Chiba T, Okimura Y, Kodama H, Kadowaki S, Chihara K, Fujita T
Third Department of Internal Medicine, Kobe University School of Medicine, Japan.
Horm Metab Res. 1988 Oct;20(10):641-4. doi: 10.1055/s-2007-1010905.
Tolbutamide significantly decreased fasting plasma gastrin after 5 min of intravenous infusion in patients with atrophic gastritis, duodenal ulcer, or insulin-dependent diabetes mellitus (IDDM) as well as in healthy volunteers. Increased plasma insulin and decreased blood glucose were observed in patients with atrophic gastritis, duodenal ulcer and healthy volunteers, but not in patients with IDDM. Suppression of plasma gastrin in healthy volunteers was also observed following oral administration of tolbutamide. Despite the observed decrease in plasma gastrin, neither basal nor tetragastrin-stimulated acid output was changed for 30 min following tolbutamide infusion in healthy volunteers. Thus, our data suggest that tolbutamide inhibits gastrin release in man via mechanisms independent of changes in plasma insulin, blood glucose or acid secretion.
在萎缩性胃炎、十二指肠溃疡或胰岛素依赖型糖尿病(IDDM)患者以及健康志愿者中,静脉输注甲苯磺丁脲5分钟后,空腹血浆胃泌素显著降低。在萎缩性胃炎、十二指肠溃疡患者及健康志愿者中观察到血浆胰岛素升高和血糖降低,但IDDM患者未出现此现象。口服甲苯磺丁脲后,健康志愿者的血浆胃泌素也受到抑制。尽管观察到血浆胃泌素降低,但在健康志愿者中,静脉输注甲苯磺丁脲后30分钟,基础胃酸分泌量和五肽胃泌素刺激的胃酸分泌量均未改变。因此,我们的数据表明,甲苯磺丁脲通过独立于血浆胰岛素、血糖或胃酸分泌变化的机制抑制人体胃泌素释放。