Studies on signal activating systems induced by an anorexigenicappetitekine, Nesfatin-1

Nesfatin-1给药可促进小鼠NB41A3细胞中CRE报告蛋白活性的剂量依赖性增加，并且Nesfatin-1结合的质膜以高亲和力的方式来源于小鼠下丘脑和NB41A3细胞。在49种gpcr中使用CRE报告基因试验，我们试图确定Nesfatin-1特异性受体，但这些努力以失败告终。Troglitazone是PPARγ的激活剂，具有显著的NUCB2基因mRNA稳定活性，Nesfatin-1激活EGF信号抑制脂肪形成。

Nesfatin-1 administration promoted a dose-dependent increase in CRE reporteractivities inmouse NB41A3cells,and Nesfatin-1 bound plasmamembranes derived frommouse hypothalami and NB41A3 cells in a high affinity manner. Using a CRE reporter assay ineachof 49 GPCRs, wetried to identify a receptorspecific to Nesfatin-1, but these efforts resulted in failure. Troglitazone, an activator for PPARγ, possessed a significantstabilizing activity of NUCB2 gene mRNA, and Nesfatin-1 activated EGF signaling tosuppress adipogenesis.