Glucose effectiveness and its components in relation to body mass index.

ABSTRACT

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 .