Objective: To assess the possible role of insulin resistance (IR) and β cell function in the pathophysiology of newly diagnosed type 2 diabetics (T2DM).
Methods: An oral glucose tolerance test was obtained at the health cohort baseline. Subjects with normal glucose tolerance (NGT, n = 269), impaired glucose regulation (IGR, n = 269) and newly diagnosed type 2 diabetics (T2DM, n = 269) were defined by ADA criteria. Subjects with NGT and IGR were selected from residents living in the same community of diabetic patients with the same gender and age (± 3 years old). The T2DM group was sub-classified as isolated fasting hyperglycemia (IFH), isolated post-challenge hyperglycemia (IPH) and combined hyperglycemia (CH). The IGR group was sub-classified as impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and combined glucose intolerance (CGI). Homeostasis model assessment of insulin resistance (HOMA-IR), β cell function (HOMA-β) and deposition index (DI) were to evaluate the insulin resistance or sensitivity, islet β cell function and that when insulin compensated respectively.
Results: From NGT to T2DM, HOMA-IR increased while HOMA-β and DI decreased significantly (P < 0.05). After the adjustment of age, gender, obesity and hypertension, IFG and CGI subgroup had statistically higher HOMA-IR and lower HOMA-β and DI, and IGT subgroup only had lower HOMA-β and DI than NGT subgroup (P < 0.05). Compared to IGT subgroup, IFG and CGI subgroup had significantly higher HOMA-IR and lower HOMA-β and DI (P < 0.05). IFH and CH subgroup had statistically higher HOMA-IR and lower HOMA-β and DI than IFH subgroup (P < 0.05), DI of CH subgroup significantly decreased than that of IPH subgroup (P < 0.05). IFH and CH subgroup had statistically higher HOMA-IR and lower HOMA-β and DI than IFG and CGI subgroup respectively. HOMA-β and DI decreased of IPH subgroup compared to IGT subgroup, and multiple linear regression analysis showed that HOMA-IR had significant influence on fasting plasma glucose (FPG) in NGT (P < 0.05), whereas two-hour plasma glucose and FPG were influenced by DI (P < 0.05) in the progression.
Conclusions: Both basic β cell dysfunction and IR exist in IFG and CGI, while only basic β cell dysfunction exist in IGT. The basic β cell dysfunction and IR are the primary features of fasting hyperglycemia, and basic β cell dysfunction also contribute to post- challenge hyperglycemia.