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dc.contributor.authorLeung, Christopher-
dc.contributor.authorHerath, Chandana B-
dc.contributor.authorJia, Zhiyuan-
dc.contributor.authorGoodwin, Michelle-
dc.contributor.authorMak, Kai Yan-
dc.contributor.authorWatt, Matthew J-
dc.contributor.authorForbes, Josephine M-
dc.contributor.authorAngus, Peter W-
dc.identifier.citationJournal of Hepatology 2013; 60(4): 832-8en_US
dc.description.abstractAdvanced glycation end-products (AGEs) levels are high in western diets and contribute to tissue injury via activation of RAGE (receptor for AGEs) and generation of reactive oxygen species (ROS). Here, we determined if high dietary AGE intake worsens progression of non-alcoholic fatty liver disease (NAFLD).Male Sprague Dawley rats were fed a methionine choline deficient (MCD) diet for 6 weeks before 6 weeks of a high AGE MCD diet through baking. They were compared with animals on MCD diet or a methionine choline replete (MCR) diet alone for 12 weeks. Hepatic ROS, triglycerides, biochemistry, picro-sirius morphometry, hepatic mRNA expression and immunohistochemistry were determined. Primary hepatic stellate cells (HSCs) from both MCR and MCD animals were exposed to AGEs. ROS, proliferation and mRNA expression were determined.The high AGE MCD diet increased hepatic AGE content and elevated triglycerides, NADPH dependent superoxide production, HNE adducts, steatosis, steatohepatitis (CD43, IL-6, TNF-α) and fibrosis (α-SMA, CTGF, COL1A, picrosirius) compared to MCD alone. In HSCs, AGEs significantly increased ROS production, bromodeoxyuridine proliferation and MCP-1, IL-6, α-SMA, and RAGE expression in HSCs from MCD but not MCR animals. These effects were abrogated by RAGE or NADPH oxidase blockade.In the MCD model of NAFLD, high dietary AGEs increases hepatic AGE content and exacerbates liver injury, inflammation, and liver fibrosis via oxidative stress and RAGE dependent profibrotic effects of AGEs on activated HSCs. This suggests that pharmacological and dietary strategies targeting the AGE/RAGE pathway could slow the progression of NAFLD.en_US
dc.subject.otherAdvanced glycation end-productsen
dc.subject.otherHepatic stellate cellen
dc.subject.otherNon-alcoholic fatty liver diseaseen
dc.subject.otherOxidative stressen
dc.subject.otherCell Proliferationen
dc.subject.otherCholine Deficiency.complicationsen
dc.subject.otherDiet.adverse effectsen
dc.subject.otherDisease Progressionen
dc.subject.otherGene Expressionen
dc.subject.otherGlycosylation End Products, Advanced.administration & dosage.metabolism.toxicityen
dc.subject.otherHepatic Stellate Cells.metabolism.pathologyen
dc.subject.otherInsulin Resistanceen
dc.subject.otherNon-alcoholic Fatty Liver Disease.etiology.metabolism.pathologyen
dc.subject.otherOxidative Stressen
dc.subject.otherRats, Sprague-Dawleyen
dc.titleDietary glycotoxins exacerbate progression of experimental fatty liver disease.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleJournal of Hepatologyen_US
dc.identifier.affiliationMedicine (University of Melbourne)en_US
dc.identifier.affiliationGastroenterology and Hepatologyen_US
dc.identifier.affiliationGlycation and Diabetes Complications Group, Mater Medical Research Institute, South Brisbane, Queensland, Australiaen_US
dc.identifier.affiliationGlycation and Diabetes Group, Baker IDI Diabetes Institute, Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationDepartment of Physiology, Monash University, Clayton, Victoria, Australiaen_US
dc.type.austinJournal Articleen, Peter W
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.grantfulltextnone- and Hepatology- of Melbourne Clinical School- Education- (University of Melbourne)- Liver Transplant Unit- and Hepatology-
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