Peters W H, Gottschling D, Ziegler M, Haude W
Acta Biol Med Ger. 1978;37(7):1007-14.
Colony-bred Wistar-rats develop obesity after long term feeding with a high-fat diet (50% fat, w/w). According to previous investigations a disturbed glucose tolerance after i.v. glucose load could be described for obese rats. Therefore, we measured peripheral IRI-concentrations before and after glucose stimulation in controls and fat-fed rats. In obese animals we observed a basal hyperinsulinemia in the dynamic phase of development of obesity. In controls and fatty rats, no differences in the peripheral insulin response to an i.v. glucose stimulation could be demonstrated, nor did we find indications of an impaired early insulin response in fatty rats. In accordance with the glucose tolerance study, obese rats in the dynamic phase showed lower FFA-levels (fasting state) and a slower decrease of FFA-concentrations after the glucose-induced insulin enhancement. Changing the feeding schedule at 20 weeks of age, e.g. feeding control diets to fatty rats for 4 weeks, reduced basal IRI-concentrations in these animals to control values. Assuming the secondary nature of the basal hyperinsulinemia in obese rats, our present results demonstrate that the observed impairment of glucose tolerance may be related to the peripheral insulin resistance of skeletal muscle and/or hypertrophied adipose tissue.
群体饲养的Wistar大鼠长期喂食高脂饮食（50%脂肪，w/w）后会发生肥胖。根据先前的研究，肥胖大鼠静脉注射葡萄糖负荷后糖耐量会受到干扰。因此，我们测量了对照组和高脂喂养大鼠在葡萄糖刺激前后的外周胰岛素抵抗指数（IRI）浓度。在肥胖动物中，我们在肥胖发展的动态阶段观察到基础高胰岛素血症。在对照组和高脂喂养大鼠中，静脉注射葡萄糖刺激后外周胰岛素反应没有差异，我们也没有发现高脂喂养大鼠早期胰岛素反应受损的迹象。与糖耐量研究一致，处于动态阶段的肥胖大鼠空腹状态下游离脂肪酸（FFA）水平较低，葡萄糖诱导胰岛素增加后FFA浓度下降较慢。在20周龄时改变喂养方案，例如给高脂喂养大鼠喂食对照饮食4周，可使这些动物的基础IRI浓度降至对照值。假设肥胖大鼠基础高胰岛素血症具有继发性，我们目前的结果表明，观察到的糖耐量受损可能与骨骼肌和/或肥大脂肪组织的外周胰岛素抵抗有关。
