Gomez P, Hallberg L, Greeley G H
Department of Surgery, The University of Texas Medical Branch, Galveston, Texas 77555-0725, USA.
Proc Soc Exp Biol Med. 1999 Jan;220(1):52-3. doi: 10.1046/j.1525-1373.1999.d01-8.x.
An obese mouse model (Cpefat/Cpefat) that has hyperproinsulinemia and late onset obesity has been described. Cpefat/Cpefat mice have a missense mutation in carboxypeptidase E (CPE), a processing enzyme essential for production of biologically active endocrine and neuroendocrine peptides. We have reported previously that CPE activity was absent in the antrum of the stomach and that processing of progastrin to the amidated biologically active form of gastrin is reduced. Since gastrin is a major secretagogue for gastric acid secretion, the purpose of the present experiments was to examine gastric acid secretion in Cpefat/Cpefat mice. In addition, secretion of amidated gastrin in response to inhibition of acid secretion was tested in Cpefat/Cpefat. Both gastric acid and challenged gastrin secretion are reduced in Cpefat/Cpefat mice. We conclude that stomach CPE activity is essential for gastric secretory activity and for challenged gastrin release.
一种具有高胰岛素原血症和迟发性肥胖的肥胖小鼠模型（Cpefat/Cpefat）已被描述。Cpefat/Cpefat小鼠在羧肽酶E（CPE）中存在错义突变，CPE是一种对生物活性内分泌和神经内分泌肽的产生至关重要的加工酶。我们之前报道过，胃窦中不存在CPE活性，且胃泌素原向酰胺化生物活性形式胃泌素的加工过程减少。由于胃泌素是胃酸分泌的主要促分泌剂，本实验的目的是检测Cpefat/Cpefat小鼠的胃酸分泌。此外，还在Cpefat/Cpefat小鼠中测试了对胃酸分泌抑制的反应中酰胺化胃泌素的分泌。Cpefat/Cpefat小鼠的胃酸分泌和刺激后的胃泌素分泌均减少。我们得出结论，胃CPE活性对于胃分泌活动和刺激后的胃泌素释放至关重要。
