Christiansen J, Bech A, Fahrenkrug J, Holst J J, Lauritsen K, Moody A J, Schaffalitzky de Muckadell O
Scand J Gastroenterol. 1979;14(2):161-6. doi: 10.3109/00365527909179862.
The effect of intrajejunal (i.j.) infusion of fat on meal-stimulated gastric acid secretion and release of pancreatic glucagon (PG), enteroglucagon (EG), gastric inhibitory polypeptide (GIP), and vasoactive intestinal polypeptide (VIP) was studied in seven healthy volunteers. I.j. fat markedly inhibited meal-stimulated acid secretion as compared to a control study with i.j. saline infusion. The acid inhibition was accompanied by augmental plasma concentrations of EG, GIP, and VIP but not of PG, suggesting that EG, GIP, and VIP may be among mediators of fat-induced jejunal inhibition of acid secretion. Concentration-time relationship makes it unlikely that the observed inhibition could be ascribed to any single peptide studied.
在七名健康志愿者中研究了空肠内输注脂肪对进餐刺激的胃酸分泌以及胰高血糖素（PG）、肠高血糖素（EG）、胃抑制性多肽（GIP）和血管活性肠肽（VIP）释放的影响。与空肠内输注生理盐水的对照研究相比，空肠内输注脂肪显著抑制了进餐刺激的胃酸分泌。胃酸抑制伴随着EG、GIP和VIP血浆浓度的升高，但PG没有升高，这表明EG、GIP和VIP可能是脂肪诱导的空肠对胃酸分泌抑制作用的介质之一。浓度-时间关系表明，观察到的抑制作用不太可能归因于所研究的任何一种单一肽。
