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

Author(s): Sachin S. Kunde | James R. Roede | Miriam B. Vos | Michael L. Orr | Young-Mi Go | Youngja Park | Thomas R. Ziegler | Dean P. Jones

Journal: Nutrients
ISSN 2072-6643

Volume: 3;
Issue: 11;
Start page: 987;
Date: 2011;
Original page

Keywords: cystine | methionine | thioredoxin | redox potential | mitochondria | obesity

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.
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