糖调节受损人群胰岛素抵抗与胰岛β细胞功能的研究

Abstract

目的评价糖调节受损(IGR)人群胰岛素抵抗(IR)与胰岛β细胞功能状态. 方法 (1)从青岛地区流行病学调查资料中,选取正常糖耐量(NGT)者447例;IGR 277例,其中空腹血糖受损(IFG)142例;糖耐量受损(IGT)93例;IFG+IGT42例.(2)测身高、体重、腰围、血压及血脂,空腹与糖负荷后血糖、胰岛素.(3)评价IR及基础与糖负荷后早期胰岛素分泌功能. 结果 IGR人群的年龄、血压、体质指数(BMI)、腰围、腰臀比均明显高于NGT人群.而IGT组的年龄、甘油三酯高于IFG组.校正年龄、性别及BMI等因素后,IGR人群HOMA-IR增高 (P<0.05), IFG、IGT及IFG+IGT组间无差异;IFG与IFG+IGT组的HOMA-β明显低于NGT和IGT组(P<0.01); IGT组△I30/△G30低于NGT(P<0.05).Logistic回归分析显示,年龄、BMI、HOMA-IR及HOMA-β与IFG的发生密切相关(P<0.01),年龄、BMI、△I30/△G30则与IGT的发生相关(P<0.05). 结论 IGR人群存在IR,同时IFG基础状态下胰岛β细胞功能轻度受损,而IGT人群的早期胰岛素分泌反应减弱.

Objective To investigate insulin resistance （IR）and dysfunction of islet β cell in 277 Chinese with impaired glucose regulation（IGR）. Methods 724 participants （256 males）in Qingdao were classified into four groups: normal glucose tolerance （NGT, n=447）, impaired fasting glucose （IFG, n=142）, impaired glucose tolerance （IGT, n=93）, combined IFG and IGT （IFG+IGT, n=42）. The levels of plasma glucose, lipids （TC, HDL-C, TG）and insulin were measured. HOMA-IR, HOMA-β and △I30/△G30 after OGTT were calculated. Multivariable logistic regression （MVLR）was used to analyze the factors related to IFG and IGT. Results The age, waist circumference, body mass index（BMI）, and blood pressure were more elevated in the groups of IFG, IGT and IFG plus IGT than those in NGT. Age and TG were higher in IGT than in IFG. After adjusting age, sex, （systolic） blood pressure and BMI, IGR had significantly increased HOMA-IR. However, there was no difference in those among IFG, IGT, and IFG+IGT. HOMA-β decreased significantly in groups of IFG（4.53±0.06） and IFG+IGT （4.38±0.10）than that in groups of NGT（5.10±0.04）and IGT（5.11±0.07）. Meanwhile, there was no difference in that between NGT and IGT. △I30/△G30 was lower in IGT（4.62±0.14） vs NGT, but was no difference among IFG（4.86±0.11）, IFG+IGT（4.70±0.22） and NGT（4.99±0.11）. Age, BMI, and IR were independent risk factors for IFG, and basic β cell function was protective factor for IFG. Age and BMI were independent risk factors, and early phase of insulin secretion was protective factor for IGT. Conclusion Both IR and insulin （secretion） deficiency （ISD）are present in IGR subjects. The IFG subjects have IR and ISD, but still maintain the early phase of insulin secretion. The IGT subjects have IR and defect of the early phase of insulin secretion, but still maintain basic β-cell function.