肥胖人群中代谢状态与胰岛素抵抗的关系  

The Relationship Between Metabolically State and Insulinresistance in Obese Population

作　　者：李珅 牛敏[1] 高政南[1] 

机构地区：[1]大连市中心医院内分泌科,116033

出　　处：《药品评价》2018年第3期19-20,48,共3页Drug Evaluation

基　　金：辽宁省自然科学基金指导计划项目;20170540229;"中心性肥胖人群胰岛功能损伤的流行病学研究及其自噬机制的探索"

摘　　要：不同代谢类型肥胖患者伴随不同的胰岛素抵抗状态,本文从肥胖患者代谢状态分型、不同类型肥胖患者发生胰岛素抵抗的基因和蛋白基础、代谢异常型肥胖引起胰岛素抵抗的病理生理机制、代谢异常型肥胖与中枢胰岛素抵抗的关系进行了简要地阐述。不同的代谢分类结果显示,约有25%的肥胖患者属于代谢正常型肥胖患者,而其余75%代谢异常型肥胖更易发生胰岛素抵抗。基因和蛋白类研究结果显示,代谢异常型肥胖患者引起胰岛素抵抗的基因基础尚未见报道,但Fetuin A蛋白被认为是代谢异常型肥胖发生胰岛素抵抗的关键蛋白。代谢异常型肥胖型患者发生胰岛素抵抗的病理机制主要为外周血白细胞中炎症和氧化应激改变了内质网信号通路,脑胰岛素抵抗似乎促进代谢异常型肥胖患者发生全身胰岛素抵抗。Different kinds of metabolic obese patients shows varying degrees of insulin resistance, this article overview that subject mainly from the following several aspects types, genes, proteins, pathophysiology and the relationship with central insulin resistance. Different studies show that about 25% obese patients are metabolically healthy obese, insulin resistance increased in metabolically abnormal obese, the gene about metabolic and insulin resistance has not been reported, and Fetuin A is considered to be A key protein which induces insulin resistance in obese population; both infiammation and oxidative stress are involved in the induction of ER stress signalling pathways in the leukocytes of metabolically unhealthy obese vs healthy obese subjects and brain insulin resistance may have played a role during the processes.

关 键 词：代谢健康型肥胖 代谢异常型肥胖 胰岛素抵抗 

分 类 号：R589.2[医药卫生—内分泌]