Heppner Kristy M, Müller Timo D, Tong Jenny, Tschöp Matthias H
Metabolic Diseases Institute, Department of Medicine, University of Cincinnati, Cincinnati, Ohio, USA.
Methods Enzymol. 2012;514:249-60. doi: 10.1016/B978-0-12-381272-8.00015-5.
The discovery of ghrelin as the endogenous ligand for the growth hormone secretagogue receptor (GHS-R) led to subsequent studies characterizing the endogenous action of this gastrointestinal hormone. Accordingly, exogenous administration of ghrelin was found to increase food intake and adiposity in a variety of species, including rodents, nonhuman primates, and humans. Later work supported these findings and confirmed that ghrelin acts through hypothalamic neurons to mediate its effects on energy metabolism. Ghrelin acts specifically through GHS-R to promote a positive energy balance as demonstrated by loss of ghrelin action after pharmacological blockade or genetic deletion of GHS-R. More recently, ghrelin was found to be a mediator of glucose metabolism and acts to inhibit insulin secretion from pancreatic β-cells. Together, the literature highlights a predominant role of ghrelin in regulating energy and glucose metabolism.
胃饥饿素作为生长激素促分泌素受体（GHS-R）的内源性配体的发现，引发了后续一系列研究，旨在阐明这种胃肠激素的内源性作用。相应地，研究发现，在包括啮齿动物、非人灵长类动物和人类在内的多种物种中，外源性给予胃饥饿素会增加食物摄入量和肥胖程度。后来的研究支持了这些发现，并证实胃饥饿素通过下丘脑神经元发挥作用，从而介导其对能量代谢的影响。胃饥饿素通过GHS-R特异性发挥作用，促进正能量平衡，药理学阻断或基因敲除GHS-R后胃饥饿素作用丧失即证明了这一点。最近，人们发现胃饥饿素是葡萄糖代谢的介质，可抑制胰腺β细胞分泌胰岛素。综合来看，文献强调了胃饥饿素在调节能量和葡萄糖代谢中的主要作用。
