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 (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 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) × ISI_M) and total DI₁₂₀ (the ratio of total insulin AUC and total glucose AUC during 0–120 min of the OGTT (InsAUC₁₂₀/GluAUC₁₂₀) × ISI_M). Compared with NGT, in IFG, ISI_M (−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, ISI_M, 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 ISI_M and DI were correlated inversely with FPG concentration (r = −0.242 for ISI_M, 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.