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Insulin as a hormone regulator of the synthesis and release of leptin by white adipose tissue

机译:胰岛素作为瘦素的胰岛素稳定剂,白脂肪组织的合成和释放

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摘要

Leptin and its receptor are widely distributed in several tissues, mainly in white adipose tissue. The serum leptin is highly correlated with body mass index in rodents and humans, being documented that leptin levels reduces in the fasting state and increase during refeeding, similarly to insulin release by pancreatic islets. Insulin appears to increase leptin mRNA and protein expression and its release by adipocytes. Some studies have suggested that insulin acts through the activation of the transcription factors: sterol regulatory element binding protein 1 (SREBP1), CCAAT enhancer binding protein-alpha (C/EBP-alpha) and specificity protein 1 (Sp1). Insulin stimulates the release of preformed and newly synthesized leptin by adipocytes through its signaling cascade. Its effects are blocked by inhibitors of the insulin signaling pathway, as well as by inhibitors of protein synthesis and agents that increase the intracellular cAMP. The literature data suggest that chronic hyperinsulinemia increases serum leptin levels in humans and rodents. In this review, we summarized the most updated knowledge on the effects of insulin on serum leptin levels, presenting the cell mechanisms that control leptin synthesis and release by the white adipose tissue.
机译:瘦素及其受体广泛分布于多种组织中,主要分布在白色脂肪组织中。血清瘦素与啮齿类动物和人类的体重指数高度相关,有文献证明,瘦素水平在禁食状态下降低,在再进食时升高,类似于胰岛释放胰岛素。胰岛素似乎可以增加瘦素mRNA和蛋白质的表达,并增加脂肪细胞对瘦素的释放。一些研究表明,胰岛素通过激活转录因子发挥作用:甾醇调节元件结合蛋白1(SREBP1)、CCAAT增强子结合蛋白α(C/EBPα)和特异性蛋白1(Sp1)。胰岛素通过其信号级联刺激脂肪细胞释放预先形成和新合成的瘦素。其作用被胰岛素信号通路的抑制剂、蛋白质合成的抑制剂和增加细胞内cAMP的药物阻断。文献数据表明,慢性高胰岛素血症会增加人类和啮齿类动物的血清瘦素水平。在这篇综述中,我们总结了胰岛素对血清瘦素水平影响的最新知识,介绍了白脂肪组织控制瘦素合成和释放的细胞机制。

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