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Journal of Lipid Research, Vol. 41, 1689-1694, October 2000
Copyright © 2000 by Lipid Research, Inc.

Original Article

Eicosanoids as endogenous regulators of leptin release and lipolysis by mouse adipose tissue in primary culture

Correspondence to: John N. Fain

Prostaglandin E₂ (PGE₂) stimulated leptin release over a 24-h incubation of mouse adipose tissue in primary culture. The maximal stimulation of leptin release was seen with 100 nM PGE₂. The role of endogenous eicosanoids in the regulation of lipolysis and leptin formation was examined in the presence of NS-398, a selective cyclooxygenase-2 inhibitor. NS-398 at a concentration of 5 µM enhanced lipolysis by 30% and lowered leptin release by 24%. This concentration of NS-398 almost completely inhibited PGE₂ formation. An inhibition of basal lipolysis by PGE₂ or N⁶-cyclopentyladenosine (CPA) was seen in the presence but not in the absence of NS-398. CPA, whose receptor, like that of PGE₂ inhibits cyclic AMP accumulation in adipose tissue, also enhanced leptin release.

These data indicate that PGE₂ can stimulate leptin release and suggest that endogenous eicosanoids affect both lipolysis and leptin formation by mouse adipose tissue. — Fain, J. N., C. W. Leffler, and S. W. Bahouth. Eicosanoids as endogenous regulators of leptin release and lipolysis by mouse adipose tissue in primary culture. J. Lipid Res. 2000. 41: 1689;–1694.

Supplementary key words: dexamethasone, NS-398, cyclooxygenase-2, PGE₂, CPA

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