Gastrin is the most important peptide in the regulation of gastric acid secretion. This communication reviews important new developments in our knowledge of its synthesis, action, and pathophysiology. The gene for human gastrin has been isolated, and it encodes a pre-pro-gastrin which is a 101-aminoacid peptide containing within it the structure of big gastrin (G34) with a C-terminal glycine extension. Post-translational processing by alpha-amidation of the glycine-extended progastrin results in generation of the active forms of the peptide (G34, G17). When gastrin binds to its receptor on the parietal cell, phosphatidylinositol biphosphate (IP2) in the plasma membrane is converted to inositol 1,4,5-triphosphate (IP3), which acts as the secondary intracellular messenger to increase intracellular calcium and initiate the process that eventually leads to acid secretion. Although an abnormality in gastrin release or action is not thought to be crucially important in the genesis of duodenal ulcer, these patients nevertheless demonstrate increased postprandial gastrin release, and a greater sensitivity of their parietal cells to gastrin. Hypergastrinemia is the cause of peptic ulceration in the Zollinger-Ellison syndrome, in primary gastrin cell hyperplasia or hyperfunction, and in the retained antrum syndrome. Ulcerogenic hypergastrinemia must be distinguished from hypergastrinemia that is secondary to hypoacidity or anacidity, as is seen in atrophic gastritis or postvagotomy.
胃泌素是调节胃酸分泌中最重要的肽。本文综述了我们在其合成、作用和病理生理学知识方面的重要新进展。人类胃泌素基因已被分离出来，它编码一种前胃泌素原，这是一种含有大胃泌素（G34）结构且C末端带有甘氨酸延伸的101个氨基酸的肽。通过对甘氨酸延伸的胃泌素原进行α-酰胺化的翻译后加工，会产生该肽的活性形式（G34、G17）。当胃泌素与其在壁细胞上的受体结合时，质膜中的磷脂酰肌醇二磷酸（IP2）会转化为肌醇1,4,5-三磷酸（IP3），IP3作为细胞内第二信使，增加细胞内钙并启动最终导致胃酸分泌的过程。尽管胃泌素释放或作用异常在十二指肠溃疡的发生中不被认为至关重要，但这些患者餐后胃泌素释放仍会增加，且其壁细胞对胃泌素的敏感性更高。高胃泌素血症是佐林格-埃利森综合征、原发性胃泌素细胞增生或功能亢进以及胃窦保留综合征中消化性溃疡形成的原因。必须将致溃疡性高胃泌素血症与继发于胃酸过少或无酸的高胃泌素血症区分开来，如在萎缩性胃炎或迷走神经切断术后所见。
