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

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Division of Gastroenterology, Hepatology and Nutrition, Emory Children’s Center, 2015 Uppergate Dr NE, Emory University School of Medicine, Atlanta, GA 30322, USA
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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
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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; https://doi.org/10.3390/nu3110987
Received: 19 September 2011 / Revised: 24 October 2011 / Accepted: 4 November 2011 / Published: 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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MDPI and ACS Style

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. https://doi.org/10.3390/nu3110987

AMA Style

Kunde SS, Roede JR, Vos MB, Orr ML, Go Y-M, Park Y, Ziegler TR, Jones DP. Hepatic Oxidative Stress in Fructose-Induced Fatty Liver Is Not Caused by Sulfur Amino Acid Insufficiency. Nutrients. 2011; 3(11):987-1002. https://doi.org/10.3390/nu3110987

Chicago/Turabian Style

Kunde, Sachin S., James R. Roede, Miriam B. Vos, Michael L. Orr, Young-Mi Go, Youngja Park, Thomas R. Ziegler, and Dean P. Jones 2011. "Hepatic Oxidative Stress in Fructose-Induced Fatty Liver Is Not Caused by Sulfur Amino Acid Insufficiency" Nutrients 3, no. 11: 987-1002. https://doi.org/10.3390/nu3110987

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