CNS leptin and insulin action in the control of energy homeostasis

被引:201
作者
Belgardt, Bengt F. [1 ,2 ]
Bruening, Jens C. [1 ,2 ]
机构
[1] Univ Cologne, Inst Genet, Dept Mouse Genet & Metab, Ctr Mol Med,Dept Internal Med 2, D-50674 Cologne, Germany
[2] Max Planck Inst Biol Ageing, Cologne, Germany
来源
YEAR IN DIABETES AND OBESITY | 2010年 / 1212卷
关键词
obesity; leptin; insulin; central nervous system (CNS); pancreas; diabetes; ENDOPLASMIC-RETICULUM STRESS; NECROSIS-FACTOR-ALPHA; HEPATIC GLUCOSE-PRODUCTION; DIET-INDUCED OBESITY; HYPOTHALAMIC PROOPIOMELANOCORTIN NEURONS; ANOREXIGENIC POMC NEURONS; UNFOLDED PROTEIN RESPONSE; ATP CHANNEL ACTIVATION; CENTRAL-NERVOUS-SYSTEM; BLOOD-BRAIN-BARRIER;
D O I
10.1111/j.1749-6632.2010.05799.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The obesity and diabetes pandemics have made it an urgent necessity to define the central nervous system (CNS) pathways controlling body weight, energy expenditure, and fuel metabolism. The pancreatic hormone insulin and the adipose tissue derived leptin are known to act on diverse neuronal circuits in the CNS to maintain body weight and metabolism in a variety of species, including humans. Because these homeostatic circuits are disrupted during the development of obesity, the pathomechanisms leading to CNS leptin and insulin resistance are a focal point of research. In this review, we summarize the recent findings concerning the mechanisms and novel neuronal mediators of both insulin and leptin action in the CNS.
引用
收藏
页码:97 / 113
页数:17
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