摘要
腺苷酸活化蛋白激酶(AMPK)也称为真核细胞的"能量感受器",下丘脑ANPK活性的下调能使摄食减少、体重降低,反之,摄食、体重增加。下丘脑AMPK能整合ghrelin等刺激食欲的信号和胰岛素、睫状神经营养因子等抑制食欲的信号,可能处于食欲、体重调节的中心环节,其机制可能在于改变了神经肽Y、刺鼠相关蛋白等的表达。对AMPK结构的阐明及对此信号通路的深入研究可能为肥胖的治疗提供新的靶点。
AMP-activated protein kinase(AMPK) is considered as the energy sensor of eukaryotic cell. Decreased activity of hypothalamic AMPK can reduce food-intake and body weight, or vice versa. Hypothalamic AMPK integrates stimulating appetite signals such as ghrelin and inhibiting appetite signals such as insulin, ciliary neurotrophic factor. It may lie at the core position of the regulation of appetite and body weight. The possible mechanism is that level of neuropeptide Y and agouti-related protein are changed. With the AMPK structure elucidated and the signal pathway further studied, new target of treating obesity may be provided.
出处
《国际内分泌代谢杂志》
2007年第4期250-252,共3页
International Journal of Endocrinology and Metabolism
关键词
腺苷酸活化蛋白激酶
食欲
体重
下丘脑
AMP-activated protein kinase
Appetite
Body weight
Hypothalamus