Glucose effectiveness and its components in relation to body mass index

Background Obesity is known to induce a deterioration of insulin sensitivity (SI), 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 (SG). This cross‐sectional study aimed to analyse SG 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 SG and its components at zero (GEZI) and at basal (BIE) insulin. Results Values for SG 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 SG and BMI (r = −0.3, P < 0.0001). SG 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 SG 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.