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

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Abstract

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.

Original languageEnglish (US)
Pages (from-to)1689-1694
Number of pages6
JournalJournal of Lipid Research
Volume41
Issue number10
StatePublished - 2000

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Eicosanoids
Lipolysis
Leptin
Adipose Tissue
Dinoprostone
Tissue
Cyclooxygenase 2 Inhibitors
Cyclic AMP
N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide

All Science Journal Classification (ASJC) codes

  • Endocrinology

Cite this

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abstract = "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.",
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