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首页> 外文期刊>Endocrine journal >Effects of Leptin on Lipid Metabolism and Gene Expression of Differentiation-Associated Growth Factors and Transcription Factors during Differentiation and Maturation of 3T3-L1 Preadipocytes
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Effects of Leptin on Lipid Metabolism and Gene Expression of Differentiation-Associated Growth Factors and Transcription Factors during Differentiation and Maturation of 3T3-L1 Preadipocytes

机译:瘦素对3T3-L1前脂肪细胞分化成熟过程中脂质代谢及分化相关生长因子和转录因子基因表达的影响

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References(42) Cited-By(11) The present study was designed to determine the effects of leptin on lipid metabolism and gene expression during differentiation and maturation of the 3T3-L1 murine preadipocyte. The preadipocytes were induced to differentiate in a growth medium containing 10% calf serum and a hormonal cocktail for 2 days. The cells were next allowed to maturate for 14 days in the growth medium supplemented with 10 μg/ml insulin or 500 ng/ml insulin-like growth factor (IGF)-I in the absence or presence of supplemented leptin. Leptin, at a dose of 5 to 500 ng/ml, had no effect on proliferation of undifferentiated 3T3-L1 cells. However, leptin suppressed the insulin- or IGF-I-stimulated lipid accumulation and enhanced the release of glycerol, a measure of lipolysis, in a dose-dependent manner during and after the maturation of the cell. Moreover, leptin at a dose of 50 ng/ml inhibited IGF-I gene expression during the entire differentiation and maturation and also peroxisome proliferator activated receptor (PPAR)-γ expression during late maturation as monitored by semi-quantitative reverse transcription-polymerase chain reaction. However, leptin exerted no effect on the expression of transforming growth factor-β, CCAT/enhancer binding protein-α and PPAR-δ. Taken together, results suggest the anti-lipogenic and lipolytic effects of leptin in differentiating and mature adipocytes may have been partly mediated by suppressing the expression of PPAR-γ and IGF-I genes.
机译:参考文献(42)Cited-By(11)本研究旨在确定瘦素对3T3-L1鼠前脂肪细胞分化和成熟过程中脂质代谢和基因表达的影响。诱导前脂肪细胞在含有10%小牛血清和激素混合物的生长培养基中分化2天。接下来,在不存在或存在瘦素的情况下,将细胞在添加有10μg/ ml胰岛素或500 ng / ml胰岛素样生长因子(IGF)-1的生长培养基中成熟14天。 5至500 ng / ml的瘦素对未分化的3T3-L1细胞的增殖没有影响。然而,瘦素在细胞成熟期间和之后以剂量依赖的方式抑制了胰岛素或IGF-I刺激的脂质蓄积,并增强了甘油的释放,这是一种脂解作用。此外,通过半定量逆转录-聚合酶链反应监测,剂量为50 ng / ml的瘦素在整个分化和成熟过程中抑制了IGF-I基因的表达,在成熟后期也抑制了过氧化物酶体增殖物激活受体(PPAR)-γ的表达。 。然而,瘦素对转化生长因子-β,CCAT /增强子结合蛋白-α和PPAR-δ的表达没有影响。两者合计,结果表明瘦素在分化和成熟的脂肪细胞中的抗脂肪形成和脂解作用可能已通过抑制PPAR-γ和IGF-I基因的表达而部分介导。

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