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Author Notes:

Author to whom correspondence should be addressed; Email: sachin.kunde@helendevoschildrens.org Tel.: +1-678-702-6595.

The authors declare no conflict of interest.

Subjects:

Research Funding:

This research was supported by grants from the National Institutes of Health (NIH) K23 DK080953 (M.B.V.), K24 RR023356 (T.R.Z.), R01 ES009047 (D.P.J.) and F32 ES019821 (J.R.R).

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Nutrition & Dietetics
  • NUTRITION & DIETETICS
  • cystine
  • methionine
  • thioredoxin
  • redox potential
  • mitochondria
  • obesity
  • SOFT DRINK CONSUMPTION
  • DIETARY FRUCTOSE
  • BODY-WEIGHT
  • HUMAN PLASMA
  • FOOD-INTAKE
  • CORN SYRUP
  • INSULIN-RESISTANCE
  • REDOX STATE
  • DISEASE
  • BEVERAGES
  • Pulmonary

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

Tools:

Journal Title:

Nutrients

Volume:

Volume 3, Number 11

Publisher:

, Pages 987-1002

Type of Work:

Article | Final Publisher PDF

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 hGSSG) 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.

Copyright information:

© 2011 by the authors.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 3.0 Unported License (http://creativecommons.org/licenses/by/3.0/).

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