Central mechanisms involved in the orexigenic actions of ghrelin

被引:123
作者
Andrews, Zane B. [1 ]
机构
[1] Monash Univ, Dept Physiol, Clayton, Vic 3183, Australia
基金
澳大利亚国家健康与医学研究理事会;
关键词
NPY; AgRP; Ghrelin; Ghrelin resistance; Intracellular; CaMKK; AMPK; CPT1; UCP; GROWTH-HORMONE SECRETAGOGUE; ACTIVATED PROTEIN-KINASE; HYPOTHALAMIC ARCUATE NUCLEUS; AGOUTI-RELATED PROTEIN; DIET-INDUCED OBESITY; HIGH-FAT DIET; NEUROPEPTIDE-Y; FOOD-INTAKE; ENERGY HOMEOSTASIS; NPY/AGRP NEURONS;
D O I
10.1016/j.peptides.2011.05.014
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Ghrelin is a stomach hormone, secreted into the bloodstream, that initiates food intake by activating NPY/AgRP neurons in the hypothalamic acruate nucleus. This review focuses on recent evidence that details the mechanisms through which ghrelin activate receptors on NPY neurons and downstream signaling within NPY neurons. The downstream signaling involves a novel CaMKK-AMPK-CPT1-UCP2 pathway that enhances mitochondrial efficiency and buffers reactive oxygen species in order to maintain an appropriate firing response in NPY. Recent evidence that shows metabolic status affects ghrelin signaling in NPY is also described. In particular, ghrelin does not activate NPY neurons in diet-induced obese mice and ghrelin does not increase food intake. The potential mechanisms and implications of ghrelin resistance are discussed. (C) 2011 Elsevier Inc. All rights reserved.
引用
收藏
页码:2248 / 2255
页数:8
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