Assessing progression to impaired glucose tolerance and type 2 diabetes mellitus

Background A prospective evaluation of the relationship between insulin secretion and insulin sensitivity, derived from the fasting state, is needed in clinical practice in order to identify the worsening of glucose metabolism. In this study the authors examine whether the product of insulin sensitivity and insulin secretion, assessed from the fasting state, predicts progression from normal glucose tolerance (NGT) to impaired fasting glucose (IFG) and from impaired glucose tolerance (IGT) to type 2 diabetes mellitus (T2DM). Materials and methods A cohort of 300 subjects with NGT and 75 subjects with IGT were followed up over a 5‐year period. Insulin sensitivity was calculated using the Belfiore index (B) and insulin secretion by the homeostasis model analysis β‐cell (HOMA‐β cell) index: the product of B‐β is expressed as: (40 × Ins0 pmol L−1)/Glu0 mmol L−1{[(Glu0 mmol L−1× Ins0 pmol L−1) + 1] − 3·5[(Glu0 mmol L−1 × Ins0 pmol L−1) − 1]}, where Glu0 is fasting glucose and Ins0 is fasting insulin. Results From baseline at the end of the follow‐up period, the product B‐β decreased 10·7% and 52·2% in progressors to IGT and T2DM, respectively. The product B‐β predicts the progression from NGT to IGT [relative risk (RR) 2·7, CI95% 1·2–9·1] and from IGT to T2DM (RR 5·3, CI95% 1·3–8·55). The cut‐off point for the product B‐β that better predicts progression from NGT to IGT is 0·25 (sensitivity 88%, specificity 92%) and from IGT to T2DM 0·15 (sensitivity 92%, specificity 95%). Conclusions Adaptation of insulin secretion to compensate for decreased insulin sensitivity during transition to IGT and T2DM can be successfully assessed with simple measures derived from the fasting state. The product B‐β predicts the development to IGT and T2DM.