血清瘦素水平与肝源性糖尿病发病机制的相关性  

Relationship between serum leptin level and pathogenesis of hepatogenous diabetes in Hainan population

作　　者：曾俊涛[1] 陈静[1] 

机构地区：[1]海南医学院附属医院消化内科,海南海口570102

出　　处：《中国热带医学》2014年第2期219-220,共2页China Tropical Medicine

基　　金：海南省卫生厅基金(No.琼卫-2011-30)

摘　　要：目的探讨瘦素(Lep)与肝源性糖尿病(Hepatogenous diabetes,HD)的关系。方法选择肝源性糖尿病患者60例归为HD组,健康体检者65例为对照组。采用ELISA法检测血清中Lep,葡萄糖氧化镁-过氧化物酶法测定空腹血糖(FPG),化学发光分析法测定空腹血清胰岛素(FINS),并计算HOMA-IR(稳态模型的胰岛素抵抗指数)。结果 HD组血清Lep、HOMA-IR分别为(10.29±1.77)ng/mL、3.40±0.29,对照组分别为(4.44±0.81)ng/mL、1.77±0.18;HD组与对照组比较差异均有统计学意义(P<0.01)。HD组患者血清Lep水平与HOMA-IR呈正相关(r=0.49,P<0.01)。结论 Lep可能通过促进胰岛素抵抗参与了肝源性糖尿病的发病机制。Objective To find out whether leptin level was associated with pathogenesis of hepatogenous diabetes in Li nationality. Methods One hundred and twenty- five patients with alcoholic liver disease（60 cases with hepatogenous diabetes and 65 cases without hepatogenous diabetes） were investigated. Serum levels of leptin were determined by ELISA. Results The levels of plasma leptin（10.29±1.77 ng/mL） and HOMA IR（2.44±0.25, 3.40±0.29） in patients with HD were significantly higher than those of the control group（P〈0.01）. In HD group, HOMA-IR was positively with the serum leptin level（P〈0.01）. Conclusion Leptin level might involve in the pathogenesis of hepatogenous diabetes.

关 键 词：瘦素 肝源性糖尿病 胰岛素抵抗 发病机制 

分 类 号：R575[医药卫生—消化系统]