Department of Endocrinology, Drum Tower Hospital Affiliated to Nanjing University Medical School, Zhongshan Road 321, 210008 Nanjing, China.
Acta Diabetol. 2012 Dec;49 Suppl 1:S51-8. doi: 10.1007/s00592-010-0194-4. Epub 2010 May 15.
To evaluate the role of insulin resistance and beta cell function to increasing fasting plasma glucose (FPG), 1,272 Chinese subjects (18-80 years of age) were divided into normal glucose tolerance (NGT), impaired fasting glucose (IFG), impaired glucose tolerance (IGT), combined glucose intolerance (CGI), and type 2 diabetes mellitus (T2DM) according to oral glucose tolerance test. Insulin sensitivity was measured by Matsuda index (ISI(M)) and homeostasis model assessment of insulin resistance (1/HOMA-IR); β-cell function adjusted by insulin sensitivity was assessed from disposition index (DI) at basal DI(0) (homeostasis model assessment of β-cell function (HOMA-B) × [1/HOMA-IR]), early-phase DI(30) (the ratio of total insulin AUC and total glucose AUC during 0-30 min of the OGTT (InsAUC(30)/GluAUC(30)) × ISI(M)) and total DI(120) (the ratio of total insulin AUC and total glucose AUC during 0-120 min of the OGTT (InsAUC(120)/GluAUC(120)) × ISI(M)). Compared with NGT, in IFG, ISI(M) (-23%), DI(0) (-38%), DI(30) (-30%), and DI(120) (-31%) were decreased significantly. As the FPG increased across categories classified by FPG levels from NGT → IFG → T2DM with 2 h PG < 7.8 mmol/l, ISI(M), DI(0), DI(30) and DI(120) showed decline beginning from normal range of FPG, compared with the reference category of FPG < 4.0 mmol/l. Correlation analysis showed that ISI(M) and DI were correlated inversely with FPG concentration (r = -0.242 for ISI(M), r = -0.933 for DI(0), r = -0.806 for DI(30), r = -0.817 for DI(120); P < 0.001). Both the impairment of beta cell function and insulin sensitivity started at the low point of FPG within the normoglycemic range and contributed to the deterioration of fasting glucose.
为了评估胰岛素抵抗和β细胞功能对空腹血糖（FPG）升高的作用，1272 名中国受试者（18-80 岁）根据口服葡萄糖耐量试验（OGTT）被分为正常糖耐量（NGT）、空腹血糖受损（IFG）、糖耐量受损（IGT）、合并糖代谢异常（CGI）和 2 型糖尿病（T2DM）。胰岛素敏感性通过 Matsuda 指数（ISI(M)）和稳态模型评估的胰岛素抵抗（1/HOMA-IR）进行测量；β细胞功能通过基础状态下的胰岛素敏感性进行调整，即基础状态下的胰岛β细胞功能（HOMA-B）与胰岛素敏感性（1/HOMA-IR）的比值（DI(0)），早期阶段的胰岛素敏感性（DI(30)）（OGTT 期间 0-30 分钟的总胰岛素 AUC 和总葡萄糖 AUC 的比值（InsAUC(30)/GluAUC(30))与 ISI(M)）和总胰岛素敏感性（DI(120)）（OGTT 期间 0-120 分钟的总胰岛素 AUC 和总葡萄糖 AUC 的比值（InsAUC(120)/GluAUC(120))与 ISI(M)）。与 NGT 相比，IFG 中 ISI(M)（-23%）、DI(0)（-38%）、DI(30)（-30%）和 DI(120)（-31%）显著降低。随着按 FPG 水平从 NGT→IFG→T2DM 进行分类的类别中 FPG 升高（2 hPG<7.8mmol/l），ISI(M)、DI(0)、DI(30)和 DI(120)从正常 FPG 范围开始下降，与 FPG<4.0mmol/l 的参考类别相比。相关性分析表明，ISI(M)和 DI 与 FPG 浓度呈负相关（ISI(M)为 r=-0.242，DI(0)为 r=-0.933，DI(30)为 r=-0.806，DI(120)为 r=-0.817；P<0.001）。β细胞功能和胰岛素敏感性的损害均在正常血糖范围内的 FPG 低值时开始，并导致空腹血糖恶化。
