肥胖相关黑棘皮病的发病机制  

Pathogenesis of obesity-related acanthosisnigricans

作　　者：尚晨[1] 龚凤英[1] 王林杰[1] 

机构地区：[1]中国医学科学院北京协和医学院北京协和医院内分泌科国家卫生和计划生育委员会内分泌重点实验室协和转化医学中心,北京100730

出　　处：《国际内分泌代谢杂志》2016年第6期416-419,共4页International Journal of Endocrinology and Metabolism

基　　金：国家自然科学基金资助项目（30540036,30771026,81370898）;北京市自然科学基金资助项目（7082079）;人社部留学人员科技活动项目择优资助经费;国家临床重点专科建设项目单位（WBYZ2011-873）

摘　　要：黑棘皮病是肥胖患者常见的皮肤过度角化伴局部肤色加深的特征性改变，是高胰岛素血症和胰岛素抵抗的可靠皮肤标志。该病是由于循环中过量的胰岛素通过直接或间接途径激活胰岛素样生长因子一1受体（IGF一1R），促进角化细胞和成纤维细胞生长所致。近年来的研究发现，肥胖患者皮肤的慢性炎性反应、维生素D浓度减低、瘦素分泌增加、色素上皮衍生因子（PEDF）水平升高、哺乳动物雷帕霉素靶蛋白（mTOR）通路过度活化与皮肤稳态受损等，也参与了黑棘皮病的发生和发展。探讨肥胖相关黑棘皮病的发病机制可以为临床诊断和治疗提供依据。Acanthosisnigricans is a disorder characterized by pigmented and hyperkeratotic skin changes, which is often seen in obesity. It is also a reliable sign of hyperinsulinemia or insulin resistance. Previous studies have revealed that high levels of insulin can result in over activation of insulin-like growth factor-1 reeeptor（IGF-1R） both directly and indirectly, which in turn lead to the proliferation of keratino- eytes and fibroblasts. Lately, it has been found that chronic skin inflammation, decreased serum vitamin D concentration, increased leptin secretion, elevated pigment epithelium derived factor （PEDF） level, exces- sive activation of the mammalian target of rapamycin （roTOR） pathway as well as impairment of skin homeo- stasis of obese patients might also play important roles in the process of acanthosisnigricans. Undoubtedly, there would be diagnostic and therapeutic potential in clarifying the pathogenesis of obesity-related acantho- sisnigrieans.

关 键 词：黑棘皮病 肥胖 高胰岛素血症 胰岛素抵抗 

分 类 号：R735.2[医药卫生—肿瘤]