Heise E, Joost H G, Hasselblatt A
Endocrinology. 1982 Mar;110(3):955-60. doi: 10.1210/endo-110-3-955.
Insulin binding to isolated fat cells from rats rendered hyperthyroid by daily injections of T4 (1 mg/kg) for 5 days was approximately doubled. The Scatchard curves reflected a large increase in receptor number, as well as an elevation in affinity of the high affinity binding sites. The response to insulin of the fat cells, however, was not increased accordingly: glucose incorporation into lipid in the presence of insulin did not differ significantly from that observed in the control group, whereas the effect of insulin on the lipolytic response to isoprenaline (isoproterenol) was even reduced in the T4-treated animals. T4 treatment had thus dissociated insulin binding from the metabolic effects of insulin, since the increase in membrane receptors was not paralleled by an enhanced effect of the hormone. Since levels of serum insulin were increased in the treated animals, the increase in number of insulin receptors was not mediated by reduced exposure to insulin. Propranolol failed to fully antagonize the effect of T4 on insulin binding, and reserpine treatment even enhanced it. It seems unlikely, therefore, that the increase in insulin receptors of adipocytes results from an augmented response to endogenous catecholamines in T4-treated rats.
通过每日注射 T4（1 毫克/千克）连续 5 天使大鼠甲状腺功能亢进，从这些大鼠分离出的脂肪细胞上胰岛素的结合量大约增加了一倍。斯卡查德曲线反映出受体数量大幅增加，以及高亲和力结合位点的亲和力提高。然而，脂肪细胞对胰岛素的反应并未相应增加：在胰岛素存在的情况下，葡萄糖掺入脂质的情况与对照组相比无显著差异，而在经 T4 处理的动物中，胰岛素对异丙肾上腺素脂解反应的作用甚至减弱。因此，T4 处理使胰岛素结合与胰岛素的代谢作用分离，因为膜受体的增加并未伴随着激素作用的增强。由于处理组动物血清胰岛素水平升高，胰岛素受体数量的增加并非由胰岛素暴露减少介导。普萘洛尔未能完全拮抗 T4 对胰岛素结合的作用，而利血平处理甚至增强了这种作用。因此，脂肪细胞胰岛素受体的增加似乎不太可能是由于 T4 处理的大鼠对内源性儿茶酚胺反应增强所致。
