Shimizu F, Kahn C R, Garzelli C, Hooks J J, Notkins A L
Diabetologia. 1983 Dec;25(6):521-4. doi: 10.1007/BF00284463.
The effect of viral infections on insulin binding in vivo was evaluated by measuring the binding of 125I-insulin to several different tissues. We found that splenic leucocytes from mice infected with either the diabetogenic (D) or non-diabetogenic (B) variants of encephalomyocarditis virus, herpes simplex virus, or lactic dehydrogenase virus showed up to a 130% increase in insulin binding. As much as a 300% increase in the binding of 125I-insulin to splenic leucocytes was observed in mice given bacterial lipopolysaccharide. In neither virus-infected nor lipopolysaccharide-treated mice was there any substantial change in insulin receptors on thymocytes, liver membranes, or peripheral erythrocytes. Thus, the increased binding of insulin appears to be limited to leucocytes and does not appear to represent a generalized metabolic alteration. These experiments suggest that during infection, the binding of insulin to leucocytes, which is widely used to measure insulin receptors, may not always accurately reflect the insulin receptor status of other tissues.
通过测量¹²⁵I-胰岛素与几种不同组织的结合,评估病毒感染对体内胰岛素结合的影响。我们发现,感染脑心肌炎病毒、单纯疱疹病毒或乳酸脱氢酶病毒的致糖尿病(D)或非致糖尿病(B)变种的小鼠脾脏白细胞,胰岛素结合增加高达130%。在给予细菌脂多糖的小鼠中,¹²⁵I-胰岛素与脾脏白细胞的结合增加高达300%。在病毒感染的小鼠和脂多糖处理的小鼠中,胸腺细胞、肝细胞膜或外周红细胞上的胰岛素受体均无实质性变化。因此,胰岛素结合增加似乎仅限于白细胞,并不代表普遍的代谢改变。这些实验表明,在感染期间,广泛用于测量胰岛素受体的胰岛素与白细胞的结合,可能并不总是准确反映其他组织的胰岛素受体状态。