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.