Petersen B, Christiansen J, Rehfeld J F
Regul Pept. 1983 Dec;7(4):323-34. doi: 10.1016/0167-0115(83)90104-0.
After a meal the serum concentrations of the N-terminal tridecapeptide-like fragment of gastrin-17, (1-13)G-17, increased markedly in patients with active duodenal ulcer, but less so in healthy subjects. Consequently the synthetic (1-13)G-17 was infused intravenously in doses that resulted in concentrations similar to those measured in duodenal ulcer patients in order to examine whether the N-terminal fragment influences gastric acid secretion. Doses of 125 and 400 pmol (1-13)G-17/kg per h inhibited the meal-stimulated acid secretion by 36% (P less than 0.05) and 66% (P less than 0.05) respectively. The release of endogenous C-terminal gastrin immunoreactivity was not influenced. The infusion of (1-13)G-17 also inhibited the acid response to exogenous gastrin-34, gastrin-17 and Peptavlon, but not to gastrin-4. The results suggest that the N-terminal gastrin-17 fragment--although devoid of the hitherto considered only active site of gastrin--plays a significant role in the regulation of the gastric acid secretion in patients with active duodenal ulcer.
餐后，活动性十二指肠溃疡患者血清中胃泌素 - 17的N端十三肽样片段（1 - 13）G - 17的浓度显著升高，而健康受试者升高幅度较小。因此，静脉输注合成的（1 - 13）G - 17，其剂量导致的浓度与十二指肠溃疡患者测得的浓度相似，以检查N端片段是否影响胃酸分泌。每小时每千克体重125和400皮摩尔的（1 - 13）G - 17剂量分别抑制进餐刺激的胃酸分泌36%（P < 0.05）和66%（P < 0.05）。内源性C端胃泌素免疫反应性的释放未受影响。输注（1 - 13）G - 17也抑制对外源性胃泌素 - 34、胃泌素 - 17和五肽胃泌素的酸反应，但不抑制对胃泌素 - 4的反应。结果表明，胃泌素 - 17的N端片段——尽管缺乏迄今认为是胃泌素唯一活性位点的结构——在活动性十二指肠溃疡患者胃酸分泌的调节中起重要作用。
