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J. Biol. Chem., Vol. 281, Issue 18, 12682-12687, May 5, 2006

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Adipose Tissue Proadipogenic Redox Changes in Obesity^*

Anne Galinier, Audrey Carrière, Yvette Fernandez, Christian Carpéné^¶, Mireille André, Sylvie Caspar-Bauguil, Jean-Paul Thouvenot, Brigitte Périquet, Luc Pénicaud, and Louis Casteilla¹

From the Unite Mixte de Recherche 5018 CNRS, Université Paul Sabatier, Institut Fedératif Recherche 31, Institut Louis Bugnard, BP 84225, 31432 Toulouse Cedex 4, Laboratoire de Biochimie Générale et Nutritionnelle, Hôpital Purpan, Place du Docteur Baylac, 31059 Toulouse Cedex 9, and ^¶Unité 586, IFR 31, Institut Louis Bugnard, BP 84225, 31432 Toulouse Cedex 4, France

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 (-tocopherol, coenzymes Q) and 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 that promotes on its own the development of a deleterious proadipogenic process.

Received for publication, June 27, 2005 , and in revised form, November 29, 2005.

^* This work was supported in part by Action Thematique Concertée Nutrition (4NUO5G) and an Agence National de Recherche sur le Sida grant (2005/003). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed. Tel.: 33-5-61323495; Fax: 33-5-62170905; E-mail: casteil{at}toulouse.inserm.fr.

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