Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/21926
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dc.contributor.authorFernando, Dinali H-
dc.contributor.authorForbes, Josephine M-
dc.contributor.authorAngus, Peter W-
dc.contributor.authorHerath, Chandana B-
dc.date2019-10-11-
dc.date.accessioned2019-10-20T22:40:33Z-
dc.date.available2019-10-20T22:40:33Z-
dc.date.issued2019-10-11-
dc.identifier.citationInternational Journal of Molecular Sciences 2019; 20(20): E5037en_US
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/21926-
dc.description.abstractNon-alcoholic fatty liver disease (NAFLD) affects up to 30% of the adult population and is now a major cause of liver disease-related premature illness and deaths in the world. Treatment is largely based on lifestyle modification, which is difficult to achieve in most patients. Progression of simple fatty liver or steatosis to its severe form non-alcoholic steatohepatitis (NASH) and liver fibrosis has been explained by a 'two-hit hypothesis'. Whilst simple steatosis is considered the first hit, its transformation to NASH may be driven by a second hit. Of several factors that constitute the second hit, advanced glycation end products (AGEs), which are formed when reducing-sugars react with proteins or lipids, have been implicated as major candidates that drive steatosis to NASH via the receptor for AGEs (RAGE). Both endogenous and processed food-derived (exogenous) AGEs can activate RAGE, mainly present on Kupffer cells and hepatic stellate cells, thus propagating NAFLD progression. This review focuses on the pathophysiology of NAFLD with special emphasis on the role of food-derived AGEs in NAFLD progression to NASH and liver fibrosis. Moreover, the effect of dietary manipulation to reduce AGE content in food or the therapies targeting AGE/RAGE pathway on disease progression is also discussed.en_US
dc.language.isoeng-
dc.subjectadvanced glycation end productsen_US
dc.subjecthepatic Kuppfer cellsen_US
dc.subjecthepatic stellate cellsen_US
dc.subjectnon-alcoholic fatty liver diseaseen_US
dc.subjectoxidative stressen_US
dc.subjectreceptor for advanced glycation end productsen_US
dc.titleDevelopment and Progression of Non-Alcoholic Fatty Liver Disease: The Role of Advanced Glycation End Products.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleInternational Journal of Molecular Sciencesen_US
dc.identifier.affiliationMedicine (University of Melbourne)en_US
dc.identifier.affiliationVictorian Liver Transplant Uniten_US
dc.identifier.affiliationMater Institute, University of Queensland, Brisbane, Australiaen_US
dc.identifier.doi10.3390/ijms20205037en_US
dc.type.contentTexten_US
dc.identifier.pubmedid31614491-
dc.type.austinJournal Article-
dc.type.austinReview-
local.name.researcherAngus, Peter W
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptVictorian Liver Transplant Unit-
crisitem.author.deptGastroenterology and Hepatology-
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