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糖尿病中国仓鼠中胰岛素受体的自身磷酸化和激酶活性降低。

Decreased autophosphorylation and kinase activity of insulin receptors in diabetic Chinese hamsters.

作者信息

Oshima E, Watanabe K, Makino I

机构信息

Second Department of Internal Medicine, Asahikawa Medical College, Japan.

出版信息

Diabetes Res Clin Pract. 1990 Aug-Sep;10(1):35-43. doi: 10.1016/0168-8227(90)90079-9.

Abstract

To clarify the role of the insulin receptor in diabetes, the hepatic insulin receptor was investigated in the spontaneously diabetic Chinese hamsters, which are the animal models for insulin-deficient diabetes. Insulin binding in the diabetic animals increased mainly due to an increase in the number of receptors. It was also observed that both the autophosphorylation and kinase activity of the hepatic insulin receptor were decreased in the diabetic animals compared to the control animals. These changes in the hepatic insulin receptor may be caused by the diabetes itself. As the phosphorylated protein of 95 kDa was immunoprecipitated by the anti-insulin receptor antibody (B-10, human) in both diabetics and controls, it was supposed that the 95 kDa protein would be the beta-subunit of insulin receptors, as in other animals. These animals seem to be useful for examining insulin receptors in diabetes.

摘要

为阐明胰岛素受体在糖尿病中的作用,对自发性糖尿病中国仓鼠的肝脏胰岛素受体进行了研究,这些仓鼠是胰岛素缺乏型糖尿病的动物模型。糖尿病动物体内的胰岛素结合增加,主要是由于受体数量增加。还观察到,与对照动物相比,糖尿病动物肝脏胰岛素受体的自身磷酸化和激酶活性均降低。肝脏胰岛素受体的这些变化可能由糖尿病本身引起。由于抗胰岛素受体抗体(B - 10,人源)在糖尿病动物和对照动物中均能免疫沉淀95 kDa的磷酸化蛋白,因此推测该95 kDa蛋白与其他动物一样,是胰岛素受体的β亚基。这些动物似乎有助于研究糖尿病中的胰岛素受体。

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