Kasuga M, Akanuma Y, Tsushima T, Iwamoto Y, Kosaka K, Kibata M, Kawanishi K
Diabetes. 1978 Sep;27(9):938-45. doi: 10.2337/diab.27.9.938.
We studied the effect of sera from two patients who had an unusual form of diabetic syndrome with extreme insulin resistance on the metabolism of human adipocytes in vitro. The IgG fractions from sera A and B, which were obtained from two patients (1 and 2) with insulin-resistant diabetes, inhibited [125I] insulin binding to human adipocytes and, at the same time, stimulated glucose oxidation and inhibited the lipolysis induced by levarterenol in human adipocytes. On the other hand, the IgG fraction from the C serum, which was obtained from patient 2 after her diabetic syndrome had completely disappeared as a result of immunosuppressive therapy, did not inhibit [125I] insulin binding to human adipocytes, stimulate glucose oxidation, or inhibit lipolysis in human adipocytes. These facts suggest that these IgG fractions bind to or near the insulin receptor of human adipocytes, that they exhibit their insulin-like effect by binding to the insulin receptor in vitro, and, furthermore, that they are responsible for the extremely insulin-resistant diabetes. However, the apparent discrepancy between the effects of these IgG fractions on man in vitro and in vivo is puzzling and needs to be explained.
我们研究了两名患有特殊形式糖尿病综合征且胰岛素抵抗极为严重的患者的血清，对人脂肪细胞体外代谢的影响。从两名胰岛素抵抗性糖尿病患者（患者1和患者2）血清中获得的A血清和B血清的IgG组分，抑制了[125I]胰岛素与人脂肪细胞的结合，同时刺激了葡萄糖氧化，并抑制了去甲肾上腺素在人脂肪细胞中诱导的脂解作用。另一方面，从患者2经免疫抑制治疗糖尿病综合征完全消失后获得的C血清的IgG组分，并不抑制[125I]胰岛素与人脂肪细胞的结合，不刺激葡萄糖氧化，也不抑制人脂肪细胞中的脂解作用。这些事实表明，这些IgG组分与人脂肪细胞的胰岛素受体或其附近结合，它们在体外通过与胰岛素受体结合发挥胰岛素样作用，此外，它们是导致这种极为严重的胰岛素抵抗性糖尿病的原因。然而，这些IgG组分在体外和体内对人体作用的明显差异令人困惑，需要加以解释。
