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 http://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 July 17, 2019. http://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. 17 Jul 2019.

Vancouver:

Kim MH. Regulation and Function of Zinc and Zinc Transporters during ER Stress. [Internet] [Doctoral dissertation]. University of Florida; 2017. [cited 2019 Jul 17]. Available from: http://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: http://ufdc.ufl.edu/UFE0051263

University of Dundee

2. 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: http://hdl.handle.net/10588/9b2509f1-3391-45fa-91eb-9b5364a9b6d9

► 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: 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 http://hdl.handle.net/10588/9b2509f1-3391-45fa-91eb-9b5364a9b6d9

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 July 17, 2019. http://hdl.handle.net/10588/9b2509f1-3391-45fa-91eb-9b5364a9b6d9.

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. 17 Jul 2019.

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 2019 Jul 17]. Available from: http://hdl.handle.net/10588/9b2509f1-3391-45fa-91eb-9b5364a9b6d9.

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: http://hdl.handle.net/10588/9b2509f1-3391-45fa-91eb-9b5364a9b6d9

Univerzitet u Beogradu

3. 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)

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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 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 July 17, 2019. 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. 17 Jul 2019.

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 2019 Jul 17]. 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 Louisville

4. Kaiser, J. Phillip, 1981-. The role of PKC-epsilon in models of alcohol- and toxin-induced liver disease.

Degree: PhD, 2009, University of Louisville

URL: 10.18297/etd/720 ; https://ir.library.louisville.edu/etd/720

► Alcoholic liver disease (ALD) is a serious concern for the world's population. It is one of the leading causes of death and is also a… (more)

▼ Alcoholic liver disease (ALD) is a serious concern for the world's population. It is one of the leading causes of death and is also a huge economic burden. The biochemical mechanisms responsible for ALD are incompletely understood, therefore there is no FDA approved therapy to treat or reverse liver damage caused by alcohol exposure. Whereas the mechanisms behind ALD are poorly understood, the disease progression is well known. The first pathological step of ALD is steatosis followed by inflammation and necrosis; if the insult(s) responsible for the previous pathologies persists, fibrosis and cirrhosis can then develop. In previous experimental studies, preventing alcohol-induced steatosis can protect against further stages of liver damage; thus, understanding the mechanisms responsible for ethanol-induced steatosis may result in a therapy to treat ALD. Previous studies have shown that protein kinase-c epsilon (PKC[varepsilon]) contributes to steatosis owing to a non-alcoholic high fat diet. However, the role of PKC[varepsilon] in alcohol-induced fatty liver is not yet known. Therefore, the goal of this work was to investigate the role of PKC[varepsilon] in not only steatosis, but also in later stages of liver disease (i.e. steatohepatitis and fibrosis). It was determined in both acute and chronic mouse models of ethanol exposure that PKC[varepsilon] plays a causal role in steatosis owing to ethanol. Surprisingly, blocking steatosis had no apparent protective effect on inflammation and necrosis in the chronic model, which implies that these pathologies may have mechanistic distinctions. Lastly, it was shown that PKC[varepsilon] plays a pivotal role in the development of fibrosis caused by chronic exposure to carbon tetrachloride (CCl 4 ). In summary, it appears that PKC[varepsilon] plays a causal role in the early (steatosis) and late (fibrosis) stages of liver disease. The inhibition of PKC[varepsilon] could therefore result in a viable therapeutic means of preventing ALD. Advisors/Committee Members: Arteel, Gavin Edward.

Subjects/Keywords: Liver disease; Alcoholic liver disease; Steatosis; Fibrosis

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APA (6^th Edition):

Kaiser, J. Phillip, 1. (2009). The role of PKC-epsilon in models of alcohol- and toxin-induced liver disease. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/720 ; https://ir.library.louisville.edu/etd/720

Chicago Manual of Style (16^th Edition):

Kaiser, J. Phillip, 1981-. “The role of PKC-epsilon in models of alcohol- and toxin-induced liver disease.” 2009. Doctoral Dissertation, University of Louisville. Accessed July 17, 2019. 10.18297/etd/720 ; https://ir.library.louisville.edu/etd/720.

MLA Handbook (7^th Edition):

Kaiser, J. Phillip, 1981-. “The role of PKC-epsilon in models of alcohol- and toxin-induced liver disease.” 2009. Web. 17 Jul 2019.

Vancouver:

Kaiser, J. Phillip 1. The role of PKC-epsilon in models of alcohol- and toxin-induced liver disease. [Internet] [Doctoral dissertation]. University of Louisville; 2009. [cited 2019 Jul 17]. Available from: 10.18297/etd/720 ; https://ir.library.louisville.edu/etd/720.

Council of Science Editors:

Kaiser, J. Phillip 1. The role of PKC-epsilon in models of alcohol- and toxin-induced liver disease. [Doctoral Dissertation]. University of Louisville; 2009. Available from: 10.18297/etd/720 ; https://ir.library.louisville.edu/etd/720

University of Sydney

5. 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 (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 July 17, 2019. 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. 17 Jul 2019.

Vancouver:

d'Avigdor WMH. Differential gene expression in HCV liver injury . [Internet] [Thesis]. University of Sydney; 2015. [cited 2019 Jul 17]. 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

University of Adelaide

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

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 July 17, 2019. 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. 17 Jul 2019.

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 2019 Jul 17]. 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

University of Minnesota

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

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 July 17, 2019. 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. 17 Jul 2019.

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 2019 Jul 17]. 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

8. Ungerleider, Nathan A. Deletions of Fstl3 and/or Fst Isoforms 303 and 315 Results in Hepatic Steatosis.

Degree: MS, Molecular & Cellular Biology, 2010, University of Massachusetts

URL: https://scholarworks.umass.edu/theses/478

► TGFβ ligands, activin and myostatin have been shown to stimulate insulin production and secretion. Antagonists, Follistatin (FST) and Follistatin like 3 (FSTL3) were partially and… (more)

Subjects/Keywords: hepatic steatosis; insulin resistance; srebp1; lipid uptake

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

APA (6^th Edition):

Ungerleider, N. A. (2010). Deletions of Fstl3 and/or Fst Isoforms 303 and 315 Results in Hepatic Steatosis. (Masters Thesis). University of Massachusetts. Retrieved from https://scholarworks.umass.edu/theses/478

Chicago Manual of Style (16^th Edition):

Ungerleider, Nathan A. “Deletions of Fstl3 and/or Fst Isoforms 303 and 315 Results in Hepatic Steatosis.” 2010. Masters Thesis, University of Massachusetts. Accessed July 17, 2019. https://scholarworks.umass.edu/theses/478.

MLA Handbook (7^th Edition):

Ungerleider, Nathan A. “Deletions of Fstl3 and/or Fst Isoforms 303 and 315 Results in Hepatic Steatosis.” 2010. Web. 17 Jul 2019.

Vancouver:

Ungerleider NA. Deletions of Fstl3 and/or Fst Isoforms 303 and 315 Results in Hepatic Steatosis. [Internet] [Masters thesis]. University of Massachusetts; 2010. [cited 2019 Jul 17]. Available from: https://scholarworks.umass.edu/theses/478.

Council of Science Editors:

Ungerleider NA. Deletions of Fstl3 and/or Fst Isoforms 303 and 315 Results in Hepatic Steatosis. [Masters Thesis]. University of Massachusetts; 2010. Available from: https://scholarworks.umass.edu/theses/478

Université Paris-Sud – Paris XI

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

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 July 17, 2019. 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. 17 Jul 2019.

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 2019 Jul 17]. 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

10. 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 July 17, 2019. 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. 17 Jul 2019.

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 2019 Jul 17]. 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/ ;

11. 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)

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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 July 17, 2019. 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. 17 Jul 2019.

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 2019 Jul 17]. 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/ ;

12. 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

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):

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 July 17, 2019. 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. 17 Jul 2019.

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 2019 Jul 17]. 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

The Ohio State University

13. Purushotham, Aparna. Role of bioactive compounds in the regulation of insulin sensitivity.

Degree: PhD, Ohio State University Nutrition, 2007, The Ohio State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1173108971

► Dietary agents have important implications in the treatment of type 2 diabetes. My first objective was to determine the effectiveness of the dietary fat, conjugated… (more)

▼ Dietary agents have important implications in the treatment of type 2 diabetes. My first objective was to determine the effectiveness of the dietary fat, conjugated linoleic acid (CLA) in the attenuation of hepatic steatosis in Wistar rats fed a CON diet or a diet containing CLA. CLA decreased hepatic triglycerides (TG) compared to the CON diet. The CLA mediated difference was associated with increases in the mRNA markers of lipid oxidation and decreased markers of lipogenesis. These effects were observed in the absence of decreases in adiposity, adipokines, body weight and food intake suggesting that CLA is protective against hepatic TG accumulation in rats by modulating hepatic lipid metabolism. CLA is associated with the development of hepatic steatosis and insulin resistance in mice along with rapid ablation of adipose tissue. Therefore, my second objective was to determine the role of adipokines in CLA mediated insulin resistance in male C57BL/6 and leptin deficient ob/ob mice that were fed a diet supplemented with or without CLA. CLA supplementation significantly decreased body fat, induced hepatic steatosis and insulin resistance in mice. Furthermore, these changes were associated with significant depletion of adiponectin, but not leptin. When adiponectin levels were restored by either removal of CLA from diet of C57BL/6 mice or administering rosiglitazone to ob/ob mice fed CLA, insulin resistance and hepatic steatosis were attenuated. Thus, we show that adiponectin is an important factor responsible for insulin resistance caused by CLA. Because increased hepatic glucose production (HGP) contributes to fasting hyperglycemia in type 2 diabetes, my third objective was to determine the effectiveness and elucidate the mechanisms by which dietary bioactive compounds, especially the citrus fruit flavonoid naringenin, exert glucose lowering effects in cultured hepatocytes. The aglycone naringenin significantly suppressed HGP from Fao hepatoma cells similar to insulin and metformin. Furthermore, naringenin, similar to metformin, decreased cellular ATP concentrations and increased p-AMPK, which when activated, suppresses hepatic glucose output. The suppressive effects of naringenin on HGP and similarity to the action of metformin are novel and intriguing and future studies using in vivo models are warranted. Advisors/Committee Members: Belury, Martha (Advisor).

Subjects/Keywords: Health Sciences, Nutrition; Insulin resistance; Hepatic steatosis; Conjugated linoleic acid; Naringenin

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

APA (6^th Edition):

Purushotham, A. (2007). Role of bioactive compounds in the regulation of insulin sensitivity. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1173108971

Chicago Manual of Style (16^th Edition):

Purushotham, Aparna. “Role of bioactive compounds in the regulation of insulin sensitivity.” 2007. Doctoral Dissertation, The Ohio State University. Accessed July 17, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1173108971.

MLA Handbook (7^th Edition):

Purushotham, Aparna. “Role of bioactive compounds in the regulation of insulin sensitivity.” 2007. Web. 17 Jul 2019.

Vancouver:

Purushotham A. Role of bioactive compounds in the regulation of insulin sensitivity. [Internet] [Doctoral dissertation]. The Ohio State University; 2007. [cited 2019 Jul 17]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1173108971.

Council of Science Editors:

Purushotham A. Role of bioactive compounds in the regulation of insulin sensitivity. [Doctoral Dissertation]. The Ohio State University; 2007. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1173108971

University of Cincinnati

14. Chen, Ying. Relationship of Glutathione Deficiency to Oxidative Stress-Related Disease and Aging.

Degree: PhD, Medicine : Toxicology (Environmental Health), 2007, University of Cincinnati

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1172086646

► Glutathione (GSH) is the most abundant cellular thiol antioxidant, disturbance in GSH homeostasis has been associated with several oxidative stress-related diseases and aging. The rate-limiting… (more)

▼ Glutathione (GSH) is the most abundant cellular thiol antioxidant, disturbance in GSH homeostasis has been associated with several oxidative stress-related diseases and aging. The rate-limiting enzyme in GSH biosynthesis, glutamate-cysteine ligase (GCL), is composed of a catalytic subunit (GCLC) and a modifier subunit (GCLM). Using mouse recombinant proteins, we demonstrate that: (a) binding of GCLM to GCLC is efficient in vitroto form the holoenyzme; (b) compared with GCLC, the holoenzyme has a higher Vmax, lower Kms for glutamate and ATP, and a higher Ki for GSH feedback inhibition; (c) GCLM may limit the levels of GSH biosynthesis in most of the tissues. In agreement with the in vitroresults, Gclm(-/-)mice have a 60-90% depletion of tissue GSH, whereas showing no overt phenotype; Gclm(-/-)mouse fetal fibroblasts (MFFs), however, are highly sensitive to oxidative insults. We therefore used Gclm(-/-)MFFs to study the role of GSH in cellular aging. Gclm(-/-)MFFs, having 25% of normal intracellular GSH, undergo premature senescence in culture. This phenotype is accompanied by increased cellular ROS and DNA damage, and induction of p53 and p21 proteins. N-acetylcysteine (NAC) supplementation restores intracellular GSH to control levels and prevents premature senescence in Gclm(-/-)MFFs. We conclude that GSH homeostasis is an important determinant in cellular senescence. As GSH depletion has been associated with numerous liver diseases, the specific role of GSH deficiency in liver pathophysiology has been investigated using the hepatocyte-specific GCLC knockout [ Gclc(h/h)] mice. Having progressive depletion of hepatic GSH to 4.5% of control levels, Gclc(h/h)mice develop severe steatosis and die of liver failure within a month. Hepatic mitochondria have concomitant depletion of GSH to 15% and appear to be the major affected organelle, showing atypical morphology and dysfunction. NAC supplementation in the drinking water prevents mortality in the Gclc(h/h)mice, by preserving mitochondrial GSH up to 65% of control levels and partially restoring their function. These NAC-rescued Gclc(h/h)mice, however, still reveal persistent oxidative stress in the liver and develop liver cirrhosis with age. These data indicate the essential role of GSH homeostasis in maintaining normal liver function. Advisors/Committee Members: Nebert, Dr. Daniel (Advisor).

Subjects/Keywords: Health Sciences, Toxicology; glutathione; oxidative stress; knockout; senescence; steatosis

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

APA (6^th Edition):

Chen, Y. (2007). Relationship of Glutathione Deficiency to Oxidative Stress-Related Disease and Aging. (Doctoral Dissertation). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1172086646

Chicago Manual of Style (16^th Edition):

Chen, Ying. “Relationship of Glutathione Deficiency to Oxidative Stress-Related Disease and Aging.” 2007. Doctoral Dissertation, University of Cincinnati. Accessed July 17, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1172086646.

MLA Handbook (7^th Edition):

Chen, Ying. “Relationship of Glutathione Deficiency to Oxidative Stress-Related Disease and Aging.” 2007. Web. 17 Jul 2019.

Vancouver:

Chen Y. Relationship of Glutathione Deficiency to Oxidative Stress-Related Disease and Aging. [Internet] [Doctoral dissertation]. University of Cincinnati; 2007. [cited 2019 Jul 17]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1172086646.

Council of Science Editors:

Chen Y. Relationship of Glutathione Deficiency to Oxidative Stress-Related Disease and Aging. [Doctoral Dissertation]. University of Cincinnati; 2007. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1172086646

Case Western Reserve University

15. Chen, Xiaocong. The Regulation of Adiponectin by Ethanol Feeding and Taurine Supplementation.

Degree: PhD, Nutrition, 2009, Case Western Reserve University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=case1221077215

► Chronic ethanol feeding to mice and rats decreases serum adiponectin concentration and adiponectin treatment during chronic ethanol feeding attenuates ethanol-induced liver injury in mice.… (more)

▼ Chronic ethanol feeding to mice and rats decreases serum adiponectin concentration and adiponectin treatment during chronic ethanol feeding attenuates ethanol-induced liver injury in mice. Here we have investigated the impact of chronic ethanol feeding on adiponectin expression and secretion by adipose tissue. Rats were fed a 36% Lieber-DeCarli ethanol-containing liquid diet or pair-fed control diet for 4 weeks. Chronic ethanol feeding decreased adiponectin mRNA, but had no effect on adiponectin protein, in subcutaneous adipose tissue. Chronic ethanol feeding also reduced adiponectin secretion by isolated subcutaneous adipocytes without affecting the intracellular adiponectin. Treatment with brefeldin A suppressed adiponectin secretion by subcutaneous adipocytes from pair-fed rats, but had little effect after ethanol feeding. In subcutaneous adipocytes from pair-fed rats, adiponectin was enriched in endoplasmic reticulum (ER)/Golgi relative to plasma membrane; however, after chronic ethanol feeding, adiponectin was equally distributed between plasma membrane and ER/Golgi fractions. These data suggested that chronic ethanol feeding decreased circulating adiponectin by inhibiting adiponectin and secretion by subcutaneous adipocytes. Chronic ethanol feeding increases oxidative stress and endoplasmic reticulum (ER) stress in adipose tissue. Here we hypothesized that supplemental taurine, an amino acid has both anti-oxidative stress and anti-ER stress, would prevent ethanol-induced decreases in adiponectin expression and attenuate liver injury. Serum adiponectin concentrations decreased as early as 4-7 days after feeding rats a 36% ethanol diet. This rapid decrease was associated with increased oxidative, but not ER stress, in subcutaneous adipose tissue. Taurine prevented ethanol-induced oxidative stress, as well as increased inflammatory cytokine expression, in adipose tissue. Taurine prevented the ethanol-induced decrease in C/EBPa and PPARa, normalizing adiponectin mRNA and serum adiponectin concentrations. Taurine also prevented ethanol-induced hepatic oxidative stress and attenuated steatosis, at least in part, by increasing expression of genes involved in fatty acid oxidation. Taken together, taurine normalized ethanol-induced decrease in adiponectin expression; this normalization was associated with prevention of ethanol-induced oxidative stress in subcutaneous adipose tissue. Taurine prevented ethanol-induced decreases in serum adiponectin; normalized adiponectin was associated with an attenuation of ethanol-induced hepatic oxidative stress and steatosis. Advisors/Committee Members: Whittaker, Jonathan (Committee Chair), Nagy, Laura (Advisor).

Subjects/Keywords: Nutrition; Adiponectin; ethanol feeding; taurine; oxidative stress; steatosis

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APA (6^th Edition):

Chen, X. (2009). The Regulation of Adiponectin by Ethanol Feeding and Taurine Supplementation. (Doctoral Dissertation). Case Western Reserve University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=case1221077215

Chicago Manual of Style (16^th Edition):

Chen, Xiaocong. “The Regulation of Adiponectin by Ethanol Feeding and Taurine Supplementation.” 2009. Doctoral Dissertation, Case Western Reserve University. Accessed July 17, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1221077215.

MLA Handbook (7^th Edition):

Chen, Xiaocong. “The Regulation of Adiponectin by Ethanol Feeding and Taurine Supplementation.” 2009. Web. 17 Jul 2019.

Vancouver:

Chen X. The Regulation of Adiponectin by Ethanol Feeding and Taurine Supplementation. [Internet] [Doctoral dissertation]. Case Western Reserve University; 2009. [cited 2019 Jul 17]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=case1221077215.

Council of Science Editors:

Chen X. The Regulation of Adiponectin by Ethanol Feeding and Taurine Supplementation. [Doctoral Dissertation]. Case Western Reserve University; 2009. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=case1221077215

University of Saskatchewan

16. 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

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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 July 17, 2019. 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. 17 Jul 2019.

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 2019 Jul 17]. 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

University of Saskatchewan

17. Jackel-Cram, Candice Marie. Molecular Mechanisms of Hepatitis C Virus- Associated Steatosis.

Degree: 2009, University of Saskatchewan

URL: http://hdl.handle.net/10388/etd-07312009-130703

► Hepatitis C virus (HCV) infects millions of people worldwide and is one of the leading causes of liver damage. Infection with HCV is strongly correlated… (more)

▼ Hepatitis C virus (HCV) infects millions of people worldwide and is one of the leading causes of liver damage. Infection with HCV is strongly correlated with an increased risk of steatosis, or fatty liver disease, which is caused by a build-up of fat deposits in hepatocytes. All genotypes of HCV appear to cause some degree of steatosis in approximately 50% of infected individuals, especially in the presence of contributing host factors such as diabetes, obesity and alcoholism. However, approximately 70% of genotype 3a infections exhibit steatosis. Furthermore, successful clearance of the genotype 3a virus results in eradication of the steatosis, suggesting the genotype 3a virus may be able to directly cause steatosis. Research suggests a role for the core protein of HCV, which forms the capsid of the virus, in the alteration of lipid metabolism pathways during infection. As such, I hypothesized that: 1) HCV alters lipid metabolism pathways and causes the build up of lipid in hepatocytes and the development of steatosis; 2) HCV-3a core protein has a differential or increased effect on these pathways in comparison to 1b core protein; and 3) other HCV proteins could also play a role in the altering of lipid metabolism. My research characterized the subcellular localization on lipid droplets of the HCV-3a core protein in comparison to HCV-1b core protein. It was found that HCV-3a core causes increased transcriptional activity from the Fatty Acid Synthase (FAS) promoter, an important enzyme involved in the synthesis of triglycerides in hepatocytes. In addition, one specific amino acid of HCV-3a core was determined to be partially responsible for this effect. Further research determined that the effect of HCV-3a core on FAS was dependent on the transcription factor Sterol Response Element Binding Protein-1 (SREBP-1) and the presence of HCV-3a core increased the processing and activity of SREBP-1. HCV core was also able to increase activity of Akt 1 and Akt2; inhibition of Akt activity resulted in decreased SREBP-1 activity thereby indicating that HCV core partially mediates SREBP-1 via Akt. Further experiments examined the role of another HCV protein, NS2, in these same lipid metabolism pathways. NS2 was also able to increase transcription from the FAS promoter via SREBP-1, suggesting that this HCV protein may also be important in the development of steatosis during HCV infection. The evidence provided in these studies shows a very important role for HCV in altering lipid metabolism during infection that may lead to the development of steatosis. Current research suggests that the SREBP-1 pathway may be critical in the life cycle of the virus and these studies have provided important information on how lipid metabolism pathways are being changed by the virus. Hopefully this work can help identify potential treatment options for HCV that can slow down disease progression by preventing the development of steatosis or by decreasing viral replication. Advisors/Committee Members: Liu, Qiang.

Subjects/Keywords: Hepatitis C Virus; Cell Signalling; Akt; FAS; SREBP; Lipid Metabolism; Steatosis

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APA (6^th Edition):

Jackel-Cram, C. M. (2009). Molecular Mechanisms of Hepatitis C Virus- Associated Steatosis. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/etd-07312009-130703

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):

Jackel-Cram, Candice Marie. “Molecular Mechanisms of Hepatitis C Virus- Associated Steatosis.” 2009. Thesis, University of Saskatchewan. Accessed July 17, 2019. http://hdl.handle.net/10388/etd-07312009-130703.

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

MLA Handbook (7^th Edition):

Jackel-Cram, Candice Marie. “Molecular Mechanisms of Hepatitis C Virus- Associated Steatosis.” 2009. Web. 17 Jul 2019.

Vancouver:

Jackel-Cram CM. Molecular Mechanisms of Hepatitis C Virus- Associated Steatosis. [Internet] [Thesis]. University of Saskatchewan; 2009. [cited 2019 Jul 17]. Available from: http://hdl.handle.net/10388/etd-07312009-130703.

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

Council of Science Editors:

Jackel-Cram CM. Molecular Mechanisms of Hepatitis C Virus- Associated Steatosis. [Thesis]. University of Saskatchewan; 2009. Available from: http://hdl.handle.net/10388/etd-07312009-130703

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

18. 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 July 17, 2019. 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. 17 Jul 2019.

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 2019 Jul 17]. 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

University of Texas Medical Branch – Galveston

19. [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 · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

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 July 17, 2019. 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. 17 Jul 2019.

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 2019 Jul 17]. 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 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 July 17, 2019. 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. 17 Jul 2019.

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 2019 Jul 17]. 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 July 17, 2019. 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. 17 Jul 2019.

Vancouver:

WEI G. Roles of the microRNAs in fatty liver lipid accumulation. [Internet] [Thesis]. National University of Singapore; 2012. [cited 2019 Jul 17]. 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

University of New South Wales

22. 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 July 17, 2019. 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. 17 Jul 2019.

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 2019 Jul 17]. 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

Virginia Commonwealth University

23. Kwong, Eric K. The Role of Sphingosine Kinase 2 in Alcoholic Liver Disease.

Degree: PhD, Microbiology & Immunology, 2019, Virginia Commonwealth University

URL: https://scholarscompass.vcu.edu/etd/5808

► Alcoholic liver disease (ALD) is one of the most common liver diseases worldwide characterized by the accumulation of lipids within the liver, inflammation and… (more)

▼ Alcoholic liver disease (ALD) is one of the most common liver diseases worldwide characterized by the accumulation of lipids within the liver, inflammation and the possibility of progressing to cirrhosis and liver failure. More importantly, there are currently no effective treatments for ALD and liver transplantation remains the only therapeutic option for end-stage liver disease. Previous studies have shown that ALD is a result of a combination of endoplasmic reticulum (ER) stress, lipid metabolism dysregulation and inflammation. It has been previously reported that alcohol disrupts gut microbiota homeostasis and causes increased endotoxins that contribute to the pathology of ALD. However, the detailed mechanism(s) underlying ALD and disease progression is poorly understood. We have discovered that sphingosine kinase 2 (SphK2) deficient (SphK2^-/-) mice on an alcohol diet exhibit increased steatosis and inflammation compared to wild type mice. Sphingosine 1-phosphate receptor 2 (S1PR2) and SphK2 have been previously shown to play a key role in nutrient metabolism and signaling. However, their roles in alcohol-induced liver injury have not been characterized. The overall objective of this study is to determine the molecular mechanism(s) by which disruption of S1PR2-mediated SphK2 signaling contributes to ALD. The effects of alcohol on mouse primary hepatocytes and cultured RAW264.7 macrophages were examined. The acute on chronic alcohol mouse model from NIAAA that recapitulates the drinking pattern of human ALD patients was used to study the effects of SphK2 deficiency in ALD. In addition, 60-day chronic alcohol mouse model was used to determine whether a more severe form of ALD was present in SphK2^-/- mice. The results indicated that SphK2^-/- mice on an alcohol diet exhibited an increased amount of hepatic steatosis compared to wild type mice. Genes regulating lipid metabolism were also dysregulated in SphK2^-/- mice. SphK2^-/- mice also had increased inflammation and liver injury as shown by an upregulation of inflammatory markers and increased levels of liver enzymes. Moreover, SphK2 protein expression levels were downregulated in the human livers of alcoholic cirrhotic and hepatocellular carcinoma (HCC) patients. These findings contribute to a greater understanding of the pathophysiology of ALD and could provide information on the development of novel therapeutics against ALD. Advisors/Committee Members: Huiping Zhou.

Subjects/Keywords: sphingolipid; steatosis; lipid signaling; inflammation; bile acids; Biology; Gastroenterology

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

APA (6^th Edition):

Kwong, E. K. (2019). The Role of Sphingosine Kinase 2 in Alcoholic Liver Disease. (Doctoral Dissertation). Virginia Commonwealth University. Retrieved from https://scholarscompass.vcu.edu/etd/5808

Chicago Manual of Style (16^th Edition):

Kwong, Eric K. “The Role of Sphingosine Kinase 2 in Alcoholic Liver Disease.” 2019. Doctoral Dissertation, Virginia Commonwealth University. Accessed July 17, 2019. https://scholarscompass.vcu.edu/etd/5808.

MLA Handbook (7^th Edition):

Kwong, Eric K. “The Role of Sphingosine Kinase 2 in Alcoholic Liver Disease.” 2019. Web. 17 Jul 2019.

Vancouver:

Kwong EK. The Role of Sphingosine Kinase 2 in Alcoholic Liver Disease. [Internet] [Doctoral dissertation]. Virginia Commonwealth University; 2019. [cited 2019 Jul 17]. Available from: https://scholarscompass.vcu.edu/etd/5808.

Council of Science Editors:

Kwong EK. The Role of Sphingosine Kinase 2 in Alcoholic Liver Disease. [Doctoral Dissertation]. Virginia Commonwealth University; 2019. Available from: https://scholarscompass.vcu.edu/etd/5808

University of Southern California

24. Josephrajan, Ajeetha. Calorie restriction reduces liver steatosis in liver specific Pten deleted mouse model.

Degree: MS, Biochemistry & Molecular Biology, 2010, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/381914/rec/1213

► Calorie restriction (CR) is an approach wherein there is moderate restriction of food intake while providing sufficient amount of essential nutrients. CR is beneficial in… (more)

Subjects/Keywords: calorie restriction; fatty acid oxidation; liver; MCAD; Pten; steatosis

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APA (6^th Edition):

Josephrajan, A. (2010). Calorie restriction reduces liver steatosis in liver specific Pten deleted mouse model. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/381914/rec/1213

Chicago Manual of Style (16^th Edition):

Josephrajan, Ajeetha. “Calorie restriction reduces liver steatosis in liver specific Pten deleted mouse model.” 2010. Masters Thesis, University of Southern California. Accessed July 17, 2019. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/381914/rec/1213.

MLA Handbook (7^th Edition):

Josephrajan, Ajeetha. “Calorie restriction reduces liver steatosis in liver specific Pten deleted mouse model.” 2010. Web. 17 Jul 2019.

Vancouver:

Josephrajan A. Calorie restriction reduces liver steatosis in liver specific Pten deleted mouse model. [Internet] [Masters thesis]. University of Southern California; 2010. [cited 2019 Jul 17]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/381914/rec/1213.

Council of Science Editors:

Josephrajan A. Calorie restriction reduces liver steatosis in liver specific Pten deleted mouse model. [Masters Thesis]. University of Southern California; 2010. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/381914/rec/1213

Boston University

25. 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 July 17, 2019. http://hdl.handle.net/2144/34923.

MLA Handbook (7^th Edition):

Yengul, Sanjay S. “Shear wave rheometry with applications in elastography.” 2019. Web. 17 Jul 2019.

Vancouver:

Yengul SS. Shear wave rheometry with applications in elastography. [Internet] [Doctoral dissertation]. Boston University; 2019. [cited 2019 Jul 17]. 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 Louisville

26. 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 (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 July 17, 2019. 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. 17 Jul 2019.

Vancouver:

Donde H. Role of ethanol as a cofactor in HAART induced hepatic steatosis and injury. [Internet] [Masters thesis]. University of Louisville; 2013. [cited 2019 Jul 17]. 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

University of New South Wales

27. 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 (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 July 17, 2019. 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. 17 Jul 2019.

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 2019 Jul 17]. 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

28. 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, Paris Saclay

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 (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). Paris Saclay. 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, Paris Saclay. Accessed July 17, 2019. 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. 17 Jul 2019.

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]. Paris Saclay; 2019. [cited 2019 Jul 17]. 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]. Paris Saclay; 2019. Available from: http://www.theses.fr/2019SACLS068

University of Toronto

29. 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

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

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 July 17, 2019. 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. 17 Jul 2019.

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 2019 Jul 17]. 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

Arizona State University

30. 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

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):

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 July 17, 2019. 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. 17 Jul 2019.

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 2019 Jul 17]. 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

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