Bhathena S J, Aparicio P, Revett K, Voyles N, Recant L
J Nutr. 1987 Jul;117(7):1291-7. doi: 10.1093/jn/117.7.1291.
Obese Zucker rats are hyperlipemic and mildly hyperglycemic. Because insulin and glucagon are involved in lipid and carbohydrate metabolism and they act via their receptors, we investigated the role of insulin and glucagon receptors in obese and lean female Zucker rats. Because dietary sucrose is more lipogenic than starch, we also studied the effect of dietary carbohydrates on the receptors. Significant phenotypic effect (obese greater than lean) was observed on plasma levels of glucose, triglyceride and insulin. Binding of insulin and glucagon to liver plasma membranes was significantly lower in obese rats than in lean rats. Lower insulin binding was due to a lower number of receptors as well as a lower affinity, whereas the lower glucagon binding was due only to a lower receptor number. Insulin binding in lean rats but not in obese rats was lower in sucrose-fed than in starch-fed rats. Diet had no effect on glucagon binding. We propose that in obese Zucker rats, in addition to hyperinsulinemia, impaired glucagon activity as manifested by decreased glucagon binding to target tissues may be an important contributor to the hyperlipemia and obesity.
肥胖的 Zucker 大鼠血脂过高且轻度血糖过高。由于胰岛素和胰高血糖素参与脂质和碳水化合物代谢且它们通过其受体发挥作用,我们研究了胰岛素和胰高血糖素受体在肥胖和瘦的雌性 Zucker 大鼠中的作用。由于膳食蔗糖比淀粉更易生成脂肪,我们还研究了膳食碳水化合物对这些受体的影响。在葡萄糖、甘油三酯和胰岛素的血浆水平上观察到显著的表型效应(肥胖大鼠大于瘦大鼠)。肥胖大鼠肝脏质膜上胰岛素和胰高血糖素的结合显著低于瘦大鼠。胰岛素结合降低是由于受体数量减少以及亲和力降低,而胰高血糖素结合降低仅归因于受体数量减少。蔗糖喂养的瘦大鼠而非肥胖大鼠的胰岛素结合低于淀粉喂养的大鼠。饮食对胰高血糖素结合无影响。我们提出,在肥胖的 Zucker 大鼠中,除了高胰岛素血症外,胰高血糖素活性受损(表现为胰高血糖素与靶组织的结合减少)可能是导致高脂血症和肥胖的一个重要因素。