Evaluation of insulin resistance in obese castrated New Zealand white rabbits.

摘要

Insulin resistance (IR) is observed in obesity and in the type 2 diabetes mellitus in humans. Although rabbits are used as experimental animal models for IR, the intravenous insulin tolerance test (IVITT), a specific test for evidencing peripheral insulin sensitivity, is not frequently used in this species. This study was conducted to evaluate insulin resistance in obese New Zealand white rabbits by IVITT. A total of 26 rabbits were randomly divided into 3 groups: castrated and obese animals (group CO, n=7), castrated animals treated with antioxidants (vitamin E and d-limonene, Immunoprotect) (group CIm, n=7) and not castrated healthy controls (group NC, n=12). After weighing and determination of the BMI (body mass index), the blood glucose concentrations were measured prior to (0 min) and 5, 10, 15, 25, 30 and 45 min after intravenous injection of human insulin (0.1 U/kg) and the following kinetic parameters were calculated: the index of insulin sensitivity (K_ivitt), the glucose disappearance rate (K_glucose), the glucose half-life time (t_{1/2 glucose}), the glucose permanence rate (AUC_glucose), the minimal glucose concentration (C_min) and its corresponding time (T_min). Whereas the K_glucose and the K_ivitt significantly decreased in castrated and obese rabbits (group CO) compared to healthy controls, the other kinetic parameters markedly and significantly increased except for the AUC_glucose. When castrated rabbits were supplemented with antioxidants (group CIm), the values of the various parameters were closely related to those calculated in controls except for the T_min which has remained significantly more elevated. The BMI negatively correlated with the K_glucose and K_ivitt and positively with the other parameters. These results demonstrate that the insulin resistance evaluating throughout the kinetic analysis of the IVITT in rabbits occurs during castration-induced obesity and that antioxidant (vitamin E, d-limonene) supplementation may alleviate this deregulation of glucose metabolism.