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Angiotensin II as a Trophic Factor of White Adipose Tissue: Stimulation of Adipose Cell Formation¹

Institut de Recherches Signalisation, Biologie du Développement et Cancer, Laboratoire Biologie du Développement du Tissu Adipeux, Centre de Biochimie, Unité Mixte de Recherches 6543, Centre National de la Recherche Scientifique, Université de Nice-Sophia Antipolis, Faculté des Sciences (P.S.-M., G.A., R.N.), 06108 Nice, France; and Pennington Biomedical Research Center, Louisiana State University (L.P.K.), Baton Rouge, Louisiana 70808-4124

Address all correspondence and requests for reprints to: Prof. Gérard Ailhaud, Institute of Signaling, Developmental Biology, and Cancer Research, Laboratory Biology of Adipose Tissue Development, Centre de Biochimie, Unité Mixte de Recherches 6543, Centre National de la Recherche Scientifique, Université de Nice-Sophia Antipolis, Faculté des Sciences, Parc Valrose, 06108 Nice Cedex 2, France. E-mail: ailhaud{at}unice.fr

White adipose tissue is known to contain the components of the renin-angiotensin system giving rise to angiotensin II (AngII). In vitro, prostacyclin is synthesized from arachidonic acid through the activity of cyclooxygenases 1 and 2 and is released from AngII-stimulated adipocytes. Prostacyclin, in turn, is able to favor adipocyte formation. Based upon in vivo and ex vivo experiments combined to immunocytochemical staining of glycerol-3-phosphate dehydrogenase (GPDH), an indicator of adipocyte formation, it is reported herein that AngII favors the appearance of GPDH-positive cells. In the presence of a cyclooxygenase inhibitor, this adipogenic effect is abolished, whereas that of (carba)prostacyclin, a stable analog of prostacyclin that bypasses this inhibition, appears unaltered. Taken together, these results are in favor of AngII acting as a trophic factor implicated locally in adipose tissue development. It is proposed that AngII enhances the formation of GPDH-expressing cells from preadipocytes in response to prostacyclin released from adipocytes.

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