ASSESSING THE RISK OF IMPAIRED GLUCOSE METABOLISM IN OVERWEIGHT ADOLESCENTS IN A CLINICAL SETTING

Objective: The study aims were to examine the relationship between adiposity and surrogate indices of pancreatic β-cell function and insulin sensitivity obtained from an oral glucose tolerance test (OGTT) in overweight adolescents and determine which factors best predict impaired glucose metabolism (IGM). Methods: In a sample of adolescents (n=209) severity of overweight was determined by relative body mass index (RBMI). Insulin sensitivity (QUICKI, CISI) and β-cell function (Fasting insulin: FI; Insulinogenic Index: ΔI30/ΔG30). Results: IGM was present in 26.8% (n=56), of which five had type 2 diabetes (T2DM). IGM prevalence was similar among RBMI strata. Once RBMI reached 150%, pronounced deterioration in CISI occurred (~55%) (P<0.0001) while less dramatic reductions were seen in QUICKI (P<0.05), with fasting blood glucose (FBG) and β-cell indices remaining stable. Compared to those with normal glucose tolerance, the IGM group exhibited higher β-cell activity (FI, P<0.0001; ΔI30/ΔG30, P=0.004) with reduced insulin sensitivity (CISI, P<0.0001; QUICKI, P<0.0002). CISI was the single predictor of IGM (P<0.0001). Low insulin sensitivity increased adolescents’ chance for IGM (CISI: OR=6.49, 95%CI=2.63, 16.05, P<0.0001; QUICKI: OR=3.16, 95%CI=1.61, 6.05, P=0.0006) as did β-cell deterioration (ΔI30/Δ G30: OR=3.18, 95%CI=1.33, 7.59, P=0.0069). Normal FBG occurred in 37.5% of youth with IGM. Conclusion: The prevalence of IGM escalates in overweight adolescents, even at lower levels of overweight, and is associated with pronounced deterioration of insulin sensitivity. Current screening recommendations for FBG underestimate the prevalence of IGM in overweight adolescents thus limiting the opportunity for earlier intervention to prevent progression to diabetes.