瘦素/瘦素受体的分子生物学特性及其与肥胖的相互关系研究进展

Progress on Molecular Biological Properties of Lep/LepR and Correlation with Obesity

目前,全球因肥胖引发的基础代谢性疾病日益严重,而由肥胖基因编码的瘦素(Lep)是中枢神经系统调节能量代谢进程中的重要能量调节因子,以下丘脑为靶点,通过激活其受体传递抑制摄食、调节脂肪沉积与能量代谢信号;但内源性瘦素升高和瘦素受体(LepR)信号的增加并不能使肥胖者的体重下降;大量研究表明瘦素多效性导致了其功能机制的复杂性。论文主要就瘦素及其受体的分子生物学特性、调控能量代谢的机制、转运缺陷及信号通路调控等及其与肥胖的关系做简要综述,以期为肥胖相关代谢性疾病的研究提供理论依据。

Obesity is one of the vital factors that results in serious metabolic diseases througout the world.Lepin(LEP)is an important energy regulator that regulates the process of energy metabolism in central nervous system(CNS).Lep,encoded by the obesity gene,can inhibit ingestion,and adjust fat deposition and energy metabolism signals through activating its receptor in hypothalamus.However,increased endogenous level of LEP and leptin receptor(LEPR)signaling can not reduce weight in obese persons.Numberous studies have shown that the pleiotropism of leptin leads to the complexity of its functional mechanism.Thus,the molecular biological properties of LEP and LEPR,regulation of energy metabolism,trafficking defect,and signaling pathway regulation involved in the obesity process were briefly summarized.