We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Hepatic oxidative stress in fructose-induced fatty liver is not caused by sulfur amino acid insufficiency.
- Authors
Kunde, Sachin S; Roede, James R; Vos, Miriam B; Orr, Michael L; Go, Young-Mi; Park, Youngja; Ziegler, Thomas R; Jones, Dean P
- Abstract
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 (E(h)GSSG) 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.
- Publication
Nutrients, 2011, Vol 3, Issue 11, p987
- ISSN
2072-6643
- Publication type
Journal Article
- DOI
10.3390/nu3110987