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J Biol Chem, Vol. 273, Issue 22, 13475-13481, May 29, 1998

Modulation of White Adipose Tissue Lipolysis by Nitric Oxide

Nicolas Gaudiot, Anne-Marie Jaubert, Elisabeth Charbonnier, Dominique Sabourault, Danièle Lacasa, Yves Giudicelli, and Catherine Ribière

From the Department of Biochemistry, INSERM CJF 94--02, Faculté de Médecine de Paris-Ouest, Universite René Descartes, Paris, France

In isolated adipocytes, the nitrosothiols S-nitroso-N-acetyl-penicillamine (SNAP) and S-nitrosoglutathione stimulate basal lipolysis, whereas the nitric oxide (NO·) donor 1-propamine, 3-(2-hydroxy-2-nitroso-1-propylhydrazine) (PAPA-NONOate) or NO gas have no effect. The increase in basal lipolysis due to nitrosothiols was prevented by dithiothreitol but not by a guanylate cyclase inhibitor. In addition the cyclic GMP-inhibited low Km, cyclic AMP phosphodiesterase activity was inhibited by SNAP suggesting that SNAP acting as NO+ donor increases basal lipolysis through a S-nitrosylation mediated inhibition of phosphodiesterase. Contrasting with these findings, SNAP reduced both isoproterenol-stimulated lipolysis and cyclic AMP production, whereas it failed to modify forskolin-, dibutyryl cyclic AMP-, or isobutylmethylxanthine-stimulated lipolysis, suggesting that SNAP interferes with the beta -adrenergic signal transduction pathway upstream the adenylate cyclase. In contrast with SNAP, PAPA-NONOate or NO gas inhibited stimulated lipolysis whatever the stimulating agents used without altering cyclic AMP production. Moreover PAPA-NONOate slightly reduces (30%) the hormone-sensitive lipase (HSL) activity indicating that stimulated lipolysis inhibition by NO· is linked to both inhibition of the HSL activity and the cyclic AMP-dependent activation of HSL. These data suggest that NO· or related redox species like NO+/NO- are potential regulators of lipolysis through distinct mechanisms.

Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.


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Copyright © 1998 by the American Society for Biochemistry and Molecular Biology.