Eicosanoids as endogenous regulators of leptin release and lipolysis by mouse adipose tissue in primary culture.
Eicosanoids as endogenous regulators of leptin release and lipolysis by mouse adipose tissue in primary culture.
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DOI：
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发表时间：
2000-10
影响因子：
6.5
通讯作者：
J. Fain;C. Leffler;S. Bahouth
中科院分区：
文献类型：
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作者：
J. Fain;C. Leffler;S. Bahouth
前列腺素E(2)(PGE(2))刺激原代培养的小鼠脂肪组织孵育24小时后释放瘦素。100 nm PGE(2)对瘦素释放的刺激作用最大。在选择性环氧合酶-2抑制剂NS-398存在下，研究了内源性二十烷类化合物在调节脂解和瘦素形成中的作用。浓度为5微米的NS-398可使脂肪分解增加30%，瘦素释放减少24%。该浓度的NS-398几乎完全抑制PGE(2)的形成。PGE(2)或N(6)-环戊基腺苷(CPA)对基础脂解有抑制作用，但不存在NS-398。CPA的受体和PGE(2)一样，可以抑制脂肪组织中循环AMP的积聚，也能促进瘦素的释放。这些数据表明，PGE2可以刺激瘦素的释放，并表明内源性二十烷类化合物影响脂肪组织的脂肪分解和瘦素的形成。
Prostaglandin E(2) (PGE(2)) 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 PGE(2). 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 microm enhanced lipolysis by 30% and lowered leptin release by 24%. This concentration of NS-398 almost completely inhibited PGE(2) formation. An inhibition of basal lipolysis by PGE(2) or N(6)-cyclopentyladenosine (CPA) was seen in the presence but not in the absence of NS-398. CPA, whose receptor, like that of PGE(2) 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.