肝源性糖尿病发病机制研究进展  

Advances in the pathogenesis of hepatogenous diabetes

作　　者：胡庆玲[1] 黄亚雄[1] 谢元林[1] 

机构地区：[1]南华大学附属长沙医院感染病科,长沙市410005

出　　处：《实用肝脏病杂志》2016年第3期377-380,共4页Journal of Practical Hepatology

基　　金：南华大学研究生科研创新专项基金资助项目(编号:No 2015XCX51)

摘　　要：肝源性糖尿病是继发于慢性肝功能损伤后发生的糖尿病。近年来,多项研究表明胰岛素抵抗与肝源性糖尿病之间的关系密切,但肝源性糖尿病的发病机制尚未完全阐明,了解肝源性糖尿病发病机制有助于提高临床对肝源性糖尿病的认识和防治水平。本文阐述了胰岛素分泌与代谢障碍、肝炎病毒感染、肝纤维化和肝硬化引起的肝脏损害、血清胰岛素样生长因子-1、肿瘤坏死因子-α和游离脂肪酸等体液因子代谢紊乱、瘦素和脂联素等脂肪细胞因子的影响以及其他方面的最新研究发现。Hepatogenous diabetes （HD） is secondary to chronic liver injury. Epidemiological studies in recent years have showed that insulin resistance is a risk factor of developing HD. However,the specific mechanism for HD occurrence remains unclear,and understanding the pathogenesis of HD can help to improve the management and prevention of HD. This article mainly reviewed the effects of insulin secretion and metabolic disturbance,hepatitis virus infection,liver fibrosis and liver cirrhosis, the involvement of insulin-like growth factor-l,tumor necrosis factor-α ,free fatty acids,adipecyte factors including leptin and adiponectin,and other aspects of the latest findings.

关 键 词：肝源性糖尿病 发病机制 研究进展 

分 类 号：R587.1[医药卫生—内分泌]