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The evolution with ageing of insulin resistance, body weight (BW) and mean arterial pressure (MAP) was studied in a group of Zucker fatty rats (ZFRs, n = 22), between 7 and 16 weeks of age, compared with an age-matched control group of Zucker lean rats (ZLRs, n = 22). The minimal model of glucose kinetics was applied to estimate glucose effectiveness, S(G), and insulin sensitivity, S(I), from insulinaemia and glycaemia measured during a 70 min intravenous glucose tolerance test. No correlation was found between S(G) and age in both ZFR and ZLR groups. No significant changes in mean S(G) between the two groups indicated no alteration of glucose-mediated glucose disposal. Estimates of S(I) from individual ZFRs were independent of age and, on average, showed 83% reduction (P < 0.001) compared with the ZLR group. Despite the lack of alteration of S(I) with age, the ZFR group showed an age-related increase of MAP, which correlated with increasing BW (r = 0.71 and P < 0.001). These results support the hypothesis that in our ZFRs, as a suitable genetic model of obesity and hypertension, insulin resistance is fully established at the age of 7 weeks and remains practically unaltered until at least the sixteenth week. An age-related increase in arterial pressure, observed in this strain, relates more properly to increasing BW, rather than insulin resistance. Development of hypertension with increasing age and BW may result from an enhanced insulin-mediated activity of the sympathetic nervous system, as observed in our previously reported study.

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. [ABSTRACT FROM AUTHOR]