Shima K, Sawazaki N, Morishita S, Tarui S, Nishikawa M
Proc Soc Exp Biol Med. 1975 Oct;150(1):232-6. doi: 10.3181/00379727-150-39009.
The effect of phenformin (DBI) on the plasma intestinal glucagon-like immunoreactivity (GLI) and pancreatic glucagon (IRG) responses to oral and intravenous glucose loads were studied in 26 gastrectomized subjects, using a cross-reacting and an IRG-specific anti-serum. The drug produced no significant changes in fasting GLI and IRG levels. Thirty minutes after oral glucose alone, the total GLI level rose to a peak of 1.55 +/- 0.17 ng/ml in the untreated subjects and to a maximum level of 1.67 +/- 0.18 ng/ml in the DBI-pretreated subjects. However, the mean GLI levels obtained 120 and 180 min after oral glucose were significantly higher after treatment with DBI. The blood sugar and IRI responses to oral glucose were lowered significantly by DBI pretreatment. DBI did not alter the glucose, IRI, IRG and GLI response to intravenous glucose. These results suggest that the release of intestinal GLI is not related to the intestinal absorption of glucose.
在26名胃切除患者中,使用交叉反应抗血清和胰高血糖素免疫反应性(IRG)特异性抗血清,研究了苯乙双胍(DBI)对口服和静脉注射葡萄糖负荷后血浆肠胰高血糖素样免疫反应性(GLI)和胰腺胰高血糖素(IRG)反应的影响。该药物对空腹GLI和IRG水平无显著影响。仅口服葡萄糖30分钟后,未治疗患者的总GLI水平升至峰值1.55±0.17 ng/ml,DBI预处理患者的总GLI水平升至最高水平1.67±0.18 ng/ml。然而,口服葡萄糖120分钟和180分钟后,DBI治疗后的平均GLI水平显著更高。DBI预处理显著降低了对口服葡萄糖的血糖和胰岛素反应。DBI未改变对静脉注射葡萄糖的葡萄糖、胰岛素、IRG和GLI反应。这些结果表明,肠GLI的释放与葡萄糖的肠道吸收无关。