具酮症倾向的肥胖糖尿病发病机制研究  

The potential pathogenesis of ketosis-prone obese diabetes

作　　者：余叶蓉[1] 谭惠文[1] 赵乃倩[1] 喻红玲[1] 耿丽杰[1] 王椿[1] 

机构地区：[1]四川大学华西医院内分泌科,成都610041

出　　处：《国际内分泌代谢杂志》2008年第4期226-229,共4页International Journal of Endocrinology and Metabolism

摘　　要：肥胖糖尿病患者自发性酮症的发生与重度胰岛素抵抗及胰岛β细胞功能显著降低有关。胰岛素抵抗及低胰岛素血症使线粒体对脂肪酸氧化能力下降，肝细胞内酮体生成增多而骨骼肌对酮体利用减少，循环中酮体水平增高。肥胖糖尿病患者持续存在的高血糖及高游离脂肪酸血症（糖脂毒性）所导致的β细胞胰岛素合成和分泌功能严重受损，可能是患者低胰岛素血症的主要原因。糖脂共同毒性所导致的胰岛素分泌显著减少与胰岛β细胞凋亡增加有关，其机制涉及启动细胞凋亡的线粒体途径。Severe peripheral insulin resistance and markedly impaired β-cell insulin secretion were observed in obese diabetic patients with unprovoked ketosis. The potential mechanism of ketone over-production in obese diabetic patients may associate with a marked synergistic effect of high glucose and FFAs which severely damaged the β-cell function. The effect of glucolipotoxicity on impaired insulin secretions relates to increased β-cell apoptosis. Mitochondria signal pathway of apoptosis plays a crucial part in the execution of apoptotic β-cell death induced by glucolipotoxicity.

关 键 词：酮症倾向糖尿病 肥胖 胰岛素抵抗 糖脂毒性 

分 类 号：R587.1[医药卫生—内分泌] R363.14[医药卫生—内科学]