空腹血糖受损、血脂与β细胞功能  被引量:2

Impaired Fasting Glucose,Lipid and beta Cell Function

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作  者:刘兆爱[1] 荣海钦[2] 

机构地区:[1]山东省医学科学院,济南250062 [2]山东省内分泌与代谢病研究所,济南250062

出  处:《医学综述》2008年第12期1881-1883,共3页Medical Recapitulate

摘  要:本文综述了空腹血糖受损(IFG)的发生率,其在不同性别、地区、种族间的分布特点。IFG伴随着脂代谢紊乱,且脂代谢紊乱早于糖代谢紊乱。由糖耐量减低(IGT)演变为2型糖尿病(T2DM)的过程中,除有前期血游离脂肪酸升高外,长期脂质代谢紊乱可引起β细胞内脂质沉积增加、线粒体形态异常、β细胞凋亡增加和功能下降。分析脂质代谢及脂毒性对胰岛β细胞功能损伤的机制并进行干预,对早期逆转β细胞功能的损伤,预防T2DM和由脂代谢紊乱所引起的与血管内皮脂质沉积有关的心、眼、肾、脑并发症的发生有重要意义。This article reviewed the prevalence of impaired fasting glucose (IFG) and its distribution characteristics in gender,geographic district and ethnic groups. IFG is often accompanied with lipid metabolism disorders before glucose metabolism disorders. During the stage of Impaired glucose tolerance (IGT) developing into type 2 diabetes meUitus (T2DM) , the levels of blood free fat acid (FFA) increase, and the prolonged lipid metabolism disorders contribute to lipid accumulation in β-cell, resulting in abnormal mitochondrial morphology,loss of β-cells and decreased β-cell functions. Thus it is of great importance to analyze the lipid metabolism and islet β-cell impairment induced by lipotoxicity for prevention of T2DM and the cardiovascular, eye, kidney and cerebral complications related to vascular endothelial lipid accumulation.

关 键 词:空腹血糖受损 脂毒性 Β细胞功能 

分 类 号:R587.1[医药卫生—内分泌]

 

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