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Papers In Press, published online ahead of print December 23, 2005
UMR 5018 CNRS-UPS, IFR 31, Institut Louis Bugnard, Toulouse 31432 Cedex 4
Corresponding Author: casteil{at}inserm.toulouse.fr
The role of inflammation and oxidative stress in the development of obesity and associated metabolic disorders is under debate. We investigated the redox metabolism in a non-diabetic obesity model, i.e. 11-week-old obese Zucker rats. Antioxidant enzyme activities,lipophilic antioxidant (a-tocopherol, coenzymes Q), hydrophilic antioxidant (glutathione, vitamin C) contents and their redox state (% oxidized form) were studied in inguinal white fat and compared with blood and liver. The adipose tissues of obese animals showed a specific higher content of hydrophilic molecules in a lower redox state than those of lean animals, which were associated with lower lipophilic molecule content and lipid peroxidation. Conversely and as expected, glutathione content decreased and its redox state increased in adipose tissues of rats subjected to lipopolysaccharide-induced systemic oxidative stress. In these in vivo models, oxidative stress and obesity thus had opposite effects on adipose tissue redox state. Moreover, the increase in glutathione content and the decrease of its redox state by antioxidant treatment promoted in vitro the accumulation of triglycerides in preadipocytes. Taken together and contrary to the emergent view, our results suggest that obesity is associated with an intracellular reduced redox state which promotes on its own the development of a deleterious proadipogenic process.
J. Biol. Chem, 10.1074/jbc.M506949200
Submitted on June 27, 2005
Revised on November 29, 2005
Accepted on December 23, 2005
Adipose tissue pro-adipogenic redox changes in obesity
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