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Dietary glycotoxins exacerbate progression of experimental fatty liver disease
Authors:Christopher Leung  Chandana B. Herath  Zhiyuan Jia  Michelle Goodwin  Kai Yan Mak  Matthew J. Watt  Josephine M. Forbes  Peter W. Angus
Affiliation:1 Department of Medicine, The University of Melbourne, Austin Health, Heidelberg, Victoria, Australia;2 Department of Gastroenterology and Hepatology, Austin Health, Austin Hospital, Heidelberg, Melbourne, Victoria, Australia;3 Glycation and Diabetes Group, Baker IDI Diabetes Institute, Melbourne, Victoria, Australia;4 Department of Physiology, Monash University, Clayton, Victoria, Australia;5 Glycation and Diabetes Complications Group, Mater Medical Research Institute, South Brisbane, Queensland, Australia
Abstract:
Keywords:AGEs, advanced glycation end-products   RAGE, receptor for AGEs   ROS, reactive oxygen species   NAFLD, non-alcoholic fatty liver disease   MCD, methionine choline deficient   MCR, methionine choline replete   CML, N-(carboxymethyl)lysine   ALT, alanine transaminase   IL-6, interleukin-6   TNF-α, tumour necrosis factor α   α-SMA, α-smooth muscle actin   COL1A, collagen-1A   CTGF, connective tissue growth factor   HSCs, hepatic stellate cells   BrDU, bromodeoxyuridine   MCP-1, monocyte chemotactic protein-1   NADPH, nicotinamide adenine dinucleotide phosphate   NASH, non-alcoholic steatohepatitis   BSA, bovine serum albumin   HNE, 4-hydroxy-2-nonenal   HOMA-IR, homeostatic model assessment of insulin resistance
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