Decreased beta cell function and insulin sensitivity contributed to increasing fasting glucose in Chinese

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 (ISIM) 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 DI0 (homeostasis model assessment of β-cell function (HOMA-B) × [1/HOMA-IR]), early-phase DI30 (the ratio of total insulin AUC and total glucose AUC during 0–30 min of the OGTT (InsAUC30/GluAUC30) × ISIM) and total DI120 (the ratio of total insulin AUC and total glucose AUC during 0–120 min of the OGTT (InsAUC120/GluAUC120) × ISIM). Compared with NGT, in IFG, ISIM (−23%), DI0 (−38%), DI30 (−30%), and DI120 (−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, ISIM, DI0, DI30 and DI120 showed decline beginning from normal range of FPG, compared with the reference category of FPG < 4.0 mmol/l. Correlation analysis showed that ISIM and DI were correlated inversely with FPG concentration (r = −0.242 for ISIM, r = −0.933 for DI0, r = −0.806 for DI30, r = −0.817 for DI120; 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.