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下丘脑是人体的摄食中枢,它通过抑制食欲的阿黑皮素原(POMC)神经元和促进食欲的神经肽相关蛋白(AgRP)神经元调节摄食及能量代谢。叉头转录因子O亚族1(FoxO1)是胰岛素信号通路和瘦素信号通路中重要的调节蛋白,FoxO1的生理作用是促进下丘脑Agrp基因表达、抑制Pomc基因表达,抑制瘦素信号通路的转录激活因子3(STAT3)蛋白对Pomc基因转录的促进作用,从而促进食欲。瘦素和胰岛素均可激活经典的IRS/PI(3)K/Akt信号通路,使FoxO1磷酸化失去活性,抑制食欲。此外,沉默信息调节因子Sirt1也可以通过去乙酰化,影响FoxO1的转录活性。本文综述了胰岛素、瘦素、Sirt1通过FoxO1调节下丘脑摄食中枢的作用机制。
The hypothalamus, the feeding center of the body, regulates food intake and energy metabolism through appetite-suppressing pro-opiomelanocortin (POMC) neurons and appetite-promoting neuropeptide-related protein (AgRP) neurons. FoxO1 is an important regulatory protein in insulin signaling pathway and leptin signaling pathway. The physiological function of FoxO1 is to promote the expression of Agrp gene in hypothalamus, inhibit the expression of Pomc gene, and inhibit the transcription of leptin signaling pathway Activator of 3 (STAT3) protein Pomc gene transcription of the promotion, thereby promoting appetite. Leptin and insulin can activate the classic IRS / PI (3) K / Akt signaling pathway, so FoxO1 phosphorylation loss of activity, inhibition of appetite. In addition, Sirt1, a silent information regulator, can also affect FoxO1 transcriptional activity through deacetylation. This review summarizes the mechanisms by which insulin, leptin, and Sirt1 regulate hypothalamic feeding through FoxO1.