Leptin inhibits rosiglitazone-induced adipogenesis in murine primary adipocytes

被引：26

作者：

Dal Rhee, Sang ^{[1
]}

Sung, Yoon-Young ^{[1
]}

Jung, Won Hoon ^{[1
]}

Cheon, Hyae Gyeong ^{[1
]}

机构：

[1] Korea Res Inst Chem Technol, Drug Discovery Div, Ctr Metab Syndrome Therapeut, Taejon 305600, South Korea

来源：

MOLECULAR AND CELLULAR ENDOCRINOLOGY | 2008年 / 294卷 / 1-2期

关键词：

Leptin; Adipogenesis; Extracellular regulated kinase; Signal transducers and activators of transcription;

D O I：

10.1016/j.mce.2008.08.018

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Leptin mainly acts on the hypothalamus in the brain, in which it regulates food intake and energy expenditure. However, the direct effects of leptin on adipocytes have been controversial in the cellular level. In this study, the effects of leptin on rosiglitazone-induced adipocyte differentiation were investigated in the primary preadipocytes prepared from Subcutaneous fat tissues of C57BL/6-Lep(ob/ob) mouse. We found that acute and prolonged treatment of leptin on preadipocytes inhibited the rosiglitazone-induced transcription factor expression and adipocyte differentiation, respectively, accompanied with decreased expression of PPAR gamma and aP2. Either PD98059, an ERK inhibitor or fludarabine, a STAT1 inhibitor restored leptin-inhibited PPAR gamma expression and subsequent lipid accumulation, but inhibitors for P1-3K (LY294002) and for STAT3 (piceatannol) did not. Furthermore, leptin decreased PPAR gamma expression also in fully differentiated adipocytes, which was reversed by either PD98059 or fludarabine. Taken together, these data suggest that leptin has a direct inhibitory effect on the rosiglitazone-induced adipocyte differentiation and PPAR gamma expression, in which ERK1/2 MAP kinase and JAK/STAT1 signaling pathways are involved. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

引用

页码：61 / 69

页数：9

共 43 条

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