链脲佐菌素糖尿病大鼠的胰岛素受体结合、胰岛素介体释放和葡萄糖氧化

INSULIN BINDING,INSULIN MEDIATOR RELEASE AND GLUCOSE OXYDATION IN STREPTOZOTOGIN-INDUGED DIABETIC RATS

作者测定了链脲佐菌素引起的糖尿病大鼠脂肪细胞膜对胰岛素特异结合率、肝细胞膜胰岛素介体释放和脂肪细胞葡萄糖氧化。结果表明:(1)糖尿病大鼠脂肪细胞膜对胰岛素特异结合率较正常大鼠显著增加,其胰岛素受体亲和力没有改变,但受体数目增加;(2)大鼠肝细胞膜加胰岛素诱导时,糖尿病鼠肝膜释放的抑制腺苷酸环化酶活力的胰岛素介体量较正常大鼠显著减少;(3)在糖尿病大鼠,基础的和胰岛素刺激的脂肪细胞葡萄糖氧化较正常大鼠显著降低。提示胰岛素介体释放量减少可能是引起受体后胰岛素抵抗的原因之一。

The percentage of specific insulin binding to adipocyte membranes, the releasing of insulin mediator from liver cell membranes and the glucose oxydation in adipocytes were measured in streptozotocin-induced diabetic rats. The results showed that 1) the weight and serum insulin were significantly decreased(P<0.01), but food and water intakes and blood glucose were markedly increased (P<0.01) in diabetic rats (n=36) as compared with normal rats (n=24); 2) the percentage of specific insulin binding to adipocyte membranes from diabetic rats was significantly greater than that from normal rats (P<0.01), this was due to increased number of receptors but the affinity of receptors for insulin was unchanged; 3) when incubated with insulin, liver cell membranes from normal rats released a great quantity of insulin mediator which inhibited adenylate cyclase activity, but this effect was blunted in diabetic rats; 4) basal and insulin-stimulated glucose oxydation in adipose cells of diabetic rats were decreased as compared with those of normal rats. It was concluded that in insulin-deficient diabetic rats, 1) the insulin binding to target cells increased; 2) the insulin resistance at post-receptor sites occurred; 3) the decreased releasing of insulin mediator may be one of the factors causing the development of insulin resistance.