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首页> 外文期刊>Cell biology international. >Co-treatment with dexamethasone and octanoate induces adipogenesis in 3T3-L1 cells.
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Co-treatment with dexamethasone and octanoate induces adipogenesis in 3T3-L1 cells.

机译：与地塞米松和辛酸酯共同处理可诱导3T3-L1细胞中的脂肪形成。

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We report here that octanoate, a medium chain fatty acid, induces adipocyte differentiation in 3T3-L1 cells by co-treatment with dexamethasone, although octanoate has been known not to stimulate 3T3-L1 adipogenesis. A low concentration of exogenous glucose prevented 3T3-L1 adipogenesis induced by 1-methyl 3-isobutylxanthine, dexamethasone, and insulin (MDI) treatment (a common protocol for adipocyte differentiation). In contrast, co-treatment with dexamethasone and octanoate (D-OCT) induced adipogenesis under the same conditions. These findings imply that octanoate, rather than glucose, is the source of accumulated lipids in D-OCT-induced adipogenesis. D-OCT increased expression of the differentiation markers peroxisome proliferator-activated receptor (PPAR)gamma2 and caveolin-1. A specific inhibitor of p38 mitogen-activated protein (MAP) kinase inhibited D-OCT-induced adipogenesis. These results suggest that the p38 MAP kinase pathway followed by up-regulation of PPARgamma2 may be involved in 3T3-L1 adipocyte differentiation induced by D-OCT, as well as by MDI.
机译：我们在这里报告辛酸，一种中链脂肪酸，通过与地塞米松的共同治疗诱导3T3-L1细胞的脂肪细胞分化，尽管已知辛酸不会刺激3T3-L1的脂肪形成。低浓度的外源葡萄糖阻止了由1-甲基3-异丁基黄嘌呤，地塞米松和胰岛素（MDI）处理（脂肪细胞分化的常用方法）诱导的3T3-L1脂肪形成。相反，在相同条件下，地塞米松和辛酸酯（D-OCT）共同处理可诱导脂肪形成。这些发现表明，辛酸而不是葡萄糖是D-OCT诱导的脂肪形成中脂质堆积的来源。 D-OCT增加了分化标记物过氧化物酶体增殖物激活受体（PPAR）γ2和小窝蛋白1的表达。 p38丝裂原活化蛋白（MAP）激酶的特异性抑制剂抑制D-OCT诱导的脂肪形成。这些结果表明，p38 MAP激酶途径继之以PPARgamma2上调可能与D-OCT以及MDI诱导的3T3-L1脂肪细胞分化有关。

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