Begum N, Tepperman H M, Tepperman J
Biochem Biophys Res Commun. 1985 Jan 16;126(1):489-95. doi: 10.1016/0006-291x(85)90632-1.
Added TAME (N alpha-p-tosyl-1-anginine methyl ester) or BAME (benzoyl-anginine methyl ester) inhibited insulin induced activation of glucose oxidation and fat cell PDH activation without affecting spermine action on PDH activation and glucose oxidation in fat cells. BAME inhibited insulin-induced generation of both PDH stimulator and PDH inhibitor from liver particulate fraction. In contrast, insulin-induced internalization of insulin receptors and negative cooperativity of insulin receptors were not affected by protease substrate inhibitors. These results suggest that certain actions of insulin (glucose oxidation, generation of PDH regulators) are mediated by proteolytic events, while insulin-induced down regulation and negative cooperativity of insulin receptors are not mediated by activation of endogenous proteases.
添加的TAME（Nα-p-甲苯磺酰基-1-精氨酸甲酯）或BAME（苯甲酰基-精氨酸甲酯）可抑制胰岛素诱导的葡萄糖氧化激活和脂肪细胞丙酮酸脱氢酶（PDH）激活，而不影响精胺对脂肪细胞中PDH激活和葡萄糖氧化的作用。BAME抑制胰岛素诱导的肝脏微粒体部分产生PDH刺激剂和PDH抑制剂。相反，胰岛素诱导的胰岛素受体内化和胰岛素受体的负协同性不受蛋白酶底物抑制剂的影响。这些结果表明，胰岛素的某些作用（葡萄糖氧化、PDH调节剂的产生）是由蛋白水解事件介导的，而胰岛素诱导的胰岛素受体下调和负协同性不是由内源性蛋白酶的激活介导的。
