Kasuga M, Akanuma Y, Iwamoto Y, Kosaka K
Am J Physiol. 1978 Aug;235(2):E175-82. doi: 10.1152/ajpendo.1978.235.2.E175.
To investigate the mechanism of the cellular insulin insensitivity of diabetic rats, insulin binding, glucose transport, and glucose oxidation were studied in adipocytes from streptozotocin-diabetic rats. Increased insulin binding was found in cells from diabetic rats, and this was due to an increased number of insulin receptors rather than a change in receptor affinity. Basal and insulin-stimulated glucose oxidation was decreased in adipocytes from diabetic rats when the data are expressed in absolute terms or as percent increased above basal. Although the absolute rate of basal and insulin-stimulated glucose transport was decreased in adipocytes from diabetic rats, the percent increase above basal of insulin-stimulated glucose transport was not decreased. In conclusion, although the cellular insulin insensitivity exists in adipocytes from diabetic rats, the number of insulin receptors was increased, coupling between insulin receptors and the glucose transport system is intact in adipocytes from diabetic rats, and a defect in intracellular glucose metabolism rather than glucose transport plays a major role in the insulin insensitivity of adipocytes from diabetic rats.
为研究糖尿病大鼠细胞胰岛素不敏感的机制,对链脲佐菌素诱导的糖尿病大鼠脂肪细胞中的胰岛素结合、葡萄糖转运及葡萄糖氧化进行了研究。发现糖尿病大鼠细胞中的胰岛素结合增加,这是由于胰岛素受体数量增加而非受体亲和力改变所致。当以绝对值或相对于基础值增加的百分比表示数据时,糖尿病大鼠脂肪细胞中基础及胰岛素刺激的葡萄糖氧化均降低。虽然糖尿病大鼠脂肪细胞中基础及胰岛素刺激的葡萄糖转运的绝对速率降低,但胰岛素刺激的葡萄糖转运相对于基础值增加的百分比并未降低。总之,虽然糖尿病大鼠脂肪细胞存在细胞胰岛素不敏感,但胰岛素受体数量增加,糖尿病大鼠脂肪细胞中胰岛素受体与葡萄糖转运系统之间的偶联完整,细胞内葡萄糖代谢而非葡萄糖转运缺陷在糖尿病大鼠脂肪细胞的胰岛素不敏感中起主要作用。