β3-肾上腺素能受体基因变异对肥胖、2型糖尿病和胰岛素抵抗发病机制的研究进展  

Advanced study of pathogenic mechanism of β3-adrenergic receptor genetic variation inducing obesity,type 2 diabetes and insulin resistance

作　　者：吴锦丹[1] 沈捷[2] 马向华[2] 

机构地区：[1]南京医科大学附属南京第一医院内分泌科,江苏南京210006 [2]南京医科大学第一附属医院内分泌科,江苏南京210029

出　　处：《医学研究生学报》2007年第9期982-984,共3页Journal of Medical Postgraduates

基　　金：江苏省自然科学基金资助项目(批准号:39170374)

摘　　要：近年来的研究发现,β3-肾上腺素能受体(β3-AR)基因变异与肥胖、2型糖尿病(T2DM)和胰岛素抵抗有关。β3-AR基因多态性是通过自主神经来影响代谢的,在β3-AR受体结合、信号转导和调节机制上的缺陷,可能会导致对脂肪组织及脂质分解反应的消失。因此,加速了肥胖及其相关的T2DM、胰岛素抵抗的发生。其他的研究表明,β3-AR可使解耦联蛋白(UCP)及过氧化物酶增殖物激活受体-γ2(PPAR-γ2)的表达增加,并且β3-AR与这两种基因联合变异在肥胖、T2DM和代谢综合征中有协同作用。Recent studies have demonstrated the correlation of genetic variation in the beta（3）-adrenergic receptor（β3AR） with obesity, type 2 diabetes mellitus, insulin resistance, The β3-adrenergic receptor plays a significant role in the control of metabolism through suppressed autonomic nervous system activity. The defects in β3-adrenergic receptor binding, signal transduction, or regulatory mechanisms, may result in diminished lipolytic response in adipose tissue, thereby exacerbating the obesity and related type 2 diabetes mellitus and insulin resistance. β3-AR stimulation induces an increase in uncoupling protein-1 （UCP） and PPAR-γ2 expression, A cross-talk between the β3-adrenergic receptor and gene variation might contribute to the development of obesity, type 2 diabetes mellitus and insulin resistance.

关 键 词：Β3-肾上腺素能受体基因 解耦联蛋白 过氧化物酶增殖物激活受体-γ2 肥胖 糖尿病 2型 胰岛素抵抗 

分 类 号：R587.1[医药卫生—内分泌]