Effects of orexin A on proliferation, survival, apoptosis and differentiation of 3T3-L1 preadipocytes into mature adipocytes
Effects of orexin A on proliferation, survival, apoptosis and differentiation of 3T3-L1 preadipocytes into mature adipocytes
复制标题
DOI：
10.1016/j.febslet.2012.10.013
复制
发表时间：
2012-11-30
期刊：
影响因子：
3.5
通讯作者：
Strowski, M. Z.
中科院分区：
文献类型：
--
作者：
Skrzypski, M.;Kaczmarek, P.;Strowski, M. Z.
食欲素A（OXA）在成熟脂肪细胞中的代谢活性通过PI 3 K/PKB和PPAR γ介导。然而，OXA对前脂肪细胞的影响在很大程度上是未知的。我们在这里报告说，OXA刺激3 T3-L1前脂肪细胞的增殖和活力，并通过ERK 1/2，而不是通过PKB保护它们免于凋亡。OXA通过ERK 1/2降低caspase-3的促凋亡活性。ERK 1/2的抑制阻止前脂肪细胞分化为脂肪细胞。与胰岛素不同，尽管ERK 1/2磷酸化增加，但3 T3-L1前脂肪细胞短期或长期暴露于OXA均不诱导前脂肪细胞分化为脂肪细胞。与胰岛素不同，OXA不能激活PKB，这解释了其不能诱导前脂肪细胞分化。(C)2012年欧洲生物化学学会联合会。由Elsevier B出版。版权所有© 2016
Metabolic activities of orexin A (OXA) in mature adipocytes are mediated via PI3K/PKB and PPAR gamma. However, the effects of OXA on preadipocytes are largely unknown. We report here that OXA stimulates the proliferation and viability of 3T3-L1 preadipocytes and protects them from apoptosis via ERK1/2, but not through PKB. OXA reduces proapoptotic activity of caspase-3 via ERK1/2. Inhibition of ERK1/2 prevents the differentiation of preadipocytes into adipocytes. Unlike insulin, neither short-term nor prolonged exposure of 3T3-L1 preadipocytes to OXA induces preadipocyte differentiation to adipocytes, despite increased ERK1/2 phosphorylation. Unlike insulin, OXA fails to activate PKB, which explains its inability to induce the differentiation of preadipocytes. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.