Potentiation of insulin stimulation of hexose transport by kallikrein and bradykinin in isolated rat adipocytes
Potentiation of insulin stimulation of hexose transport by kallikrein and bradykinin in isolated rat adipocytes
复制标题
激肽释放酶和缓激肽对离体大鼠脂肪细胞中己糖转运的胰岛素刺激的增强作用
DOI：
10.1016/0303-7207(87)90016-5
复制
发表时间：
1987
影响因子：
4.1
通讯作者：
R. Vukmirovich
中科院分区：
文献类型：
--
作者：
J. Goldman;D. Pfister;R. Vukmirovich
在最大内源性胰岛素刺激条件下，激肽释放酶和缓激肽增加脂肪细胞己糖转运，而在没有胰岛素的情况下没有这种作用。这种胰岛素作用的增强遵循与激肽释放酶和缓激肽浓度的剂量-反应关系，这与后者在胰岛素作用调节中的生理作用一致。胰岛素降解分离的脂肪细胞和胰岛素结合脂肪细胞质膜上的受体不受激肽释放酶或缓激肽。因此，激肽释放酶和缓激肽增强胰岛素作用发生在后胰岛素结合位点。总之，激肽释放酶-缓激肽系统通过血管舒张和增强血液灌注增加靶组织的底物供应，并且还通过其增强胰岛素作用刺激葡萄糖摄取和代谢。这些作用表明，激肽释放酶-缓激肽系统调节靶组织中代谢底物的可用性和利用。
Kallikrein and bradykinin additively increased adipocyte hexose transport under conditions of maximal intrinsic insulin stimulation, while no such effect occurred in the absence of insulin. This potentiation of insulin action follows a dose-response relationship with kallikrein and bradykinin concentrations consistent with a physiological role for the latter in the modulation of insulin action. Insulin degradation by isolated adipocytes and insulin binding to its receptors on adipocyte plasma membranes were not affected by either kallikrein or bradykinin. Thus, the kallikrein and bradykinin potentiation of insulin action occur at post-insulin binding sites. In conclusion, the kallikrein-bradykinin system increases the supply of substrates to target tissues through vasodilation and augmented blood perfusion, and it also stimulates glucose uptake and metabolism via its potentiation of insulin action. These actions suggest that the kallikrein-bradykinin system regulate both the availability and utilization of metabolic substrates, in target tissues.