Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Nutrients. 2011 Nov;3(11):987-1002. doi: 10.3390/nu3110987. Epub 2011 Nov 18.

Hepatic oxidative stress in fructose-induced fatty liver is not caused by sulfur amino acid insufficiency.

Author information

  • 1Division of Gastroenterology, Hepatology and Nutrition, Emory Children's Center, Emory University School of Medicine, Atlanta, GA 30322, USA. sachin.kunde@helendevoschildrens.org

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.

KEYWORDS:

cystine; methionine; mitochondria; obesity; redox potential; thioredoxin

PMID:
22254090
[PubMed - indexed for MEDLINE]
PMCID:
PMC3257721
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Multidisciplinary Digital Publishing Institute (MDPI) Icon for PubMed Central
    Loading ...
    Write to the Help Desk