糖尿病前期人群的胰岛β细胞功能和胰岛素抵抗的探讨

目的评价糖调节受损（IGR）不同组分的胰岛素抵抗（IR）和胰岛β细胞功能状况。方法OGTT筛查北京地区无DM史中老年人群，据2003年ADA标准，分为正常糖耐量（NGT）组、空腹血糖受损（IFG）组、糖耐量减低（IGT）组、及IFG合并IGT（IFG＋IGT）组，检测各组胰岛素抵抗指数（HO-MA-IR）、胰岛素敏感指数（ISI-Stumvoll）、β细胞功能指数（HBCI/IR）及第一、二时相胰岛素分泌指数。结果（1）IFG组：HOMA-IR显著高于NGT组和IGT组，ISI-Stumvoll高于IGT组（P均〈0.05），HBCI/IR显著低于NGT组和IGT组（P〈0.05）；（2）IGT组：HOMA-IR和HBCI/IR均位于NGT组和IFG组之间，ISI-Stumvoll、第一时相和第二时相胰岛素分泌指数显著低于NGT组和IFG组（P均〈0.05）；（3）IFG＋IGT组：HOMA-IR高于NGT组、IFG组和IGT组，ISI-Stumvoll显著低于NGT组和IFG组（P均〈0.05），HBCI/IR显著低于NGT组和IGT组（P均〈0.05）；（4）在非糖尿病人群中，随着FPG及2hPG的升高，HOMA-IR有递增趋势，ISI-Stumvoll、第一时相和第二时相胰岛素分泌指数有递减趋势（P均〈0.05）。结论IFG主要是肝脏IR和基础状态时的胰岛β细胞分泌功能受损。IGT的肌肉IR较重，其糖负荷后的胰岛β细胞分泌功能受损较重。在非糖尿病人群，FPG和2hPG的升高与IR呈正相关，与胰岛β细胞功能呈负相关。

Study on the islet β cell function and insulin resistance of prediabetic population

Objective To analyze the islet β cell function and the insulin resistance of different components of impaired glucose regulation （1GR）. Methods A total of 463 adults diagnosed as IGR and 200 adults diagnosed as NGT by 75g OGTT, were included for the analysis of the islet beta cell function and insulin resistance. Resets In the IFG group, HOMA-IR was significantly higher than in NGT and IGT group（P〈0. 05） ,ISI-Stumvoll was lower than in NGT group, but higher than in IGT group （P〈0. 05） ; HBCI/IR were lower than in the two groups （P〈0. 05）. HOMA-IR and HBCI/IR of IGT group were between the NGT group and the IFG group. ISI-Stumvoll, the first and second phase insulin secretion index were significantly lower in IGT group than in NGT group and IFG group（P〈0. 05）. In the IFG plus IGT group, HOMA IR was the highest among all the groups; ISI-Stumvoll was lower than the NGT group and the IFG group; HBCI/IR were lower than the NGT group and the IGT group; the first and second phase insulin secretion index were the lowest among all the groups. In the non-diabetic population, along with the increasing of fasting plasma glucose （FPG） or 2h plasma glucose （2hPG）, HOMA IR was increased gradually, ISI-Stumvoll and the first and second phase insulin secretion indexes were decreased gradually （P 〈 0.05 ）. Conclusions IFG is originatd from severe hepatic insulin resistance and basal islet β cell dysfunction. IGT is originated from marked peripheral insulin resistance, and post-glucose-loading β cell dysfunction with near-normal basal insulin secretion. In the non-diabetic groups, FPG and 2hPG are positively correlated with insulin resistance, and negatively correlated with islet β cell function.