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Taurine supplementation prevents ethanol‐induced decreases in serum adiponectin and reduces hepatic steatosis in rats
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.702.33
Subject(s) - steatosis , medicine , taurine , endocrinology , oxidative stress , adiponectin , adipose tissue , chemistry , fatty liver , white adipose tissue , liver injury , insulin , insulin resistance , biology , biochemistry , amino acid , disease
Adiponectin (Acrp) has important insulin sensitizing functions and acts to increase fatty acid oxidation in liver. Chronic ethanol feeding (EF) results in hepatic steatosis, associated with decreased serum Acrp, due, at least in part, to a decrease in Acrp secretion by adipocytes. In other model systems, decreased Acrp expression is associated with oxidative stress in adipose. If EF increases oxidative stress in adipose, leading to decreased serum Acrp and contributing to ethanol‐induced steatosis, then treatment with taurine, an amino acid with anti‐oxidant properties, should prevent oxidative stress in adipose and restore Acrp during EF. Male Wistar rats were allowed free access to a 36% ethanol (% calories) liquid diet or pair‐fed control diets supplemented or not with taurine for 1 week. EF increased 4‐hydroxynonenol (4HNE) adducts, a marker of oxidative stress, in both subcutaneous adipose and liver, decreased serum Acrp and resulted in hepatic steatosis. Taurine supplementation prevented EF‐induced 4HNE adducts in adipose and liver, normalized serum Acrp and attenuated liver steatosis. Taken together, these data suggest that oxidative stress in adipose is an important contributor to EF‐induced decreases in serum Acrp and the development of hepatic steatosis. These data also identify adipose as a potential target for therapeutic intervention to prevent ethanol‐induced liver injury.