Glucose effectiveness and its components in relation to body mass index

Background Obesity is known to induce a deterioration of insulin sensitivity ( S I ), one of the insulin‐dependent components of glucose tolerance. However, few studies investigated whether obesity affects also the insulin‐independent component, that is glucose effectiveness ( S G ). This cross‐sectional study aimed to analyse S G and its components in different body mass index (BMI) categories. Materials and methods Three groups of subjects spanning different BMI (kg m −2 ) categories underwent a 3‐h frequently sampled intravenous glucose tolerance test: Lean (LE; 18.5 ≤ BMI < 25, n = 73), Overweight (OW; 25 ≤ BMI < 30, n = 90), and Obese (OB; BMI ≥ 30, n = 41). OB has been further divided into two subgroups, namely Obese I (OB‐I; 30 ≤ BMI < 35, n = 27) and Morbidly Obese (OB‐M; BMI ≥ 35, n = 14). Minimal model analysis provided S G and its components at zero (GEZI) and at basal (BIE) insulin. Results Values for S G were 1.98 ± 1.30 × 10 −2 ·min −1 in all subjects grouped and 2.38 ± 1.23, 1.84 ± 0.82, 1.59 ± 0.61 10 −2 ·min −1 in LE, OW and OB, respectively. In all subjects grouped, a significant inverse linear correlation was found between the log‐transformed values of S G and BMI ( r  = −0.3, P  < 0.0001). S G was significantly reduced in OW and OB with respect to LE ( P  < 0.001) but no significant difference was detected between OB and OW ( P  = 0.35) and between OB‐I and OB‐M ( P  = 0.25). Similar results were found for GEZI. BIE was not significantly different among NW, OW and OB ( P  = 0.11) and between OB‐I and OB‐M ( P  ≥ 0.07). Conclusions S G and its major component GEZI deteriorate in overweight individuals compared to those in the normal BMI range, without further deterioration when BMI increases above 30 kg m −2 .