Villar A, D'Ocón M P, Anselmi E
Rev Esp Fisiol. 1985 Dec;41(4):451-5.
Glycemia and insulinemia in rat blood samples have been determined at different times before and after administration of glibenclamide, PGE1, glibenclamide and PGE1, glibenclamide and glucose, PGE1 and glucose, and glibenclamide, PGE1 and glucose. PGE1 led to a partial inhibition of glibenclamide induced insulin release, with and without glucose administration, but a total inhibition did not occur. The inhibitory action of PGE1 on insulin secretion was also reflected on the glycemia curves. Defects in insulin release in diabetes could be due in part to an excessive production of PGs, that involve a failure in the beta-cells to respond to glucose signals. The present paper shows that glibenclamide secretory action was not cancelled out by PGE1. These results could explain the availability of glibenclamide in the treatment of diabetes mellitus.
在给予格列本脲、前列腺素E1、格列本脲与前列腺素E1、格列本脲与葡萄糖、前列腺素E1与葡萄糖以及格列本脲、前列腺素E1与葡萄糖之前及之后的不同时间，对大鼠血样中的血糖和胰岛素血症进行了测定。无论是否给予葡萄糖，前列腺素E1都会部分抑制格列本脲诱导的胰岛素释放，但并未出现完全抑制的情况。前列腺素E1对胰岛素分泌的抑制作用也反映在血糖曲线上。糖尿病患者胰岛素释放缺陷可能部分归因于前列腺素过度产生，这涉及β细胞对葡萄糖信号反应失败。本文表明前列腺素E1并未抵消格列本脲的分泌作用。这些结果可以解释格列本脲在糖尿病治疗中的有效性。
