Molecular mechanisms of appetite and obesity: a role for brain AMPK

被引:18
|
作者
Martinez de Morentin, Pablo B. [1 ,2 ]
Urisarri, Adela [3 ]
Couce, Maria L. [3 ]
Lopez, Miguel [1 ,2 ]
机构
[1] Univ Santiago de Compostela, Inst Invest Sanitaria, CIMUS, Dept Physiol, Santiago De Compostela 15782, Spain
[2] CIBER Fisiopatol Obesidad & Nutr CIBERobn, Santiago De Compostela 15706, Spain
[3] Univ Clin Hosp Santiago de Compostela, Dept Pediat, Neonatol Unit, IDIS,CIBERER, Santiago De Compostela 15706, Spain
关键词
AMPK; energy balance; food intake; hypothalamus; obesity; ACTIVATED PROTEIN-KINASE; FATTY-ACID-METABOLISM; GLUCAGON-LIKE PEPTIDE-1; ACETYL-COA CARBOXYLASE; AGOUTI-RELATED PEPTIDE; ENERGY-SENSOR; FOOD-INTAKE; STRUCTURAL BASIS; POMC NEURONS; PROOPIOMELANOCORTIN DEFICIENCY;
D O I
10.1042/CS20160048
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Feeding behaviour and energy storage are both crucial aspects of survival. Thus, it is of fundamental importance to understand the molecular mechanisms regulating these basic processes. The AMP-activated protein kinase ( AMPK) has been revealed as one of the key molecules modulating energy homoeostasis. Indeed, AMPK appears to be essential for translating nutritional and energy requirements into generation of an adequate neuronal response, particularly in two areas of the brain, the hypothalamus and the hindbrain. Failure of this physiological response can lead to energy imbalance, ultimately with extreme consequences, such as leanness or obesity. Here, we will review the data that put brain AMPK in the spotlight as a regulator of appetite.
引用
收藏
页码:1697 / 1709
页数:13
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