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A more recent version of this article appeared on January 1, 2005

Papers In Press, published online ahead of print October 1, 2004
J. Lipid Res., doi:10.1194/jlr.M400344-JLR200
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Submitted on September 9, 2004
Revised on September 27, 2004
Accepted on September 28, 2004

Inducible nitric oxide synthase modulates lipolysis in adipocytes

Patrice Penfornis and André Marette

Department of Physiology and CRML, Laval University Hospital Research Center, Ste-Foy, Quebec G1V4G2

Corresponding Author: andre.marette{at}crchul.ulaval.ca

The role of inducible nitric oxide (NO) synthase (iNOS) in the modulation of adipocyte lipolysis was investigated in the present study. Treatment of white and brown adipose cell lines and mouse adipose explants with a mixture of TNF-a, interferon-g and lipopolysaccharide (LPS) doubled the lipolytic rate and this was associated with marked induction of iNOS expression and NO production. iNOS inhibition by 1400W, aminoguanidine or L-NIL pre-treatment further increased the cytokine/LPS-mediated lipolysis by 30% (P<0.05) in cultured adipocytes and in adipose explants. However, this potentiating effect of iNOS inhibition was abolished in adipose explants isolated from iNOS-/- mice. Pharmacological inhibitors of adenylyl cyclase or protein kinase A reduced cytokine/LPS-induced lipolysis and also blunted the potentiating effect of iNOS inhibition on the lipolytic rate. Furthermore, addition of the antioxidants L-cystine and L-glutathione to cytokine/LPS-stimulated adipocytes mimicked the lipolytic effect of iNOS inhibition. In conclusion, inhibition of iNOS activity in adipocytes potentiates cytokine/LPS-induced lipolysis. This effect was fully reversed by adenylyl cyclase and protein kinase A inhibitors but was mimicked by cellular antioxidants. These data suggest that iNOS-mediated NO production counteracts cytokine/LPS-mediated lipolysis in adipocytes and that this feedback mechanism involves an oxidative process upstream of cAMP production in the signaling pathway.


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[Abstract] [Full Text] [PDF]


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