Röjdmark S, Andersson D E
Am J Cardiol. 1986 Feb 26;57(7):39D-43D. doi: 10.1016/0002-9149(86)90804-0.
Studies have indicated that verapamil inhibits insulin release from pancreatic beta cells in vitro. Studies in this clinic, however, showed that both oral pretreatment with verapamil for 1 week and intravenous infusion of the drug over a period of 3 hours improved oral glucose tolerance in patients with type II diabetes without affecting insulin release. In contrast, verapamil failed to increase further the hypoglycemic effect of oral glibenclamide therapy when administered intravenously in diabetic patients. This hypoglycemic effect of verapamil does not appear to be caused by reduced glucose absorption from the gut because intravenous infusion of verapamil left the portal vein glucose response to glucose ingestion unaffected in normoglycemic patients who underwent portal vein catheterization for diagnostic purposes. It is more likely that verapamil affects the liver, leading to decreased hepatic glucose output, which supports previous reports that have shown an inhibitory influence of verapamil on enzymes involved in the gluconeogenetic and glycogenolytic processes.
研究表明，维拉帕米在体外可抑制胰腺β细胞释放胰岛素。然而，该诊所的研究显示，对II型糖尿病患者而言，口服维拉帕米预处理1周以及在3小时内静脉输注该药，均可改善口服葡萄糖耐量，且不影响胰岛素释放。相比之下，在糖尿病患者中静脉注射维拉帕米时，它未能进一步增强口服格列本脲疗法的降糖效果。维拉帕米的这种降糖作用似乎并非由肠道葡萄糖吸收减少所致，因为对因诊断目的而行门静脉插管的血糖正常患者静脉输注维拉帕米后，门静脉对摄入葡萄糖的反应未受影响。维拉帕米更有可能作用于肝脏，导致肝脏葡萄糖输出减少，这支持了之前的报道，即维拉帕米对参与糖异生和糖原分解过程的酶具有抑制作用。
