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Hepatic Oxidative Stress in Fructose-Induced Fatty Liver Is Not Caused by Sulfur Amino Acid Insufficiency

Division of Gastroenterology, Hepatology and Nutrition, Emory Children’s Center, 2015 Uppergate Dr NE, Emory University School of Medicine, Atlanta, GA 30322, USA
Whitehead Biomedical Research Bldg. Division of Pulmonary, Allergy and Critical Care Medicine, 615 Michael St, Emory University School of Medicine, Ste 205P, Atlanta, GA 30322, USA
Department of Medicine, GG23 Emory University Hospital, 1600/002/1AA, 1364 Clifton Rd, Atlanta, GA 30322, USA
Author to whom correspondence should be addressed.
Nutrients 2011, 3(11), 987-1002;
Received: 19 September 2011 / Revised: 24 October 2011 / Accepted: 4 November 2011 / Published: 18 November 2011
PDF [921 KB, uploaded 18 November 2011]


Fructose-sweetened liquid consumption is associated with fatty liver and oxidative stress. In rodent models of fructose-mediated fatty liver, protein consumption is decreased. Additionally, decreased sulfur amino acid intake is known to cause oxidative stress. Studies were designed to test whether oxidative stress in fructose-sweetened liquid-induced fatty liver is caused by decreased ad libitum solid food intake with associated inadequate sulfur amino acid intake. C57BL6 mice were grouped as: control (ad libitum water), fructose (ad libitum 30% fructose-sweetened liquid), glucose (ad libitum 30% glucose-sweetened water) and pair-fed (ad libitum water and sulfur amino acid intake same as the fructose group). Hepatic and plasma thiol-disulfide antioxidant status were analyzed after five weeks. Fructose- and glucose-fed mice developed fatty liver. The mitochondrial antioxidant protein, thioredoxin-2, displayed decreased abundance in the liver of fructose and glucose-fed mice compared to controls. Glutathione/glutathione disulfide redox potential (EhGSSG) and abundance of the cytoplasmic antioxidant protein, peroxiredoxin-2, were similar among groups. We conclude that both fructose and glucose-sweetened liquid consumption results in fatty liver and upregulated thioredoxin-2 expression, consistent with mitochondrial oxidative stress; however, inadequate sulfur amino acid intake was not the cause of this oxidative stress. View Full-Text
Keywords: cystine; methionine; thioredoxin; redox potential; mitochondria; obesity cystine; methionine; thioredoxin; redox potential; mitochondria; obesity

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Kunde, S.S.; Roede, J.R.; Vos, M.B.; Orr, M.L.; Go, Y.-M.; Park, Y.; Ziegler, T.R.; Jones, D.P. Hepatic Oxidative Stress in Fructose-Induced Fatty Liver Is Not Caused by Sulfur Amino Acid Insufficiency. Nutrients 2011, 3, 987-1002.

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