Mitochondrial uncoupling protein 2 (UCP2) in glucose and lipid metabolism

被引:173
作者
Diano, Sabrina [1 ,2 ,3 ,4 ]
Horvath, Tamas L. [1 ,2 ,3 ,4 ]
机构
[1] Yale Univ, Sch Med, Program Integrat Cell Signaling & Neurobiol Metab, New Haven, CT 06520 USA
[2] Yale Univ, Sch Med, Dept Ob Gyn, New Haven, CT 06520 USA
[3] Yale Univ, Sch Med, Dept Comparat Med, New Haven, CT 06520 USA
[4] Yale Univ, Sch Med, Dept Neurobiol, New Haven, CT 06520 USA
关键词
FATTY-ACID OXIDATION; BETA-CELL FUNCTION; REACTIVE OXYGEN; ARCUATE NUCLEUS; ENERGY-BALANCE; FREE-RADICALS; FOOD-INTAKE; NEURONS; OBESITY; HOMEOSTASIS;
D O I
10.1016/j.molmed.2011.08.003
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
Nutrient availability is critical for the physiological functions of all tissues. By contrast, an excess of nutrients such as carbohydrate and fats impair health and shorten life due by stimulating chronic diseases, including diabetes, cancer and neurodegeneration. The control of circulating glucose and lipid levels involve mitochondria in both central and peripheral mechanisms of metabolism regulation. Mitochondrial uncoupling protein 2 (UCP2) has been implicated in physiological and pathological processes related to glucose and lipid metabolism, and in this review we discuss the latest data on the relationships between UCP2 and glucose and lipid sensing from the perspective of specific hypothalamic neuronal circuits and peripheral tissue functions. The goal is to provide a framework for discussion of future therapeutic strategies for metabolism-related chronic diseases.
引用
收藏
页码:52 / 58
页数:7
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