidade (VLDL) a partir do órgão são os principais mecanismos etiopatogênicos envolvidos com a EH. A patogênese da DHGNA é multifatorial e diversos fatores ou condições têm sido relacionados à predisposição para o seu desenvolvimento. Atualmente, diferentes tratamentos farmacológicos para DHGNA estão sendo propostos, mas ainda não há nenhum estudo comprobatório da sua eficácia. Objetiva-se avaliar os efeitos da suplementação da colina e do frutooligossacarídeo (FOS) na dieta de ratos Wistar, no modelo de esteatose hepática, induzido por dieta hiperglicídica. Foram utilizados 46 ratos machos, da raça Wistar adultos com peso variando entre 250 - 320 g, vindos do Biotério Central do Campus da USP Ribeirão Preto. Do lote inicial de animais foram distribuídos de forma aleatória nos diferentes grupos de estudo de I a IV, dependendo da indução ou não da esteatose. Considerou-se fase I o período correspondente a indução de esteatose e fase II quando se submeteu os animais a suplementação com nutrientes (Grupos III e IV), ou quando os animais receberam dieta padrão pós fase I (Grupo II) . Os animais do Grupo I (controle) receberam ração padrão do biotério que foi igual para todos os animais, sendo separado um lote da mesma ração para todo o experimento. Foi analisado as seguintes variáveis: Ingestão alimentar semanal, evolução do peso dos animais, nitrogênio urinário, amônia urinária, colesterol total e triacilgliceróis séricos, peso úmido de fígado e coração, nitrogênio e gordura tecidual, dosagem de vitamina E, malondialdeído (MDA) e glutationa no tecido hepático e análise histopatológica. Observamos que nenhum dos nutrientes empregados (colina e FOS) foi eficaz na redução da quantidade de gordura do fígado pela análise histológica. Nenhum dos nutrientes adicionados foi capaz de proteger o fígado da ação dos radicais livres, já que o MDA, um marcador indireto da geração do estresse oxidativo, manteve-se com valores elevados mesmo na fase de tratamento. Ocorreu diminuição dos níveis de triacilgliceróis em todos os grupos submetidos à indução de esteatose, do início ao final do experimento. O frutooligossacarídeo foi capaz de reduzir os níveis de colesterol sérico, em relação aos seus níveis basais, quando suplementado após indução de esteatose.

Non-alcoholic fatty liver disease (NAFLD) is a common clinical pathological condition characterized by fat accumulation in the the hepatic parenchyma hepatocyte. Liver steatosis (HS) is one of the components of NAFLD and is characterized by the presence of lipids vacuoles, mainly triacylglycerol, within the hepatocites. Alterations…

Advisors/Committee Members: Marchini, Julio Sérgio.

Subjects/Keywords: choline; colina; esteatose hepática; fructoologosaccharide; frutooligossacarídeo; liver steatosis

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

APA (6^th Edition):

Borges, N. J. B. G. (2008). Efeitos da suplementação da colina e de frutooligossacarídeos na esteatose hepática em ratos wistar. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/17/17138/tde-28032012-085320/ ;

Chicago Manual of Style (16^th Edition):

Borges, Nádia Juliana Beraldo Goulart. “Efeitos da suplementação da colina e de frutooligossacarídeos na esteatose hepática em ratos wistar.” 2008. Masters Thesis, University of São Paulo. Accessed January 26, 2021. http://www.teses.usp.br/teses/disponiveis/17/17138/tde-28032012-085320/ ;.

MLA Handbook (7^th Edition):

Borges, Nádia Juliana Beraldo Goulart. “Efeitos da suplementação da colina e de frutooligossacarídeos na esteatose hepática em ratos wistar.” 2008. Web. 26 Jan 2021.

Vancouver:

Borges NJBG. Efeitos da suplementação da colina e de frutooligossacarídeos na esteatose hepática em ratos wistar. [Internet] [Masters thesis]. University of São Paulo; 2008. [cited 2021 Jan 26]. Available from: http://www.teses.usp.br/teses/disponiveis/17/17138/tde-28032012-085320/ ;.

Council of Science Editors:

Borges NJBG. Efeitos da suplementação da colina e de frutooligossacarídeos na esteatose hepática em ratos wistar. [Masters Thesis]. University of São Paulo; 2008. Available from: http://www.teses.usp.br/teses/disponiveis/17/17138/tde-28032012-085320/ ;

9. Saviani, Gisele. Anatomia das vias sanguíneas e biliares e histologia do fígado de Avestruz (Struthio camelus, Linnaeus, 1758).

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

URL: http://www.teses.usp.br/teses/disponiveis/10/10132/tde-20072009-095137/ ;

►

Hoje a criação de avestruz ((Struthio camelus, Linnaeus 1758)) é uma atividade de grande potencial, porém não existem padrões definidos sobre a histologia do seu… (more)

▼

Hoje a criação de avestruz ((Struthio camelus, Linnaeus 1758)) é uma atividade de grande potencial, porém não existem padrões definidos sobre a histologia do seu fígado, que é um órgão de grande importância no metabolismo, o conhecimento de sua histologia e anatomia pode contribuir para a detecção de doenças e deficiências nutricionais que influenciam no crescimento e desenvolvimento do animal. Os objetivos desta pesquisa são: Estudar a anatomia e histologia do fígado e a ramificação de sua artéria hepática, veia porta hepática e ducto biliar. Para a realização da parte macroscópica foram utilizados quinze avestruzes com idades entre 12 e 18 meses (com peso médio em torno de 80 a 100 kg), provenientes do abatedouro Don Pig, situado próximo à cidade de Botucatu no estado de São Paulo. Os animais foram abatidos com pistola pneumática e posteriormente submetidos a sangria. Foram injetadas com látex a artéria hepática, o ducto biliar e a veia porta. O fígado dos avestruzes apresentam dois lobos (direito e esquerdo). No caso o direito é maior que o esquerdo e ambos são subdivididos em dorsal, intermédio e ventral. Além disso, amostras do fígado foram processadas para a observação em microscopia de luz e microscopia eletrônica de transmissão (MET). A hematoxilina e eosina (H.E), picrossírius, Gordon e Sweets, Sudan black e o ácido peródico de Schiff (PAS) são colorações usadas respectivamente para observar a morfologia do fígado, colágeno, fibras reticulares, gordura e glicogênio. Foram encontrados os espaços porta- hepáticos (artéria hepática, veia porta e ducto biliar e as veias centrolobulares). O glicogênio presente mostrou a média de 5,68%. O conteúdo lipídico, conferiu um aspecto goticular compatível com um quadro de esteatose hepática e a média obtida foi de 9,83%. Foi encontrado colágeno ao redor dos espaços porta-hepáticos, artérias centrolobulares e capilares sinusóides e a média foi de 14,71%. Encontrou-se também fibras reticulares ao redor dos capilares sinusóides e a média foi de 5,96%. Quanto à MET notou-se que no citoplasma dos hepatócitos desses animais existem numerosas mitocôndrias, glicogênio, muitas gotas de gordura, alguns lisossomos, retículo endoplasmático granular ao redor das mitocôndrias, algumas células estreladas, eritrócitos, núcleo, célula em degeneração e o canalículo biliar ao centro. Provavelmente o quadro sugestivo de esteatose é resultante do estado nutricional dos animais, já que nenhum outro aspecto relevante foi encontrado. Como estas aves são destinadas ao abate, sua alimentação é formulada para que os animais apresentem rápido desenvolvimento e alto ganho de peso, provavelmente com níveis de lipídios acima do necessário, causando uma deposição de micelas de gordura nos hepatócitos. Estes resultados demontraram que os hepatócitos dos avestruzes são muito simulares as outras aves apesar de também serem muito similares na estrutura das células do fígado de mamíferos.

At present the ostrich (Struthio camelus) breeding has been showing a great economical potential, although yet there…

Advisors/Committee Members: Hernandez-Blazquez, Francisco Javier.

Subjects/Keywords: Avestruzes; Colágeno; Collagen; Esteatose; Fígado; Glicogenio; Glicogênio; Liver; Ostriches; Steatosis

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

APA (6^th Edition):

Saviani, G. (2009). Anatomia das vias sanguíneas e biliares e histologia do fígado de Avestruz (Struthio camelus, Linnaeus, 1758). (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/10/10132/tde-20072009-095137/ ;

Chicago Manual of Style (16^th Edition):

Saviani, Gisele. “Anatomia das vias sanguíneas e biliares e histologia do fígado de Avestruz (Struthio camelus, Linnaeus, 1758).” 2009. Doctoral Dissertation, University of São Paulo. Accessed January 26, 2021. http://www.teses.usp.br/teses/disponiveis/10/10132/tde-20072009-095137/ ;.

MLA Handbook (7^th Edition):

Saviani, Gisele. “Anatomia das vias sanguíneas e biliares e histologia do fígado de Avestruz (Struthio camelus, Linnaeus, 1758).” 2009. Web. 26 Jan 2021.

Vancouver:

Saviani G. Anatomia das vias sanguíneas e biliares e histologia do fígado de Avestruz (Struthio camelus, Linnaeus, 1758). [Internet] [Doctoral dissertation]. University of São Paulo; 2009. [cited 2021 Jan 26]. Available from: http://www.teses.usp.br/teses/disponiveis/10/10132/tde-20072009-095137/ ;.

Council of Science Editors:

Saviani G. Anatomia das vias sanguíneas e biliares e histologia do fígado de Avestruz (Struthio camelus, Linnaeus, 1758). [Doctoral Dissertation]. University of São Paulo; 2009. Available from: http://www.teses.usp.br/teses/disponiveis/10/10132/tde-20072009-095137/ ;

University of Louisville

10. Donde, Hridgandh. Role of ethanol as a cofactor in HAART induced hepatic steatosis and injury.

Degree: MS, 2013, University of Louisville

URL: 10.18297/etd/363 ; https://ir.library.louisville.edu/etd/363

► Highly Active Antiretroviral Therapy (HAART) has led to a significant increase in the life expectancy of HIV patients; however, there are significant side effects… (more)

Subjects/Keywords: HAART; Hepatic injury; Ethanol; Steatosis; Pharmacy and Pharmaceutical Sciences

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

APA (6^th Edition):

Donde, H. (2013). Role of ethanol as a cofactor in HAART induced hepatic steatosis and injury. (Masters Thesis). University of Louisville. Retrieved from 10.18297/etd/363 ; https://ir.library.louisville.edu/etd/363

Chicago Manual of Style (16^th Edition):

Donde, Hridgandh. “Role of ethanol as a cofactor in HAART induced hepatic steatosis and injury.” 2013. Masters Thesis, University of Louisville. Accessed January 26, 2021. 10.18297/etd/363 ; https://ir.library.louisville.edu/etd/363.

MLA Handbook (7^th Edition):

Donde, Hridgandh. “Role of ethanol as a cofactor in HAART induced hepatic steatosis and injury.” 2013. Web. 26 Jan 2021.

Vancouver:

Donde H. Role of ethanol as a cofactor in HAART induced hepatic steatosis and injury. [Internet] [Masters thesis]. University of Louisville; 2013. [cited 2021 Jan 26]. Available from: 10.18297/etd/363 ; https://ir.library.louisville.edu/etd/363.

Council of Science Editors:

Donde H. Role of ethanol as a cofactor in HAART induced hepatic steatosis and injury. [Masters Thesis]. University of Louisville; 2013. Available from: 10.18297/etd/363 ; https://ir.library.louisville.edu/etd/363

11. Rafiei, Hossein 1981-. Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease.

Degree: 2017, University of Saskatchewan

URL: http://hdl.handle.net/10388/7946

► Non-alcoholic fatty liver disease (NAFLD) is a public health burden. Steatosis as the “first hit”, and oxidative stress, inflammation, mitochondrial dysfunction, and endoplasmic reticulum stress… (more)

▼ Non-alcoholic fatty liver disease (NAFLD) is a public health burden. Steatosis as the “first hit”, and oxidative stress, inflammation, mitochondrial dysfunction, and endoplasmic reticulum stress as the “second hits” are the main contributors of the progression of fatty liver to non-alcoholic steatohepatitis (NASH). Dietary polyphenols have shown promise in protecting the liver against NAFLD. The relative effectiveness and mechanisms of different polyphenols however is mostly unknown. In this thesis HepG2 hepatocytes exposed to oleic or palmitic acid were used as a model system to explore the ability of selected polyphenols (resveratrol, quercetin, catechin, cyanidin, cyanidin-3-glucoside, berberine) from different classes to protect against molecular aspects of NAFLD and NASH. In an investigation of the “first hit” (Chapter 3), different polyphenols protected similarly against oleic acid-induced intracellular lipid accumulation, but differed in their effects on the expression of genes and proteins involved in lipogenesis, fatty acid oxidation, mitochondrial biogenesis, and bioenergetics. In an investigation of “second hits” (Chapter 4), most of the polyphenols decreased reactive oxygen species (ROS), prevented the decrease in uncoupling protein 2 (UCP2) mRNA, prevented the increase in tumor necrosis factor alpha (TNFα) mRNA, reversed decreases in mitochondrial biogenesis and increased expression of mitochondrial respiratory complexes and manganese superoxide dismutase (MnSOD). The anthocyanins were unique in decreasing ROS without inducing mitochondrial biogenesis or Mn-SOD mRNA expression. In investigations with palmitic acid (Chapter 5), exposure of HepG2 cells to palmitic acid induced endoplasmic reticulum (ER) stress evidenced by upregulated mRNA for the ER chaperones glucose-regulated protein 94 and 78 (GRP94, GRP78) and oxygen-regulated protein 150 (ORP150), cochaperone endoplasmic reticulum-localized DnaJ homologue 4 (ERdj4), and proapoptotic CCAAT-enhancer-binding protein homologous protein (CHOP). A few of the polyphenols (quercetin, catechin, cyanidin) protected against these changes. In a comparison of flavonoids with their phenolic breakdown/digestion products (Chapter 6), the polyphenols 2,4,6-trihydroxybenzaldehyde, protocatechuic acid, and caffeic acid protected similarly to quercetin and cyanidin against oleic and palmitic acid-induced steatosis and ROS generation. Moreover, in a short-term 1 h exposure (to limit spontaneous degradation in the medium), only breakdown/digestion products prevented an oleic acid-induced decrease of mitochondrial biogenesis. In conclusion, different classes of dietary polyphenols were all able to protect against steatosis and ROS generation in this in vitro model of NAFLD. Part of the mechanism for some polyphenols was through effects on mitochondrial biogenesis and function, bioenergetics, and ER stress. Phenolic breakdown/digestion products of flavonoids were shown to contribute to the protective effects of parent polyphenols. Advisors/Committee Members: Bandy, Brian, Arnason, Terra, Paterson, Phyllis, Krol, Edward, Zello, Gordon.

Subjects/Keywords: Non-alcoholic fatty liver disease; Mitochondrial dysfunction; endoplasmic reticulum stress; Steatosis

10 more images…

Record Details Similar Records Cite « Share

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

APA (6^th Edition):

Rafiei, H. 1. (2017). Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/7946

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):

Rafiei, Hossein 1981-. “Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease.” 2017. Thesis, University of Saskatchewan. Accessed January 26, 2021. http://hdl.handle.net/10388/7946.

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

MLA Handbook (7^th Edition):

Rafiei, Hossein 1981-. “Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease.” 2017. Web. 26 Jan 2021.

Vancouver:

Rafiei H1. Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease. [Internet] [Thesis]. University of Saskatchewan; 2017. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10388/7946.

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

Council of Science Editors:

Rafiei H1. Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease. [Thesis]. University of Saskatchewan; 2017. Available from: http://hdl.handle.net/10388/7946

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

Penn State University

12. Huang, Kuan-Hsun. Exogenous Lipids Regulate the Development of Hepatic Steatosis in a Lean NAFLD model-fed a High Carbohydrate Diet.

Degree: 2016, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/13342kxh359

► Non-alcoholic fatty liver disease (NAFLD), an umbrella term that encompasses hepatic steatosis, steatohepatitis, fibrosis, and cirrhosis, has become the most common chronic liver disease in… (more)

▼ Non-alcoholic fatty liver disease (NAFLD), an umbrella term that encompasses hepatic steatosis, steatohepatitis, fibrosis, and cirrhosis, has become the most common chronic liver disease in the developed countries. NAFLD has been shown to be positively associated with obesity, and thus not surprisingly the majority of NAFLD studies have utilized obese models to explore NAFLD causality. However, previous studies indicated that 25% of patients with NAFLD are not obese and that 7.4% of lean adults have steatosis, and they are more likely to be younger and female, suggesting that these people with lean NAFLD were metabolically obese. Additionally, insulin resistance is an independent risk factor to the development of lean NAFLD, which has been shown to be related to cardiovascular disease and diabetes mellitus. Therefore, understanding the etiology of lean NAFLD in the early stage of the development of steatosis becomes an urgent need. On the other hand, lifestyle modification intervention including diet and physical activity is believed to improve NAFLD or even reverse it, but very few studies have focused on the reversal of hepatic steatosis in the lean NAFLD model. Thus, the overall research hypothesis in this dissertation is that the exogenous lipids as a form of lipid emulsion (LE) and physical activity are capable to reverse hepatic triacylglycerol (TG) accumulation in the lean mouse model with preexisting steatosis. Previous work in our laboratory indicated that 13.5% (percent of total energy, en-%) Intralipid® given orally ameliorated TG accumulation in the liver of nonobese mice fed a high carbohydrate diet (HCD) for 5 weeks. Here, in my first study (chapter 3) I examined whether HCD can induce hepatic steatosis in a short period of time (8d) and whether Intralipid® and voluntary exercise can prevent liver triacylglycerol (TG) accumulation by regulating the de novo lipogenesis-associated transcripts and the concentrations of total fatty acids, in 8 d, on the development of steatosis in a lean mouse model. The results revealed that hepatic TG contents in the HCD-fed mice were significantly increased, confirmed by Oil Red O staining, suggesting the 8d period of induction of steatosis was sufficient to induce mild steatosis. Supplementation with 13.5% Intralipid®, with or without exercise, also suppressed HCD-induced steatosis. qRT-PCR analysis showed that including 13.5% Intralipid® to the HCD significantly decreased the transcript levels for lipogenesis-associated genes, whereas mice-fed HCD with exercise had less beneficial effect in the early stage of steatosis, as compared to HCD supplemented with 13.5% Intralipid®. Fatty acid profiling also showed a consistency with transcriptional data that the concentration of monounsaturated FA was decreased significantly. As noted in the previous study that HCD is capable to induce mild hepatic steatosis within 8d, I conducted a second study (chapter 4) to test whether the beneficial effect contributed by 13.5% Intralipid® supplementation will be extended to the mouse… Advisors/Committee Members: A. Catharine Ross, Dissertation Advisor/Co-Advisor, A. Catharine Ross, Committee Chair/Co-Chair, Michael H. Green, Committee Member, Connie J. Rogers, Committee Member, Andrew D. Patterson, Outside Member.

Subjects/Keywords: Lean NAFLD; Glucose metabolism; lipidmetabolism; hepatic steatosis; metabolomics; high carbohydrate diet

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

APA (6^th Edition):

Huang, K. (2016). Exogenous Lipids Regulate the Development of Hepatic Steatosis in a Lean NAFLD model-fed a High Carbohydrate Diet. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/13342kxh359

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):

Huang, Kuan-Hsun. “Exogenous Lipids Regulate the Development of Hepatic Steatosis in a Lean NAFLD model-fed a High Carbohydrate Diet.” 2016. Thesis, Penn State University. Accessed January 26, 2021. https://submit-etda.libraries.psu.edu/catalog/13342kxh359.

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

MLA Handbook (7^th Edition):

Huang, Kuan-Hsun. “Exogenous Lipids Regulate the Development of Hepatic Steatosis in a Lean NAFLD model-fed a High Carbohydrate Diet.” 2016. Web. 26 Jan 2021.

Vancouver:

Huang K. Exogenous Lipids Regulate the Development of Hepatic Steatosis in a Lean NAFLD model-fed a High Carbohydrate Diet. [Internet] [Thesis]. Penn State University; 2016. [cited 2021 Jan 26]. Available from: https://submit-etda.libraries.psu.edu/catalog/13342kxh359.

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

Council of Science Editors:

Huang K. Exogenous Lipids Regulate the Development of Hepatic Steatosis in a Lean NAFLD model-fed a High Carbohydrate Diet. [Thesis]. Penn State University; 2016. Available from: https://submit-etda.libraries.psu.edu/catalog/13342kxh359

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

13. Castro benitez, Carlos. Innovative strategies to improve liver grafts quality before transplantation : Stratégies innovantes pour l’amélioration des greffons hépatiques avant la transplantation.

Degree: Docteur es, Toxicologie, 2019, Université Paris-Saclay (ComUE)

URL: http://www.theses.fr/2019SACLS068

►

La préservation statique à froid (SCS) est l’étalon-or de la préservation des organes après une greffe. En raison de la pénurie d’organes et de l’augmentation… (more)

▼

La préservation statique à froid (SCS) est l’étalon-or de la préservation des organes après une greffe. En raison de la pénurie d’organes et de l’augmentation du nombre de patients figurant sur la liste d’attente, le recours aux organes provenant des donneurs à critères élargis, lesquels sont très sensibles au syndrome d’ischémie-reperfusion (IRS), ce qui entraîne une non-fonction primaire (PNF) ou un dysfonctionnement précoce (EAD), est de plus en plus fréquent.Cette recherche avait pour but d’étudier et d’identifier de nouvelles stratégies pour améliorer la qualité de la préservation des organes - d'atténuer les séquelles de l'IRS en utilisant la machine de perfusion hépatique à différentes températures et à différentes périodes d'utilisation après le prélèvement de l'organe ou en ajoutant une hémoglobine extracellulaire en tant que transporteur d'oxygène pendant le SCS.Deux modèles différents ex-vivo ont été analysés : L’un chez le petit animal avec des foies de rats normaux et stéatosiques, pour la perfusion hypothermique (HMP) et SCS avec le transporteur d'oxygène et au niveau préclinique, des foies humains stéatosiques récusés, pour la perfusion normothermique (NMP).Les résultats ont confirmé de manière significative l'intérêt de l’HMP dans la phase pré-ischémique du SCS et celui de l'utilisation de l'hémoglobine extracellulaire en améliorant la fonction hépatique, le maintien de l'anatomie des hépatocytes et en réduisant des marqueurs du stress oxydatif, de l'apoptose et de l'inflammation. Egalement, l'utilisation de NMP a permis d'analyser les foies sévèrement stéatosiques pouvant être récupérés pour une transplantation dans un avenir très proche.Cette recherche met en évidence de nouvelles approches en matière de préservation d'organes susceptibles d'augmenter le pool d'organes et d'améliorer les résultats en transplantation hépatique.Mots-clés : greffe de foie, stockage froid dans le froid, perfusion dans une machine à foie, lésion de reperfusion par ischémie, transporteur d'oxygène.

Static cold storage (SCS) is the gold standard of organ preservation after being procured for transplantation. Due to the organ shortage and the increase of number of patients in the waiting list have pushed the use organs from extended criteria donors which are very susceptible to the ischemia reperfusion syndrome (IRS) leading to primary non-function (PNF) or to early allograft dysfunction (EAD).This research was aimed to study and identify new strategies to improve the quality of organ preservation -liver, to attenuate the IRS sequels by using the liver perfusion machine (LPM) at different temperatures and times of usage after the organ procurement or by adding an extracellular hemoglobin as an oxygen carrier during SCS.Two different ex-vivo models were analyzed: small animal -normal and steatotic rat livers, for hypothermic perfusion (HMP) and SCS with the oxygen carrier and preclinical -steatotic discarded human livers, for normothermic perfusion (NMP).The results significantly confirmed the benefit of the HMP in the…

Advisors/Committee Members: Adam, René (thesis director).

Subjects/Keywords: Transplantation Hépatique; Solution de préservation; Stéatose; Liver Transplant; Preservation Solution; Steatosis

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

APA (6^th Edition):

Castro benitez, C. (2019). Innovative strategies to improve liver grafts quality before transplantation : Stratégies innovantes pour l’amélioration des greffons hépatiques avant la transplantation. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2019SACLS068

Chicago Manual of Style (16^th Edition):

Castro benitez, Carlos. “Innovative strategies to improve liver grafts quality before transplantation : Stratégies innovantes pour l’amélioration des greffons hépatiques avant la transplantation.” 2019. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed January 26, 2021. http://www.theses.fr/2019SACLS068.

MLA Handbook (7^th Edition):

Castro benitez, Carlos. “Innovative strategies to improve liver grafts quality before transplantation : Stratégies innovantes pour l’amélioration des greffons hépatiques avant la transplantation.” 2019. Web. 26 Jan 2021.

Vancouver:

Castro benitez C. Innovative strategies to improve liver grafts quality before transplantation : Stratégies innovantes pour l’amélioration des greffons hépatiques avant la transplantation. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2019. [cited 2021 Jan 26]. Available from: http://www.theses.fr/2019SACLS068.

Council of Science Editors:

Castro benitez C. Innovative strategies to improve liver grafts quality before transplantation : Stratégies innovantes pour l’amélioration des greffons hépatiques avant la transplantation. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2019. Available from: http://www.theses.fr/2019SACLS068

14. Groebner, Jennifer. Alcohol-induced tubulin hyperacetylation impairs microtubule dynamics and motor function: contributions to hepatic injury.

Degree: 2018, The Catholic University of America

URL: http://hdl.handle.net/1961/cuislandora:213557

►

Although the progression of alcoholic liver disease (ALD) is clinically well described, there are currently no treatments to relieve or reverse the disease state. Our… (more)

▼

Although the progression of alcoholic liver disease (ALD) is clinically well described, there are currently no treatments to relieve or reverse the disease state. Our previous work has shown that ethanol metabolism induces microtubule acetylation and stability, which strongly correlates with defects in microtubule motor-mediated protein trafficking including secretion and nuclear translocation. Because transcytosis is also microtubule motor-dependent, we examined this process and found that it was also significantly impaired by ethanol treatment. Not only did dynein/dynactin, the minus end-directed motor complex, colocalize with stalled transcytosing proteins on acetylated microtubules, dynein was also more strongly associated with microtubules, which we suggest leads to decreased motor processivity resulting in vesicle stalling and impaired delivery. Since microtubule acetylation has been shown to mediate lipid droplet biogenesis and because fatty liver is an early stage of ALD, we examined lipid droplet dynamics in ethanol-treated cells. Ethanol metabolism enhanced lipid droplet accumulation and enlargement with a reciprocal decrease in droplet degradation. Since droplet motility is also microtubule motor-dependent and implicated in droplet growth and degradation, we performed live cell imaging of fluorescently-labeled droplets. Lipid droplet motility was significantly impaired and large droplets were essentially stationary in ethanol-treated cells. In cells depleted of intact microtubules, lipid droplets were immobile and redistributed from the cell periphery to more apical regions, indicating that intact microtubules are required for droplet motility and distributions. To directly assess if microtubule acetylation can directly explain defects in motor-mediated motility, we overexpressed α-tubulin acetyltransferase (αTAT1) to induce acetylation levels (~3-fold) similar to those observed in ethanol-treated cells. Live cell imaging revealed that lipid droplet motility was decreased in cells overexpressing αTAT1, but to a lesser extent than in ethanol-treated cells. Dynein/dynactin colocalized with large, immotile droplets in both ethanol-treated cells and in cells overexpressing αTAT1, suggesting that enhanced droplet binding leads to stalled droplets. We further determined that ethanol-induced impairment of microtubule-dependent STAT5B nuclear translocation attenuated growth hormone-mediated hepatoprotective signaling, further suggesting that modulating tubulin acetylation levels is a novel therapeutic target for ALD.

Cellular biology

alcoholic liver disease, dynein, lipid droplets, microtubule acetylation, steatosis, tubulin acetyltransferase

Biology

Degree Awarded: Ph.D. Biology. The Catholic University of America

Advisors/Committee Members: The Catholic University of America (Degree granting institution), Tuma, Pamela (Thesis advisor), Golin, John (Committee member), Mullins, J. Michael (Committee member), Nieh, Sen (Committee member), McRae, Farzana (Committee member).

Subjects/Keywords: alcoholic liver disease; dynein; lipid droplets; microtubule acetylation; steatosis; tubulin acetyltransferase

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APA (6^th Edition):

Groebner, J. (2018). Alcohol-induced tubulin hyperacetylation impairs microtubule dynamics and motor function: contributions to hepatic injury. (Thesis). The Catholic University of America. Retrieved from http://hdl.handle.net/1961/cuislandora:213557

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):

Groebner, Jennifer. “Alcohol-induced tubulin hyperacetylation impairs microtubule dynamics and motor function: contributions to hepatic injury.” 2018. Thesis, The Catholic University of America. Accessed January 26, 2021. http://hdl.handle.net/1961/cuislandora:213557.

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

MLA Handbook (7^th Edition):

Groebner, Jennifer. “Alcohol-induced tubulin hyperacetylation impairs microtubule dynamics and motor function: contributions to hepatic injury.” 2018. Web. 26 Jan 2021.

Vancouver:

Groebner J. Alcohol-induced tubulin hyperacetylation impairs microtubule dynamics and motor function: contributions to hepatic injury. [Internet] [Thesis]. The Catholic University of America; 2018. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/1961/cuislandora:213557.

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

Council of Science Editors:

Groebner J. Alcohol-induced tubulin hyperacetylation impairs microtubule dynamics and motor function: contributions to hepatic injury. [Thesis]. The Catholic University of America; 2018. Available from: http://hdl.handle.net/1961/cuislandora:213557

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

Colorado State University

15. Nivala, Angela Marie. Novel therapies for NAFLD.

Degree: PhD, Food Science and Human Nutrition, 2011, Colorado State University

URL: http://hdl.handle.net/10217/49853

► Background/Aims Non Alcoholic Fatty Liver Disease (NAFLD) is a chronic liver disease often associated with metabolic disorders like type 2 diabetes, cardiovascular disease, obesity, and… (more)

▼ Background/Aims Non Alcoholic Fatty Liver Disease (NAFLD) is a chronic liver disease often associated with metabolic disorders like type 2 diabetes, cardiovascular disease, obesity, and metabolic syndrome. It is characterized by hepatic fat accumulation (steatosis) that is at or above 5% of liver weight in the absence of excessive alcohol consumption (< 20 g/day). Current treatment for NAFLD focuses on reducing body weight and improving insulin action. The intent of this thesis was to identify therapies that targeted the liver. In the first aim, we examined whether secretions from plant roots contained compounds that restricted lipid accumulation or improved insulin action. The second aim examined whether taurine could prevent characteristic features of disease progression. Specifically, we hypothesized that (1) onion root exudates will prevent or reduce lipid accumulation and improve insulin signaling and (2) taurine will prevent or reduce endoplasmic reticulum (ER) stress, oxidative stress and liver injury. Methods To examine these hypotheses, liver cells and dietary models of NAFLD were employed. Analyses focused on hepatic triglycerides, insulin signaling, ER stress, oxidative stress and inflammation using basic biochemical methods such as western blotting, Real Time PCR, immunohistochemistry and enzyme-linked assays. Results Onion root exudates prevented fatty acid-mediated lipid accumulation and enhanced insulin signaling in H4IIE liver cells. Onion root exudates reduced plasma glucose, free fatty acids (FFA), and improved insulin action in rats fed a high fat diet. Taurine mitigated palmitate-mediated caspase-3 activity, cell death, ER stress, and oxidative stress in H4IIE liver cells and primary hepatocytes. In rats fed a high sucrose diet, taurine supplementation significantly reduced hepatic lipid accumulation, liver injury, inflammation, plasma triglycerides and insulin levels. The high sucrose diet resulted in an induction of multiple components of the unfolded protein response (UPR) in the liver consistent with ER stress which was ameliorated by taurine supplementation. Treatment of mice with the ER stress inducing agent tunicamycin resulted in liver injury, UPR induction and hepatic lipid accumulation, and this was significantly ameliorated by supplementation with taurine. Conclusion Both onion root exudates and taurine reduced metabolic abnormalities associated with NAFLD. Onion root exudates appear to exert this effect through reduced lipid accumulation and enhanced insulin sensitivity in the liver, while taurine reduced hepatic steatosis, ER stress, oxidative stress and liver injury. Overall, onion root exudates and taurine show promise as novel therapies for the treatment of NAFLD. Advisors/Committee Members: Pagliassotti, Michael (advisor), Vivanco, Jorge (committee member), Frye, Melinda (committee member), Vanamala, Jairam (committee member).

Subjects/Keywords: hepatic steatosis; insulin resistance; lipotoxicity; NAFLD; root exudates; taurine

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APA (6^th Edition):

Nivala, A. M. (2011). Novel therapies for NAFLD. (Doctoral Dissertation). Colorado State University. Retrieved from http://hdl.handle.net/10217/49853

Chicago Manual of Style (16^th Edition):

Nivala, Angela Marie. “Novel therapies for NAFLD.” 2011. Doctoral Dissertation, Colorado State University. Accessed January 26, 2021. http://hdl.handle.net/10217/49853.

MLA Handbook (7^th Edition):

Nivala, Angela Marie. “Novel therapies for NAFLD.” 2011. Web. 26 Jan 2021.

Vancouver:

Nivala AM. Novel therapies for NAFLD. [Internet] [Doctoral dissertation]. Colorado State University; 2011. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10217/49853.

Council of Science Editors:

Nivala AM. Novel therapies for NAFLD. [Doctoral Dissertation]. Colorado State University; 2011. Available from: http://hdl.handle.net/10217/49853

University of Texas Medical Branch – Galveston

16. [No author]. Glucose and Lipid Dysregulation Following Loss of Hepatic Aryl Hydrocarbon Receptor in Mice.

Degree: University of Texas Medical Branch – Galveston

URL: http://hdl.handle.net/2152.3/11212

► The aryl hydrocarbon receptor (AhR) is a cytosolic, ligand activated transcription factor commonly known for its role in environmental toxicant metabolism. However, the generation of… (more)

▼ The aryl hydrocarbon receptor (AhR) is a cytosolic, ligand activated transcription factor commonly known for its role in environmental toxicant metabolism. However, the generation of AhR knockout (AhR-KO) mice has shown physiological roles for the AhR in normal liver growth and development, insulin homeostasis, glucose homeostasis, and lipid metabolism. The liver is a major regulator of energy and glucose homeostasis and recent data have also shown that reduced AhR activity results in increased energy expenditure and susceptibility to weight gain and hepatic steatosis on an obesogenic diet. To date, no one has conclusively shown how AhR activity in the liver affects overall mouse lipid energy and glucose metabolism. To investigate how AhR activity in the mouse liver affects glucose and lipid metabolism, we utilized liver specific, AhR conditional knockout (AhR-CKO) mice. We discovered a novel phenotype wherein, AhR-CKO mice exhibited reduced body weight with age, reduced adiposity and increased expression of thermogenic gene, uncoupling protein 1 (UCP1) or the browning of the white adipose tissue (WAT) vs. controls. Next generation RNA sequencing of AhR-CKO vs. control mice liver transcriptomes revealed significantly increased expression of fibroblast growth factor (FGF) 21, a known hepatokine and activator of thermogenesis in mice WAT. We hypothesized that hepatic AhR activity alters the thermogenic gene program in white adipocytes by driving beige adipocyte recruitment through direct regulation of the metabolic hormone, FGF21. Using ChIP analyses and a luciferase reporter system we demonstrated that AhR directly regulates FGF21 at the gene level. The generation and utilization of AhR/FGF21 double conditional knockout mice demonstrated that FGF21 is responsible for the browning of white fat seen after hepatic loss of AhR as evident by no increased UCP1 expressions in the white fat taken from mice after hepatic loss of AhR and FGF21. Advisors/Committee Members: Denner, Larry (advisor), Elferink, Cornelis (committeeMember), Edwards, Dean (committeeMember), Rastellini, Cristiana (committeeMember), Belalcazar, Maria L (committeeMember).

Subjects/Keywords: AhR FGF21 Steatosis Obesity

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APA (6^th Edition):

author], [. (n.d.). Glucose and Lipid Dysregulation Following Loss of Hepatic Aryl Hydrocarbon Receptor in Mice. (Thesis). University of Texas Medical Branch – Galveston. Retrieved from http://hdl.handle.net/2152.3/11212

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

author], [No. “Glucose and Lipid Dysregulation Following Loss of Hepatic Aryl Hydrocarbon Receptor in Mice. ” Thesis, University of Texas Medical Branch – Galveston. Accessed January 26, 2021. http://hdl.handle.net/2152.3/11212.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

author], [No. “Glucose and Lipid Dysregulation Following Loss of Hepatic Aryl Hydrocarbon Receptor in Mice. ” Web. 26 Jan 2021.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

author] [. Glucose and Lipid Dysregulation Following Loss of Hepatic Aryl Hydrocarbon Receptor in Mice. [Internet] [Thesis]. University of Texas Medical Branch – Galveston; [cited 2021 Jan 26]. Available from: http://hdl.handle.net/2152.3/11212.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

author] [. Glucose and Lipid Dysregulation Following Loss of Hepatic Aryl Hydrocarbon Receptor in Mice. [Thesis]. University of Texas Medical Branch – Galveston; Available from: http://hdl.handle.net/2152.3/11212

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

University of Toronto

17. Tersigni, Claudia Ariana. Effect of Autophagy Induction via TRPML1 Activation on Hepatic Steatosis.

Degree: 2019, University of Toronto

URL: http://hdl.handle.net/1807/98408

►

Discrepancies between the number of liver transplant candidates and available organs has led to an increased use of marginal grafts, including steatotic liver grafts. Steatotic… (more)

Subjects/Keywords: autophagy; fatty liver; hepatic steatosis; mucolipin 1; transplant; TRPML1; 0306

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APA (6^th Edition):

Tersigni, C. A. (2019). Effect of Autophagy Induction via TRPML1 Activation on Hepatic Steatosis. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/98408

Chicago Manual of Style (16^th Edition):

Tersigni, Claudia Ariana. “Effect of Autophagy Induction via TRPML1 Activation on Hepatic Steatosis.” 2019. Masters Thesis, University of Toronto. Accessed January 26, 2021. http://hdl.handle.net/1807/98408.

MLA Handbook (7^th Edition):

Tersigni, Claudia Ariana. “Effect of Autophagy Induction via TRPML1 Activation on Hepatic Steatosis.” 2019. Web. 26 Jan 2021.

Vancouver:

Tersigni CA. Effect of Autophagy Induction via TRPML1 Activation on Hepatic Steatosis. [Internet] [Masters thesis]. University of Toronto; 2019. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/1807/98408.

Council of Science Editors:

Tersigni CA. Effect of Autophagy Induction via TRPML1 Activation on Hepatic Steatosis. [Masters Thesis]. University of Toronto; 2019. Available from: http://hdl.handle.net/1807/98408

University of Toronto

18. Brandt, Sydney Laura. The Circulating Furan Fatty Acid Metabolite CMPF Directly Enhances Hepatic FGF21 Secretion and Lipid Metabolism.

Degree: 2017, University of Toronto

URL: http://hdl.handle.net/1807/88616

►

Elevation of the fish oil metabolite 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF) induces metabolic remodeling within the -cell to a preferential use of fatty acids. Although detrimental to… (more)

Subjects/Keywords: ACC Inhibition; CMPF; FGF21; Lipid metabolism; NAFLD; Steatosis; 0719

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APA (6^th Edition):

Brandt, S. L. (2017). The Circulating Furan Fatty Acid Metabolite CMPF Directly Enhances Hepatic FGF21 Secretion and Lipid Metabolism. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/88616

Chicago Manual of Style (16^th Edition):

Brandt, Sydney Laura. “The Circulating Furan Fatty Acid Metabolite CMPF Directly Enhances Hepatic FGF21 Secretion and Lipid Metabolism.” 2017. Masters Thesis, University of Toronto. Accessed January 26, 2021. http://hdl.handle.net/1807/88616.

MLA Handbook (7^th Edition):

Brandt, Sydney Laura. “The Circulating Furan Fatty Acid Metabolite CMPF Directly Enhances Hepatic FGF21 Secretion and Lipid Metabolism.” 2017. Web. 26 Jan 2021.

Vancouver:

Brandt SL. The Circulating Furan Fatty Acid Metabolite CMPF Directly Enhances Hepatic FGF21 Secretion and Lipid Metabolism. [Internet] [Masters thesis]. University of Toronto; 2017. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/1807/88616.

Council of Science Editors:

Brandt SL. The Circulating Furan Fatty Acid Metabolite CMPF Directly Enhances Hepatic FGF21 Secretion and Lipid Metabolism. [Masters Thesis]. University of Toronto; 2017. Available from: http://hdl.handle.net/1807/88616

Boston University

19. Yengul, Sanjay S. Shear wave rheometry with applications in elastography.

Degree: PhD, Mechanical Engineering, 2019, Boston University

URL: http://hdl.handle.net/2144/34923

► The goal of elastography is to map the mechanical properties of soft tissues associated with health and disease. The mechanical property of interest in this… (more)

▼ The goal of elastography is to map the mechanical properties of soft tissues associated with health and disease. The mechanical property of interest in this work is the complex shear modulus, composed of a real part, the storage modulus, which is a measure of elasticity, and an imaginary part, the loss modulus, which is a measure of viscosity. Together, they determine the speed and attenuation of shear waves in the medium. Elastography techniques based on either ultrasound imaging or MRI can image shear wave propagation and thus are capable of measuring shear wave speed and attenuation. Dispersion, or the frequency-dependence of material parameters, is a primary confounding factor when comparing measurements between different shear wave elastography implementations. Prior attempts at quantifying this frequency-dependence suffered from inaccurate modeling assumptions and low signal-to-noise ratios (SNR). To overcome these limitations, a high-fidelity forward model of shear wave propagation in homogeneous media was developed. The model is an exact semi-analytical solution of Navier's equation and is well-suited for acoustic radiation force impulse shear wave elastography (ARFI-SWE) because it does not require precise knowledge of the strength of the source, nor its spatial or temporal distribution. Unlike models used in ARFI-SWE heretofore, it accounts for the vector polarization of shear waves and exactly represents geometric spreading of the shear wavefield, whether spherical, cylindrical, or neither. Furthermore, it is material-model independent, i.e. it makes no assumption about the frequency-dependence of material parameters. It overcomes the problem of low SNR through spatial averaging and enables estimation of the frequency-dependent complex shear modulus over a wider frequency range than has hitherto been possible. This improved ARFI-SWE was named Shear Wave Rheometry (SWR). By combining SWR with a novel torsional vibration rheometry, dispersion in tissue-mimicking gels was quantified from 1 – 1800 Hz. The measurements show sizable frequency-dependent variation in the shear modulus of gelatin, a material often assumed to be non-dispersive based on narrow-band measurements. SWR measurements in ex vivo bovine liver tissue yielded complex shear modulus estimates from 25 – 250 Hz and showed that liver tissue exhibits significant dispersion in this frequency range: a factor of 4 increase in the storage modulus and a factor of 10 increase in the loss modulus. Quality metrics showed that liver tissue can be reasonably approximated as homogeneous and isotropic for ARFI-SWE measurements in this frequency range. Results demonstrate that accounting for dispersion is essential for meaningful comparisons of measurements between systems. Moreover, improved tissue characterization enabled by SWR may have clinical relevance, for example, in the diagnosis and monitoring of chronic liver disease. Advisors/Committee Members: Barbone, Paul E. (advisor), Madore, Bruno (advisor).

Subjects/Keywords: Acoustics; Elastic wave; Liver fibrosis; Medical imaging; NAFLD; Steatosis; Viscoelasticity

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APA (6^th Edition):

Yengul, S. S. (2019). Shear wave rheometry with applications in elastography. (Doctoral Dissertation). Boston University. Retrieved from http://hdl.handle.net/2144/34923

Chicago Manual of Style (16^th Edition):

Yengul, Sanjay S. “Shear wave rheometry with applications in elastography.” 2019. Doctoral Dissertation, Boston University. Accessed January 26, 2021. http://hdl.handle.net/2144/34923.

MLA Handbook (7^th Edition):

Yengul, Sanjay S. “Shear wave rheometry with applications in elastography.” 2019. Web. 26 Jan 2021.

Vancouver:

Yengul SS. Shear wave rheometry with applications in elastography. [Internet] [Doctoral dissertation]. Boston University; 2019. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/2144/34923.

Council of Science Editors:

Yengul SS. Shear wave rheometry with applications in elastography. [Doctoral Dissertation]. Boston University; 2019. Available from: http://hdl.handle.net/2144/34923

University of Dundee

20. Garbacz, Wojciech G. Cooperation between peroxisome proliferator activated receptor alpha and delta in regulation of body weight and hepatic steatosis in mice.

Degree: PhD, 2012, University of Dundee

URL: https://discovery.dundee.ac.uk/en/studentTheses/9b2509f1-3391-45fa-91eb-9b5364a9b6d9 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.578897

► Peroxisome proliferator-activated receptor alpha (PPARa) and delta (PPARd) belong to the nuclear receptor superfamily. PPARa is a target of lipid-lowering drugs and PPARd promotes fatty… (more)

Subjects/Keywords: 616.3; Peroxisome Proliferator Activator Receptor (PPAR); Liver; Steatosis

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APA (6^th Edition):

Garbacz, W. G. (2012). Cooperation between peroxisome proliferator activated receptor alpha and delta in regulation of body weight and hepatic steatosis in mice. (Doctoral Dissertation). University of Dundee. Retrieved from https://discovery.dundee.ac.uk/en/studentTheses/9b2509f1-3391-45fa-91eb-9b5364a9b6d9 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.578897

Chicago Manual of Style (16^th Edition):

Garbacz, Wojciech G. “Cooperation between peroxisome proliferator activated receptor alpha and delta in regulation of body weight and hepatic steatosis in mice.” 2012. Doctoral Dissertation, University of Dundee. Accessed January 26, 2021. https://discovery.dundee.ac.uk/en/studentTheses/9b2509f1-3391-45fa-91eb-9b5364a9b6d9 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.578897.

MLA Handbook (7^th Edition):

Garbacz, Wojciech G. “Cooperation between peroxisome proliferator activated receptor alpha and delta in regulation of body weight and hepatic steatosis in mice.” 2012. Web. 26 Jan 2021.

Vancouver:

Garbacz WG. Cooperation between peroxisome proliferator activated receptor alpha and delta in regulation of body weight and hepatic steatosis in mice. [Internet] [Doctoral dissertation]. University of Dundee; 2012. [cited 2021 Jan 26]. Available from: https://discovery.dundee.ac.uk/en/studentTheses/9b2509f1-3391-45fa-91eb-9b5364a9b6d9 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.578897.

Council of Science Editors:

Garbacz WG. Cooperation between peroxisome proliferator activated receptor alpha and delta in regulation of body weight and hepatic steatosis in mice. [Doctoral Dissertation]. University of Dundee; 2012. Available from: https://discovery.dundee.ac.uk/en/studentTheses/9b2509f1-3391-45fa-91eb-9b5364a9b6d9 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.578897

21. GENG WEI. Roles of the microRNAs in fatty liver lipid accumulation.

Degree: 2012, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/33282

Subjects/Keywords: microRNA; NAFLD; lipid; steatosis

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APA (6^th Edition):

WEI, G. (2012). Roles of the microRNAs in fatty liver lipid accumulation. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/33282

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):

WEI, GENG. “Roles of the microRNAs in fatty liver lipid accumulation.” 2012. Thesis, National University of Singapore. Accessed January 26, 2021. http://scholarbank.nus.edu.sg/handle/10635/33282.

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

MLA Handbook (7^th Edition):

WEI, GENG. “Roles of the microRNAs in fatty liver lipid accumulation.” 2012. Web. 26 Jan 2021.

Vancouver:

WEI G. Roles of the microRNAs in fatty liver lipid accumulation. [Internet] [Thesis]. National University of Singapore; 2012. [cited 2021 Jan 26]. Available from: http://scholarbank.nus.edu.sg/handle/10635/33282.

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

Council of Science Editors:

WEI G. Roles of the microRNAs in fatty liver lipid accumulation. [Thesis]. National University of Singapore; 2012. Available from: http://scholarbank.nus.edu.sg/handle/10635/33282

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

Arizona State University

22. Crawford, Meli'sa Shaunte. Examining the Effects of a High Fat Diet on the Development of Metabolic Syndrome and Gut Leakiness in Male Sprague-Dawley Rats.

Degree: Biology, 2019, Arizona State University

URL: http://repository.asu.edu/items/53625

► The prevalence of obesity and obesity-related disorders have increased world-wide. In the last decade, the intestinal microbiome has become a major indicator of metabolic and… (more)

▼ The prevalence of obesity and obesity-related disorders have increased world-wide. In the last decade, the intestinal microbiome has become a major indicator of metabolic and gastrointestinal health. Previous research has shown that high-fat diet (HFD) consumption can alter the microbial composition of the gut by increasing the abundance of gram-positive bacteria associated with the onset of obesity and type 2 diabetes. Although, the most common form of obesity and metabolic syndrome intervention is exercise and diet, these recommendations may not improve severe cases of obesity. Thus, an important relevance of my project was to investigate whether the intake of an organometallic complex (OMC) would prevent the onset of metabolic and gastrointestinal complications associated with high-fat diet intake. I hypothesized that the consumption of a HFD for 6 weeks would promote the development of metabolic and gastrointestinal disease risk factors. Next, it was hypothesized that OMC treatment would decrease metabolic risk factors by improving insulin sensitivity and decreasing weight gain. Finally, I hypothesized that HFD-intake would increase the abundance of gram-positive bacteria associated with gastrointestinal disease. My preliminary data investigated the effects of a 6-week HFD on the development of hepatic steatosis, intestinal permeability and inflammation in male Sprague Dawley rats. I found that a 6-week HFD increases hepatic triglyceride concentrations, plasma endotoxins and promotes the production of pro-inflammatory cytokines in the cecum wall. I then investigated whether OMC treatment could prevent metabolic risk factors in male Sprague-Dawley rats fed a HFD for 10 weeks and found that OMC can mitigate risk factors such hyperglycemia, liver disease, impaired endothelial function, and inflammation. Lastly, I investigated the effects of a 10-week HFD on the gastrointestinal system and found an increase in liver triglycerides and free glycerol and alterations of the distal gut microbiome. My results support the hypothesis that a HFD can promote metabolic risk factors, alter the gut microbiome and increase systemic inflammation and that OMC treatment may help mitigate some of these effects. Together, these studies are among the first to demonstrate the effects of a soil-derived compound on metabolic complications. Additionally, these conclusions also provide an essential basis for future gastrointestinal and microbiome studies of OMC treatment.

Subjects/Keywords: Physiology; High Fat Diet; Inflammation; Metabolic Syndrome; Microbiome; Obesity; Steatosis

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

APA (6^th Edition):

Crawford, M. S. (2019). Examining the Effects of a High Fat Diet on the Development of Metabolic Syndrome and Gut Leakiness in Male Sprague-Dawley Rats. (Doctoral Dissertation). Arizona State University. Retrieved from http://repository.asu.edu/items/53625

Chicago Manual of Style (16^th Edition):

Crawford, Meli'sa Shaunte. “Examining the Effects of a High Fat Diet on the Development of Metabolic Syndrome and Gut Leakiness in Male Sprague-Dawley Rats.” 2019. Doctoral Dissertation, Arizona State University. Accessed January 26, 2021. http://repository.asu.edu/items/53625.

MLA Handbook (7^th Edition):

Crawford, Meli'sa Shaunte. “Examining the Effects of a High Fat Diet on the Development of Metabolic Syndrome and Gut Leakiness in Male Sprague-Dawley Rats.” 2019. Web. 26 Jan 2021.

Vancouver:

Crawford MS. Examining the Effects of a High Fat Diet on the Development of Metabolic Syndrome and Gut Leakiness in Male Sprague-Dawley Rats. [Internet] [Doctoral dissertation]. Arizona State University; 2019. [cited 2021 Jan 26]. Available from: http://repository.asu.edu/items/53625.

Council of Science Editors:

Crawford MS. Examining the Effects of a High Fat Diet on the Development of Metabolic Syndrome and Gut Leakiness in Male Sprague-Dawley Rats. [Doctoral Dissertation]. Arizona State University; 2019. Available from: http://repository.asu.edu/items/53625

23. Villemain Le Hagre, Laure. Le récepteur Sigma 1 : implication dans la prolifération et la stéatose des hépatocytes : Sigma 1 Receptor : Role in Hepatocyte Proliferation and Steatosis.

Degree: Docteur es, Sciences de la vie et de la santé, 2019, Université Paris-Saclay (ComUE)

URL: http://www.theses.fr/2019SACLS370

►

Le récepteur Sigma 1 (SigR1) est une protéine transmembranaire du RE, enrichie dans les MAMs, qui agirait comme une chaperonne. Ubiquitaire, SigR1 est très exprimé… (more)

▼

Le récepteur Sigma 1 (SigR1) est une protéine transmembranaire du RE, enrichie dans les MAMs, qui agirait comme une chaperonne. Ubiquitaire, SigR1 est très exprimé dans le système nerveux central (SNC) et le foie. Dans le SNC, SigR1 est impliqué dans un grand nombre de maladies neurodégénératives mais aussi dans le mécanisme de la douleur et dans la dépression. SigR1 est aussi impliqué dans les cancers. Il est surexprimé dans de nombreuses tumeurs cancéreuses et particulièrement dans les tumeurs hormonodépendantes dans lesquelles son expression est corrélée au statut hormonal de la tumeur. Malgré sa très forte expression dans le foie, son rôle y est inconnu. Dans l’objectif de déterminer le rôle de SigR1 dans le foie nous étudions son expression dans les différents types de tumeurs hépatiques. SigR1 est significativement surexprimé dans les adénomes hépatocellulaires (HCA) et particulièrement le sous-type muté pour le gène HNF1α, les H-HCA. Les H-HCA sont des tumeurs hépatiques bénignes stéatosées majoritairement observées chez des femmes jeunes prenant des contraceptifs oraux (œstrogènes). Quelles sont les causes et les conséquences de cette surexpression dans les hépatocytes ? En utilisant des modèles cellulaires hépatocytaires (HepG2 et Huh7) et des souris KO pour le gène HNF1α nous mettons en évidence les résultats suivants. Les œstrogènes induisent l’expression de SigR1 via son récepteur nucléaire ERα. De même, l’inhibition d’HNF1α induit une surexpression de SigR1. Cette surexpression entraine une prolifération et une stéatose des hépatocytes, correspondant au phénotype des patientes atteintes de H-HCAs.

Sigma 1 receptor (SigR1) is a transmembrane protein of the RE, enriched in the MAMs, which would act like a chaperone. Although ubiquitous, SigR1 is especially expressed in the central nervous system (CNS) and the liver. In the CNS, SigR1 has been linked to neurodegenerative diseases and also pain and depression. SigR1 is also involved in cancer. SigR1 is overexpressed in many cancer tumors and especially in hormone dependent tumors where its expression is correlated to the hormonal status of the tumor. Although SigR1 is highly expressed in the liver, its role in this organ is unknown. Aiming at finding the role of this protein in the liver we analyze its expression in several liver tumors. SigR1 is significantly overexpressed in hepatocellular adenomas mutated for HNF1α gene, H-HCA. H-HCA are benign liver tumors with marked steatosis. They are mostly found in women taking oral contraceptives (estrogens). Why is SigR1 overexpressed in H-HCA ans what are the consequences of this overexpression? Using hepatocyte cellular models (HepG2 and Huh7) and mice that are KO for HNF1α gene, we found the following results. Estrogens induce the expression of SigR1 through its nuclear receptor ERα. HNF1α inhibition also induces its expression. This overexpression leads to an increase of the cell proliferation rate and steatosis. These effects resume H-HCA patients’ phenotype.

Advisors/Committee Members: Combettes, Laurent (thesis director).

Subjects/Keywords: Adénome hépatocellulaire; Prolifération; Stéatose; Hepatocellular adenoma; Proliferation; Steatosis

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

APA (6^th Edition):

Villemain Le Hagre, L. (2019). Le récepteur Sigma 1 : implication dans la prolifération et la stéatose des hépatocytes : Sigma 1 Receptor : Role in Hepatocyte Proliferation and Steatosis. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2019SACLS370

Chicago Manual of Style (16^th Edition):

Villemain Le Hagre, Laure. “Le récepteur Sigma 1 : implication dans la prolifération et la stéatose des hépatocytes : Sigma 1 Receptor : Role in Hepatocyte Proliferation and Steatosis.” 2019. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed January 26, 2021. http://www.theses.fr/2019SACLS370.

MLA Handbook (7^th Edition):

Villemain Le Hagre, Laure. “Le récepteur Sigma 1 : implication dans la prolifération et la stéatose des hépatocytes : Sigma 1 Receptor : Role in Hepatocyte Proliferation and Steatosis.” 2019. Web. 26 Jan 2021.

Vancouver:

Villemain Le Hagre L. Le récepteur Sigma 1 : implication dans la prolifération et la stéatose des hépatocytes : Sigma 1 Receptor : Role in Hepatocyte Proliferation and Steatosis. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2019. [cited 2021 Jan 26]. Available from: http://www.theses.fr/2019SACLS370.

Council of Science Editors:

Villemain Le Hagre L. Le récepteur Sigma 1 : implication dans la prolifération et la stéatose des hépatocytes : Sigma 1 Receptor : Role in Hepatocyte Proliferation and Steatosis. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2019. Available from: http://www.theses.fr/2019SACLS370

University of Toronto

24. Prentice, Kacey June. Identification and Characterization of the Role of the Circulating Metabolite 3-Carboxy-4-Methyl-5-Propyl-2-Furanpropanoic Acid (CMPF) in Diabetes.

Degree: PhD, 2015, University of Toronto

URL: http://hdl.handle.net/1807/75688

►

Both gestational diabetes (GDM) and type 2 diabetes (T2D) are caused by a failure of the pancreatic beta cell to compensate for increased insulin demand.… (more)

▼

Both gestational diabetes (GDM) and type 2 diabetes (T2D) are caused by a failure of the pancreatic beta cell to compensate for increased insulin demand. The underlying cause of this failure, particularly the rapid transition from prediabetes to diabetes, and between GDM and T2D is largely unknown. To identify circulating factors that may play a causal role in beta cell dysfunction we performed global metabolomics profiling on the plasma of GDM and T2D patients compared to normal glucose tolerant controls. We identified the furan fatty acid metabolite 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF) as being highly elevated in diabetic plasma. In vivo and in vitro assays demonstrated that CMPF induces glucose intolerance by impairing glucose-stimulated insulin secretion (GSIS), suggesting CMPF may play a causal role in diabetes. Analysis of human patients showed that rapid elevation in CMPF is associated with a significantly increased risk of diabetes development, consistent with elevated CMPF being the “tipping point” in the progression from prediabetes to overt diabetes. The mechanism underlying this dysfunction involves increasing reactive oxygen species (ROS), resulting in altered gene expression, inhibition of beta cell transcription factor activity, as well as uncoupling of glucose metabolism to ATP production, thus reducing insulin biosynthesis and secretion. Additionally, CMPF induces a state of preferential fatty acid utilization, which persists for months following treatment. This suggests that CMPF exposure during GDM may be responsible for the extremely high rate of progression to T2D postpartum. While detrimental for beta cell function, this ability of CMPF to drive fatty acid oxidation has beneficial effects for hepatic insulin sensitivity due to the prevention of steatosis. CMPF induces beta-oxidation, simulating a “fasting-like” state and promoting expression of FGF21, which is required to impair triglyceride synthesis and promote beta-oxidation long-term. Overall, CMPF is significantly elevated in human diabetes and has direct effects on beta cell function and insulin sensitivity in rodent models.

2017-02-12 00:00:00

Advisors/Committee Members: Wheeler, Michael B, Physiology.

Subjects/Keywords: Beta Cell; Diabetes; Gestational Diabetes; Insulin; Metabolomics; Steatosis; 0719

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

APA (6^th Edition):

Prentice, K. J. (2015). Identification and Characterization of the Role of the Circulating Metabolite 3-Carboxy-4-Methyl-5-Propyl-2-Furanpropanoic Acid (CMPF) in Diabetes. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/75688

Chicago Manual of Style (16^th Edition):

Prentice, Kacey June. “Identification and Characterization of the Role of the Circulating Metabolite 3-Carboxy-4-Methyl-5-Propyl-2-Furanpropanoic Acid (CMPF) in Diabetes.” 2015. Doctoral Dissertation, University of Toronto. Accessed January 26, 2021. http://hdl.handle.net/1807/75688.

MLA Handbook (7^th Edition):

Prentice, Kacey June. “Identification and Characterization of the Role of the Circulating Metabolite 3-Carboxy-4-Methyl-5-Propyl-2-Furanpropanoic Acid (CMPF) in Diabetes.” 2015. Web. 26 Jan 2021.

Vancouver:

Prentice KJ. Identification and Characterization of the Role of the Circulating Metabolite 3-Carboxy-4-Methyl-5-Propyl-2-Furanpropanoic Acid (CMPF) in Diabetes. [Internet] [Doctoral dissertation]. University of Toronto; 2015. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/1807/75688.

Council of Science Editors:

Prentice KJ. Identification and Characterization of the Role of the Circulating Metabolite 3-Carboxy-4-Methyl-5-Propyl-2-Furanpropanoic Acid (CMPF) in Diabetes. [Doctoral Dissertation]. University of Toronto; 2015. Available from: http://hdl.handle.net/1807/75688

University of South Carolina

25. Havighorst, Amanda Rose. Susceptibility to Metabolic Disease and Individual Variations in Unfolded Protein Response in Deer Mice (Peromyscus Maniculatus).

Degree: PhD, College of Pharmacy, 2019, University of South Carolina

URL: https://scholarcommons.sc.edu/etd/5610

► The endoplasmic reticulum is the site where integral membrane and secreted proteins are synthesized and folded, and is also the site of synthesis of… (more)

▼ The endoplasmic reticulum is the site where integral membrane and secreted proteins are synthesized and folded, and is also the site of synthesis of steroids, lipids, and other macromolecules. While ER is found in most cell types, hepatocytes in particular contain large amounts of both rough and smooth ER to facilitate their tasks, which include lipoprotein assembly and secretion, cholesterol biosynthesis, and lipid metabolism. As such, stress in the ER – and the cells’ ability to respond to it – plays a key role in disease pathogenesis. In particular, hepatic steatosis, or fatty liver, is linked to ER stress. However, if and how inherent variations in the resulting unfolded protein response (UPR) affect the predisposition to ER stress-associated metabolic conditions, including hepatic steatosis, remains to be established. By using genetically diverse deer mice (Peromyscus maniculatus) as a model, we show that the profile of tunicamycininduced UPR in fibroblasts isolated at puberty varies between individuals and predicts deregulation of lipid metabolism and diet induced hepatic steatosis later in life. Among the different UPR targets tested, CHOP more consistently predicted elevated plasma cholesterol and hepatic steatosis. Compared to baseline levels or inducibility, the maximal intensity of the UPR following stimulation best predicts the onset of pathology. Differences in the expression profile of the UPR recorded in cells from different populations of deer mice correlate with the varying response to ER stress in altitude adaptation. Upon analysis of gene expression in the livers, no differences in the expression levels of various UPR-associated genes between steatotic and nonsteatotic vi livers were recorded. Then we asked if there is a change in the relative levels of these genes as compared to each other. While we did not note any changes to the coordination of UPR genes among themselves, we did note that there was a loss of coordination between ER stress genes and autophagy and metabolic genes, particularly hepatic lipase (HL), but only in the livers of mice who had developed steatosis. Additionally, using rat hepatoma cells which naturally express HL, we demonstrated that induction of ER stress leads to the downregulation of HL alongside the upregulation of ER stress-induced genes. Together, this data demonstrates the ability of tunicamycin-treated fibroblasts isolated early in life to predict the propensity of an individual to develop hepatic steatosis; this approach might also be useful for other conditions associated with ER stress, both metabolic and otherwise. The results of the liver analysis imply that ER stress plays a role in the expression of HL and potentially other important metabolic genes, and that the loss of coordination of ER stress response with other cellular responses could be a more important factor in the transition to disease than the levels of individual transcripts alone. Advisors/Committee Members: Hippokratis Kiaris.

Subjects/Keywords: Pharmacy and Pharmaceutical Sciences; ER stress; liver; NAFLD; steatosis; UPR; variation

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APA (6^th Edition):

Havighorst, A. R. (2019). Susceptibility to Metabolic Disease and Individual Variations in Unfolded Protein Response in Deer Mice (Peromyscus Maniculatus). (Doctoral Dissertation). University of South Carolina. Retrieved from https://scholarcommons.sc.edu/etd/5610

Chicago Manual of Style (16^th Edition):

Havighorst, Amanda Rose. “Susceptibility to Metabolic Disease and Individual Variations in Unfolded Protein Response in Deer Mice (Peromyscus Maniculatus).” 2019. Doctoral Dissertation, University of South Carolina. Accessed January 26, 2021. https://scholarcommons.sc.edu/etd/5610.

MLA Handbook (7^th Edition):

Havighorst, Amanda Rose. “Susceptibility to Metabolic Disease and Individual Variations in Unfolded Protein Response in Deer Mice (Peromyscus Maniculatus).” 2019. Web. 26 Jan 2021.

Vancouver:

Havighorst AR. Susceptibility to Metabolic Disease and Individual Variations in Unfolded Protein Response in Deer Mice (Peromyscus Maniculatus). [Internet] [Doctoral dissertation]. University of South Carolina; 2019. [cited 2021 Jan 26]. Available from: https://scholarcommons.sc.edu/etd/5610.

Council of Science Editors:

Havighorst AR. Susceptibility to Metabolic Disease and Individual Variations in Unfolded Protein Response in Deer Mice (Peromyscus Maniculatus). [Doctoral Dissertation]. University of South Carolina; 2019. Available from: https://scholarcommons.sc.edu/etd/5610

26. chouzouri, vasiliki. Συσχέτιση αρτηριακής πίεσης με μη αλκοολική στεάτωση.

Degree: 2016, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/36863

►

Over the past five decades the association of essential hypertension with non-alcoholic fatty liver disease is a field of study. It is assumed that essential… (more)

▼

Over the past five decades the association of essential hypertension with non-alcoholic fatty liver disease is a field of study. It is assumed that essential hypertension is an independent predictor of cardiovascular risk. On the other hand, increasingly recently scientific data highlight the role of non-alcoholic fatty liver disease in the occurrence of cardiovascular disease. So a question arose on how two independent risk factors of cardiovascular disease could be associated with each other. The existence of correlation between the two factors was reinforced by the latest scientific data showing that treatment of hypertension with certain classes of drugs, particularly for angiotensin converting enzyme inhibitors or blockers of angiotensin II receptors improves steatosis.The main finding of the study is that newly diagnosed and untreated essential hypertension, as defined by the 24-hour ambulatory recording, correlated independently with non-alcoholic fatty liver disease even after adjustment for the characteristics of the study population. Furthermore, a novel finding of our study is that the levels of the 24hour daytime systolic blood pressure correlated independently with non-alcoholic fatty liver disease. Moreover, the results of our study verify earlier data revealing a correlation between the end-diastolic diameter of the left ventricle with non-alcoholic fatty liver disease.

Τις τελευταίες πέντε δεκαετίες η συσχέτιση της ιδιοπαθούς αρτηριακής υπέρτασης με την μη αλκοολική λιπώδη διήθηση του ήπατος αποτελεί πεδίο μελέτης. Είναι δεδομένο ότι η αρτηριακή υπέρταση αποτελεί ανεξάρτητο προγνωστικό παράγοντα καρδιαγγειακού κινδύνου. Όμως ολοένα νεώτερα επιστημονικά δεδομένα τονίζουν τον ρόλο της μη αλκοολικής λιπώδους διήθησης του ήπατος στην εμφάνιση καρδιαγγειακής νόσου. Έτσι, δημιουργήθηκε το ερώτημα κατά πόσο δύο ανεξάρτητοι παράγοντες καρδιαγγειακού κινδύνου θα μπορούσαν να συσχετίζονται μεταξύ τους. Η ύπαρξη συσχέτισης μεταξύ των δύο παραγόντων ενισχύθηκε από τα τελευταία επιστημονικά δεδομένα που δείχνουν ότι η θεραπεία της αρτηριακής υπέρτασης με συγκεκριμένες κατηγορίες φαρμάκων, ειδικότερα με τους αναστολείς του μετατρεπτικού ενζύμου της αγγειοτενσίνης ή με τους αποκλειστές των υποδοχέων της αγγειοτενσίνης ΙΙ, βελτιώνει την στεάτωση. Το κύριο εύρημα της παρούσας διδακτορικής διατριβής είναι ότι η νεοδιαγνωσθείσα και αθεράπευτη ιδιοπαθής αρτηριακή υπέρταση, όπως ορίζεται από την 24ωρη καταγραφή, συσχετίζεται ανεξάρτητα με την μη αλκοολική λιπώδη διήθηση του ήπατος. Επιπλέον, ένα νέο εύρημα της δικής μας μελέτης είναι ότι τα επίπεδα της 24ωρης πρωινής συστολικής αρτηριακής πίεσης συσχετίζονται ανεξάρτητα με την μη αλκοολική λιπώδη διήθηση του ήπατος. Ακόμη, τα αποτελέσματα της μελέτης μας επαληθεύουν προγενέστερα δεδομένα που ανέδειξαν τη συσχέτιση μεταξύ της τελοδιαστολικής διαμέτρου της αριστερής κοιλίας με την μη αλκοολική λιπώδη διήθηση του ήπατος.

Subjects/Keywords: Αρτηριακή υπέρταση; Στεάτωση ήπατος; Arterial hypertension; Liver steatosis

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

APA (6^th Edition):

chouzouri, v. (2016). Συσχέτιση αρτηριακής πίεσης με μη αλκοολική στεάτωση. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/36863

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):

chouzouri, vasiliki. “Συσχέτιση αρτηριακής πίεσης με μη αλκοολική στεάτωση.” 2016. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed January 26, 2021. http://hdl.handle.net/10442/hedi/36863.

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

MLA Handbook (7^th Edition):

chouzouri, vasiliki. “Συσχέτιση αρτηριακής πίεσης με μη αλκοολική στεάτωση.” 2016. Web. 26 Jan 2021.

Vancouver:

chouzouri v. Συσχέτιση αρτηριακής πίεσης με μη αλκοολική στεάτωση. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2016. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/10442/hedi/36863.

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

Council of Science Editors:

chouzouri v. Συσχέτιση αρτηριακής πίεσης με μη αλκοολική στεάτωση. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2016. Available from: http://hdl.handle.net/10442/hedi/36863

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

University of New South Wales

27. Clark, Paul James. Translational genomics, transcriptomics and metabolomics analyses of the metabolic effects of chronic hepatitis C infection and their clinical implications.

Degree: Kirby Institute, 2012, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/52447 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11120/SOURCE01?view=true

► Background: The hepatitis C virus (HCV) relies on host lipid pathways for its life cycle, leading to metabolicconsequences including hypocholesterolemia, insulin resistance and hepatic steatosis.… (more)

▼ Background: The hepatitis C virus (HCV) relies on host lipid pathways for its life cycle, leading to metabolicconsequences including hypocholesterolemia, insulin resistance and hepatic steatosis. These sequelae have varyingclinical implications, including poorer sustained viral response (SVR) to pegylated interferon/ribavirin (PEG/RBV)therapy, increased risk of hepatic fibrosis and residual risk of liver disease (eg fibrosis, steatosis) and complications(eg hepatocellular carcinoma), even after SVR.Aims: To define host genomic and metabolomic profiles associated with hypocholesterolemia, hepatic steatosis,hepatic fibrosis and hepatic inflammation in chronic HCV infection, and to assess their clinical impacts.Methods: Genome wide association studies, candidate gene studies, microarray based mRNA transcription profiling,liquid chromatography/mass spectrometry metabolomic assays, multivariable regression models (MVR).Results: In HCV genotype 1 (G1), IL28B genotype is the only common variant associated with LDL-C levels. LDL-Clevels remain significant predictors of SVR. Host IL28B and PNPLA3 polymorphism are significant host determinantsof susceptibility to hepatic steatosis in chronic HCV G1 infection. Lower PNPLA3 genotype frequency in AfricanAmerican (AA) patients may explain their lower frequency of hepatic steatosis relative to Caucasian Americans,despite greater metabolic risk factors in AA patients. PNPLA3 was associated with Mallory bodies and lobularinflammation (a pattern seen in non-alcoholic fatty liver disease) but not fibrosis. Gene expression enrichmentassociated with PNPLA3 genotype and varied phenotypes of histopathological injury include a number of novelgenetic associations as well as transcripts previously identified which warrant further investigation. HCV perturbs thedistal cholesterol synthesis pathway in a HCV genotype-specific manner but the levels of the proximal sterollanosterol, which has important cholesterol regulation effects, is preserved.Conclusions: Taken together, these translational genomics and metabolics studies provide insights into the nature ofhost-virus metabolic interactions in chronic HCV and their clinical sequelae. Advisors/Committee Members: Dore, Gregory, Kirby Institute, Faculty of Medicine, UNSW.

Subjects/Keywords: Trascriptomics; Hepatitis C; Genomics; Metabolomics; Steatosis; IL28B; PNPLA3; GWAS

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APA (6^th Edition):

Clark, P. J. (2012). Translational genomics, transcriptomics and metabolomics analyses of the metabolic effects of chronic hepatitis C infection and their clinical implications. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/52447 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11120/SOURCE01?view=true

Chicago Manual of Style (16^th Edition):

Clark, Paul James. “Translational genomics, transcriptomics and metabolomics analyses of the metabolic effects of chronic hepatitis C infection and their clinical implications.” 2012. Doctoral Dissertation, University of New South Wales. Accessed January 26, 2021. http://handle.unsw.edu.au/1959.4/52447 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11120/SOURCE01?view=true.

MLA Handbook (7^th Edition):

Clark, Paul James. “Translational genomics, transcriptomics and metabolomics analyses of the metabolic effects of chronic hepatitis C infection and their clinical implications.” 2012. Web. 26 Jan 2021.

Vancouver:

Clark PJ. Translational genomics, transcriptomics and metabolomics analyses of the metabolic effects of chronic hepatitis C infection and their clinical implications. [Internet] [Doctoral dissertation]. University of New South Wales; 2012. [cited 2021 Jan 26]. Available from: http://handle.unsw.edu.au/1959.4/52447 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11120/SOURCE01?view=true.

Council of Science Editors:

Clark PJ. Translational genomics, transcriptomics and metabolomics analyses of the metabolic effects of chronic hepatitis C infection and their clinical implications. [Doctoral Dissertation]. University of New South Wales; 2012. Available from: http://handle.unsw.edu.au/1959.4/52447 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11120/SOURCE01?view=true

University of New South Wales

28. Wainwright, Camilla. Assessment of myocardial and hepatic steatosis, fibrosis and viability using ex vivo, in vivo and advanced imaging techniques.

Degree: Clinical School - St Vincent's Hospital, 2016, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/60083 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:51140/SOURCE2?view=true

► The novel technique of 1H MRS at a high-field strength (3 Tesla) was demonstrated to be a reproducible method to assess hepatic lipid content.This technique… (more)

▼ The novel technique of 1H MRS at a high-field strength (3 Tesla) was demonstrated to be a reproducible method to assess hepatic lipid content.This technique was then used with another novel MR sequence of T1 mapping (ShMOLLI) at 3T to evaluate liver steatosis and fibrosis in subjectswith early type 2 diabetes. It was found that these subjects with early diabetes already had marked liver steatosis, compared to a matched controlgroup. There was no evidence of increased T1 values, as a measure of fibrosis. These advanced MR and MRS techniques were then used at 3Tto evaluate the myocardium in subjects with early type 2 diabetes. It was demonstrated that cardiac lipid content was elevated and PCr/ATP wasreduced, but cardiac systolic and diastolic function remained normal in these subjects. There was also no significant difference in myocardial strainbetween the group of diabetics and matched controls.Most of the previous MR studies looking at subjects with diabetes include patients who have had the disease for a longer duration and are often onmultiple medications. The subjects in the MR studies in this thesis had been recently diagnosed with diabetes and had not developed symptoms ofend-organ disease. The work presented here shows that, even in the early stages of diabetes, the metabolic abnormalities occurring in diabeteshad already begun to produce sub-clinical end-organ changes.Finally, an anti-fibrotic compound called Tranilast was investigated to assess its effect on the myocardial reperfusion-injury and fibrosis pathwaysin the isolated rat heart model. At lower dose Tranilast (10uM), it was shown there was marginal improvement in several of the parameters toassess recovery of cardiac function. There was also a reduction of LDH, a marker of cardiomyocyte injury. Advisors/Committee Members: McCrohon, Jane, Clinical School - St Vincent's Hospital, Faculty of Medicine, UNSW, Holloway, Cameron, Clinical School - St Vincent's Hospital, Faculty of Medicine, UNSW, MacDonald, Peter Simon, Clinical School - St Vincent's Hospital, Faculty of Medicine, UNSW.

Subjects/Keywords: Advanced imaging techniques; Myocardial and hepatic steatosis; Vivo

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

APA (6^th Edition):

Wainwright, C. (2016). Assessment of myocardial and hepatic steatosis, fibrosis and viability using ex vivo, in vivo and advanced imaging techniques. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/60083 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:51140/SOURCE2?view=true

Chicago Manual of Style (16^th Edition):

Wainwright, Camilla. “Assessment of myocardial and hepatic steatosis, fibrosis and viability using ex vivo, in vivo and advanced imaging techniques.” 2016. Doctoral Dissertation, University of New South Wales. Accessed January 26, 2021. http://handle.unsw.edu.au/1959.4/60083 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:51140/SOURCE2?view=true.

MLA Handbook (7^th Edition):

Wainwright, Camilla. “Assessment of myocardial and hepatic steatosis, fibrosis and viability using ex vivo, in vivo and advanced imaging techniques.” 2016. Web. 26 Jan 2021.

Vancouver:

Wainwright C. Assessment of myocardial and hepatic steatosis, fibrosis and viability using ex vivo, in vivo and advanced imaging techniques. [Internet] [Doctoral dissertation]. University of New South Wales; 2016. [cited 2021 Jan 26]. Available from: http://handle.unsw.edu.au/1959.4/60083 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:51140/SOURCE2?view=true.

Council of Science Editors:

Wainwright C. Assessment of myocardial and hepatic steatosis, fibrosis and viability using ex vivo, in vivo and advanced imaging techniques. [Doctoral Dissertation]. University of New South Wales; 2016. Available from: http://handle.unsw.edu.au/1959.4/60083 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:51140/SOURCE2?view=true

29. Pais, Raluca. L’inflammation hépatique dans les formes sévères de NAFLD : implications cliniques, médiateurs et stratégies diagnostiques : Role of chronic inflammation in advanced NAFLD : mechanisms, clinical impact and diagnostic strategies.

Degree: Docteur es, Physiologie et Physiopathologie, 2015, Université Pierre et Marie Curie – Paris VI

URL: http://www.theses.fr/2015PA066223

►

L’objectif général de ce travail était de mieux définir à travers des études cliniques le rôle de l’inflammation hépatique dans l’histoire naturelle de la NAFLD.… (more)

▼

L’objectif général de ce travail était de mieux définir à travers des études cliniques le rôle de l’inflammation hépatique dans l’histoire naturelle de la NAFLD. La première étude a montré que les lésions d’inflammation lobulaire ou de fibrose, même minimes, sont associées avec un risque de progression de la maladie à moyen terme. Souvent cette progression s’accompagnait d’une aggravation des facteurs de risque métabolique. La deuxième étude a démontré que les facteurs de risque métaboliques sont fréquents chez les patients avec une maladie alcoolique du foie et augmentent significativement le risque de carcinome hépatocellulaire au stade de cirrhose. Ces résultats permettent d’identifier un groupe des patients buveurs excessifs ayant un risque élevé de carcinome hépatocellulaire. La troisième étude a porté sur une cohorte transversale de plus de 5000 patients. La stéatose était un facteur associé avec la présence des lésions d’athérosclérose indépendamment des facteurs de risque cardiovasculaire classiques. Dans une cohorte de 1800 patients suivis en moyenne 8 ans, nous avons montré que la stéatose était associée à la survenue des lésions d’athérosclérose carotidienne. Ces résultats, suggèrent que la stéatose est non seulement un marqueur de risque mais un facteur qui intervient dans la pathogenèse de l’athérosclérose carotidienne. En conclusion, nos résultats suggèrent que l'inflammation hépatique, dans un contexte de stéatose contribue à la progression des lésions hépatiques, favorise l'expression de médiateurs pro-athérogènes et l’activation des voies de carcinogenèse ce qui aurait pour effet l'apparition des complications extrahépatiques chez les patients avec NAFLD.

The aim of this work was to analyze the role of chronic systemic inflammation into the natural history of NAFLD. We first undertook a study of NAFLD patients with repeat liver biopsies and demonstrated that mild lobular or portal inflammation or fibrosis in any location substantially increases the risk of progression to steatohepatitis or advanced fibrosis. Disease progression occurred concomitant with worsening of the metabolic conditions during follow-up. In the second study, we analyzed the prevalence and the impact of steatosis and metabolic risk factors on the risk of developing hepatocellular carcinoma in patients with alcoholic cirrhosis undergoing liver transplantation. The main finding of this study was that patients with advanced ALD have a high prevalence of NAFLD, and that this comorbid association confers a significantly increased risk of hepatocellular carcinoma. These findings are important for risk stratification of HCC in patients with ALD. In the third study we demonstrated that steatosis predicted carotid atherosclerosis independently of the association with classical cardiovascular risk factors. Second, in a subset of patients with longitudinal follow-up we demonstrated that baseline NAFLD was an independent predictor for incident carotid plaques. These results suggest that NAFLD is not only a marker but also an “active…

Advisors/Committee Members: Ratziu, Vlad (thesis director), Housset, Chantal (thesis director).

Subjects/Keywords: Stéatose; Steatohépatite; Fibrose; Inflammation; Carcinome hépatocellulaire; Athérosclérose; Steatosis; Atherosclerosis; 616.3

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

APA (6^th Edition):

Pais, R. (2015). L’inflammation hépatique dans les formes sévères de NAFLD : implications cliniques, médiateurs et stratégies diagnostiques : Role of chronic inflammation in advanced NAFLD : mechanisms, clinical impact and diagnostic strategies. (Doctoral Dissertation). Université Pierre et Marie Curie – Paris VI. Retrieved from http://www.theses.fr/2015PA066223

Chicago Manual of Style (16^th Edition):

Pais, Raluca. “L’inflammation hépatique dans les formes sévères de NAFLD : implications cliniques, médiateurs et stratégies diagnostiques : Role of chronic inflammation in advanced NAFLD : mechanisms, clinical impact and diagnostic strategies.” 2015. Doctoral Dissertation, Université Pierre et Marie Curie – Paris VI. Accessed January 26, 2021. http://www.theses.fr/2015PA066223.

MLA Handbook (7^th Edition):

Pais, Raluca. “L’inflammation hépatique dans les formes sévères de NAFLD : implications cliniques, médiateurs et stratégies diagnostiques : Role of chronic inflammation in advanced NAFLD : mechanisms, clinical impact and diagnostic strategies.” 2015. Web. 26 Jan 2021.

Vancouver:

Pais R. L’inflammation hépatique dans les formes sévères de NAFLD : implications cliniques, médiateurs et stratégies diagnostiques : Role of chronic inflammation in advanced NAFLD : mechanisms, clinical impact and diagnostic strategies. [Internet] [Doctoral dissertation]. Université Pierre et Marie Curie – Paris VI; 2015. [cited 2021 Jan 26]. Available from: http://www.theses.fr/2015PA066223.

Council of Science Editors:

Pais R. L’inflammation hépatique dans les formes sévères de NAFLD : implications cliniques, médiateurs et stratégies diagnostiques : Role of chronic inflammation in advanced NAFLD : mechanisms, clinical impact and diagnostic strategies. [Doctoral Dissertation]. Université Pierre et Marie Curie – Paris VI; 2015. Available from: http://www.theses.fr/2015PA066223

30. Monteiro, Paula Alves [UNESP]. Efeito de diferentes modelos de exercício físico sobre a composição corporal, marcadores metabólicos e inflamatórios em adolescentes obesos.

Degree: 2017, Universidade Estadual Paulista

URL: http://hdl.handle.net/11449/150365

►

A prevalência da obesidade na população pediátrica aumenta a um ritmo acelerado em muitos países, e tem se tornado um importante problema de saúde pública.… (more)

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A prevalência da obesidade na população pediátrica aumenta a um ritmo acelerado em muitos países, e tem se tornado um importante problema de saúde pública. O exercício físico (crônico e agudo) continua sendo uma pedra angular nas intervenções com a população pediátrica obesa. Assim, o objetivo do estudo foi investigar o efeito de modelos distintos de exercício físico agudo e crônico na composição corporal, variáveis metabólicas e resposta dos marcadores inflamatórios em adolescentes obesos com ou sem esteatose hepática (EH). Materiais e Métodos: Estudo crônico - 32 adolescentes obesos participaram de dois grupos de treinamento randomizados, concorrente ou aeróbico durante 20 semanas (50 minutos x 3 por semana), e foram comparados a um grupo controle de 16 sujeitos. Estudo Agudo - 19 adolescentes obesos realizaram duas sessões experimentais, separadas por uma semana, Exercício Intermitente de Intensidade Moderada (EIIM) (3 min: 1 min a 65% velocidade máxima atingida durante o teste de esteira, totalizando ~ 3 km) e Exercício Intermitente de Alta Intensidade (EIAI) (2 min: 1 min a 95% da velocidade máxima alcançada durante o teste de esteira, totalizando ~ 3 km). Ambos os estudos mensuraram a composição corporal dos voluntários utilizando-se a absortometria de raio-x de dupla energia, perfil metabólico e inflamatório, bem como o diagnóstico da EH e a espessura da gordura subcutânea e visceral utilizando-se o ultrassom. Resultados: No estudo crônico após 20 semanas, ambos os grupos de treinamento reduziram significativamente o % GC por 2,9-3,6% em comparação ao grupo controle que não obteve mudanças (p = 0,042). Houve também mudanças positivas no perfil lipídico dos grupos que treinaram. No entanto, as variáveis inflamatórias não se alteraram. Não houve diferença entre as mudanças dos grupos de treinamento aeróbio e concorrente. Já o estudo agudo houve alterações significativas no grupo EIAI com EH, no triacilglicerol (aumentou de 17,9%) e cortisol (aumentou 93,03%) e no grupo EIAI sem EH, houve alterações no triacilglicerol (aumentou de 10,6%), no cortisol (aumentou de 18,1%) e IL-6 (aumentou de 20,4%). No grupo EIIM com EH, houve alteração significativa apenas no cortisol (diminuição de 46,9%) e no grupo EIIM sem EH foram observadas alterações no triacilglicerol (aumento de 9,4%) e cortisol (diminuição de 41%). Concluímos que os treinamentos concorrente e aeróbio foram capazes de propiciar benefícios na composição corporal e nas variáveis metabólicas em adolescentes com e sem EH, e só o esforço aeróbio agudo de alta intensidade propiciou alterações inflamatórias nos adolescentes sem EH.

The prevalence of obesity in pediatric population is increasing at an accelerated rate in many countries, and has become a major public health concern. Physical activity, particularly exercise training (chronic and acute), remains to be a cornerstone of pediatric obesity interventions, and of diseases associated, such as the hepatic steatosis. Thus the aim of the study was analyze the effect of different types of exercise on body…

Advisors/Committee Members: Freitas Junior, Ismael Forte [UNESP], Lira, Fabio Santos [UNESP], Universidade Estadual Paulista (UNESP).

Subjects/Keywords: Gordura corporal; Treinamento físico; Obesidade; Esteatose hepática; Body fat; Physical training; Obesity; Hepatic steatosis

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

APA (6^th Edition):

Monteiro, P. A. [. (2017). Efeito de diferentes modelos de exercício físico sobre a composição corporal, marcadores metabólicos e inflamatórios em adolescentes obesos. (Thesis). Universidade Estadual Paulista. Retrieved from http://hdl.handle.net/11449/150365

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):

Monteiro, Paula Alves [UNESP]. “Efeito de diferentes modelos de exercício físico sobre a composição corporal, marcadores metabólicos e inflamatórios em adolescentes obesos.” 2017. Thesis, Universidade Estadual Paulista. Accessed January 26, 2021. http://hdl.handle.net/11449/150365.

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

MLA Handbook (7^th Edition):

Monteiro, Paula Alves [UNESP]. “Efeito de diferentes modelos de exercício físico sobre a composição corporal, marcadores metabólicos e inflamatórios em adolescentes obesos.” 2017. Web. 26 Jan 2021.

Vancouver:

Monteiro PA[. Efeito de diferentes modelos de exercício físico sobre a composição corporal, marcadores metabólicos e inflamatórios em adolescentes obesos. [Internet] [Thesis]. Universidade Estadual Paulista; 2017. [cited 2021 Jan 26]. Available from: http://hdl.handle.net/11449/150365.

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

Council of Science Editors:

Monteiro PA[. Efeito de diferentes modelos de exercício físico sobre a composição corporal, marcadores metabólicos e inflamatórios em adolescentes obesos. [Thesis]. Universidade Estadual Paulista; 2017. Available from: http://hdl.handle.net/11449/150365

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

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Open Access Theses and Dissertations