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J. Biol. Chem., Vol. 281, Issue 19, 13141-13149, May 12, 2006

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Rosiglitazone Controls Fatty Acid Cycling in Human Adipose Tissue by Means of Glyceroneogenesis and Glycerol Phosphorylation^*

Stéphanie N. Leroyer¹, Joan Tordjman, Geneviève Chauvet, Joëlle Quette¹, Charles Chapron, Claude Forest, and Bénédicte Antoine¹²

From the INSERM-UMR-S 530/747, Université Paris Descartes, 45 Rue des Saints-Pères, 75006 Paris, France and Groupe Hospitalier Universitaire Ouest, Centre Hospitalier Universitaire Cochin, Paris, France

Control of fatty acid homeostasis is crucial to prevent insulin resistance. During fasting, the plasma fatty acid level depends on triglyceride lipolysis and fatty acid re-esterification within fat cells. In rodents, Rosiglitazone® controls fatty acid homeostasis by stimulating two pathways in the adipocytes, glyceroneogenesis and glycerol phosphorylation, that provide the glycerol 3-phosphate necessary for fatty acid re-esterification. Here, we analyzed the functionality of both pathways for controlling fatty acid release in subcutaneous adipose tissue samples from lean and overweight women before and after Rosiglitazone® ex vivo treatment. In controls, pyruvate, used as a substrate of glyceroneogenesis, could contribute to the re-esterification of up to 65% of the fatty acids released after basal lipolysis, whereas glycerol phosphorylation accounted for only 14 ± 9%. However, the efficiency of glyceroneogenesis diminished as body mass index (BMI) of women increased. After Rosiglitazone treatment, increase of either pyruvate- or glycerol-dependent fatty acid re-esterification was strictly correlated to that of phosphoenolpyruvate carboxykinase and glycerol kinase, the key enzymes of each pathway, but depended on BMI of the women. Whereas the Rosiglitazone® responsiveness of glyceroneogenesis was rather constant according to the BMI of the women, glycerol phosphorylation was mostly enhanced in lean women (BMI < 27). Overall, these data indicate that, whereas glyceroneogenesis is more utilized than glycerol phosphorylation for fatty acid re-esterification in human subcutaneous adipose tissue in the physiological situation, both are solicited in response to Rosiglitazone® but with lower efficiency when BMI is increased.

Received for publication, December 5, 2005 , and in revised form, February 27, 2006.

^* This work was supported by the Institut National de la Santé et de la Recherche Médicale, the Université René Descartes, and a grant from the Association de Langue Française pour l'Etude du Diabète et des Maladies Métaboliques-GlaxoSmithKline (to C. F.). 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 Present address: INSERM U. 680, Centre Universitaire St. Antoine, 27 Rue de Chaligny, 75012 Paris, France.

² A CNRS researcher. To whom correspondence should be addressed: Inserm U. 680, Centre Universitaire St. Antoine, 27 Rue de Chaligny, 75012 Paris, France. Tel.: 33-1-40-01-13-21; Fax: 33-1-40-01-13-52; E-mail: benedicte.antoine{at}univ-paris5.fr.

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