Early insulin secretion failure leads to diabetes in Chinese subjects with impaired glucose regulation

Abstract

Both beta-cell dysfunction and decreased insulin sensitivity are involved in the pathogenesis of impaired glucose tolerance (IGT) and impaired fasting glucose (IFG), while their relative contribution in the progression to type 2 diabetes still remains controversial. The aim of the present study is to clarify this process in Chinese subjects by using cross-sectional method. 2,975 Chinese subjects were classified into: normal glucose tolerance (NGT), impaired glucose regulations (IGR), and diabetes mellitus (DM) based on oral glucose tolerance test (OGTT). The IGR group was sub-classified as isolated IFG, isolated IGT and combined glucose intolerance (CGI). The DM group was sub-classified as normal fasting plasma glucose and 2-hour hyperglycemia (N0D2), fasting hyperglycemia and normal 2-hour plasma glucose (D0N2), and both fasting and 2-hour hyperglycemia (D0D2). As far as insulinogenic index (IGI) was concerned, there was no difference between IFG and IGT in either gender, however, HOMA2-B% (homeostasis model assessment for beta-cell function) of IGT was higher than that of IFG and CGI in both male and female (P < 0.05). In the diabetic sub-groups, IGI of N0D2 was higher than that of D0N2, and both deteriorated compared with those of IGT and IFG, respectively. HOMA2-B% of N0D2 was still higher than that of D0N2 and D0D2. No significant difference was detected in OGIS and HOMA2-S% (homeostasis model assessment for insulin sensitivity) between IFG and IGT, and this was the case between N0D2 and D0N2. OGIS and HOMA-IR of IGR sub-groups were not different from those of their diabetic counterparts. Failure of beta-cell function might be the main reason for both IGT and IFG developing into diabetes instead of aggravated insulin resistance.