Laboratory of Physiology, Federal University of São João del-Rei, Divinópolis, Minas Gerais, Brazil.
Laboratory of Molecular Genetic, Federal University of São João del-Rei, Divinópolis, Minas Gerais, Brazil.
Peptides. 2018 Aug;106:49-58. doi: 10.1016/j.peptides.2018.06.007. Epub 2018 Jun 25.
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-α (C/EBP-α) 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.
瘦素及其受体广泛分布于多种组织中,主要分布于白色脂肪组织。在啮齿动物和人类中,血清瘦素与体重指数高度相关,有文献记载,瘦素水平在禁食状态下降低,在再喂养期间升高,类似于胰岛释放胰岛素。胰岛素似乎增加了脂肪细胞中瘦素 mRNA 和蛋白质的表达及其释放。一些研究表明,胰岛素通过激活转录因子:固醇调节元件结合蛋白 1(SREBP1)、CCAAT 增强子结合蛋白-α(C/EBP-α)和特异性蛋白 1(Sp1)起作用。胰岛素通过其信号级联刺激脂肪细胞释放预先形成的和新合成的瘦素。其作用被胰岛素信号通路抑制剂、蛋白质合成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动物的血清瘦素水平。在这篇综述中,我们总结了关于胰岛素对血清瘦素水平影响的最新知识,介绍了控制白色脂肪组织中瘦素合成和释放的细胞机制。