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J. Biol. Chem., Vol. 276, Issue 15, 11512-11516, April 13, 2001

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Progesterone Stimulates Adipocyte Determination and Differentiation 1/Sterol Regulatory Element-binding Protein 1c Gene Expression
POTENTIAL MECHANISM FOR THE LIPOGENIC EFFECT OF PROGESTERONE IN ADIPOSE TISSUE^*

Danièle Lacasa, Xavier Le Liepvre, Pascal Ferre, and Isabelle Dugail^§

From the  Laboratoire de Biochimie et Biologie Moléculaire, Faculté de Médecine Paris Ouest, Université René Descartes, 75270 Paris, France and INSERM U 465, Nutrition, Métabolisme, Obésité, 15 Rue de l'École de Médecine, 75006 Paris, France

Fatty acid synthase (FAS), a nutritionally regulated lipogenic enzyme, is transcriptionally controlled by ADD1/SREBP1c (adipocyte determination and differentiation 1/sterol regulatory element-binding protein 1c), through insulin-mediated stimulation of ADD1/SREBP1c expression. Progesterone exerts lipogenic effects on adipocytes, and FAS is highly induced in breast tumor cell lines upon progesterone treatment. We show here that progesterone up-regulates ADD1/SREBP1c expression in the MCF7 breast cancer cell line and the primary cultured preadipocyte from rat parametrial adipose tissue. In MCF7, progesterone induced ADD1/SREBP1c and Metallothionein II (a well known progesterone-regulated gene) mRNAs, with comparable potency. In preadipocytes, progesterone increased ADD1/SREBP1c mRNA dose-dependently, but not SREBP1a or SREBP2. Run-on experiments demonstrated that progesterone action on ADD1/SREBP1c was primarily at the transcriptional level. The membrane-bound and mature nuclear forms of ADD1/SREBP1 protein accumulated in preadipocytes cultured with progesterone, and FAS induction could be abolished by adenovirus-mediated overexpression of a dominant negative form of ADD1/SREBP1 in these cells. Finally, in the presence of insulin, progesterone was unable to up-regulate ADD1/SREBP1c mRNA in preadipocytes, whereas its effect was restored after 24 h of insulin deprivation. Together these results demonstrate that ADD1/SREBP1c is controlled by progesterone, which, like insulin, acts by increasing ADD1/SREBP1c gene transcription. This provides a potential mechanism for the lipogenic actions of progesterone on adipose tissue.

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