Bryer-Ash M
Department of Medicine, University of British Columbia, Vancouver, Canada.
Diabetes. 1991 May;40(5):633-40. doi: 10.2337/diab.40.5.633.
The effects of acute and chronic hyperglycemia on the kinase activity of insulin receptors in vivo were studied in the rat. Skeletal muscle-derived insulin receptors were isolated, with preservation of the in vivo phosphorylation state, from nondiabetic rats subjected to hyperinsulinemic clamps at either euglycemia (mean 5.2 mM) or hyperglycemia (14.4 mM) or from streptozocin-induced diabetic rats at euglycemia (5.1 mM) or hyperglycemia (14.2 mM). Kinase activity toward histone of insulin receptors from nondiabetic animals rendered hyperglycemic for 80-90 min was 50% higher than that of receptors from rats clamped at euglycemia (mean +/- SE 4.5 +/- 0.4 vs. 3.0 +/- 0.3 fmol of phosphate into histone, respectively, P less than 0.02), although kinase activity of receptors isolated from animals rendered diabetic for 10-14 days before hyperglycemic or euglycemic clamps showed no such effect. These results suggest that acute hyperglycemia may increase insulin-receptor kinase activity in vivo, possibly augmenting glucose disposal thereby, whereas the chronic hyperglycemia of diabetes mellitus results in metabolic derangements that nullify this effect.
在大鼠体内研究了急性和慢性高血糖对胰岛素受体激酶活性的影响。从正常血糖（平均5.2 mM）或高血糖（14.4 mM）下接受高胰岛素钳夹的非糖尿病大鼠，或从链脲佐菌素诱导的糖尿病大鼠在正常血糖（5.1 mM）或高血糖（14.2 mM）下，分离出保留体内磷酸化状态的骨骼肌来源的胰岛素受体。使非糖尿病动物高血糖80 - 90分钟后，胰岛素受体对组蛋白的激酶活性比正常血糖钳夹的大鼠的受体高50%（平均±SE分别为4.5±0.4对3.0±0.3 fmol磷酸盐掺入组蛋白，P<0.02），尽管在高血糖或正常血糖钳夹前10 - 14天患糖尿病的动物分离出的受体的激酶活性没有这种效应。这些结果表明，急性高血糖可能会增加体内胰岛素受体激酶活性，从而可能增强葡萄糖的处置，而糖尿病的慢性高血糖会导致代谢紊乱，使这种效应无效。
