Yahav J, Fradkin A, Diver-Haber A, Jonas A
Pediatric Gastroenterology Service, SHEBA Medical Centre, Tel-Hashomer, Israel.
Acta Physiol Scand. 1990 May;139(1):193-201. doi: 10.1111/j.1748-1716.1990.tb08912.x.
Post-natal malnutrition was induced in rats using the expanded litter model. Pepsinogen secretion of isolated gastric glands in response to several secretagogues was measured. Malnourished 19-day-old pups showed no response to carbachol, CCK-8, gastrin, secretin and ionophore A23187 compared to well-nourished animals, but showed comparable secretion of pepsinogen after stimulation with dibutyryl cAMP (DiBcAMP). Hydrocortisone treatment for 48 h caused increased pepsinogen accumulation and elevated pepsinogen secretory responsiveness to carbachol and secretin of gastric glands isolated from post-natal malnourished pups. Our results indicate that isolated gastric glands obtained from well-nourished rat possess two functionally distinct receptors for gastrin and C-terminal fragment of CCK. Our study supports the concept that in malnourished rats there is a decreased number of binding sites or/and some post-receptor defects. Pepsinogen release mechanisms remain unaffected.
采用扩大窝仔数模型诱导大鼠产后营养不良。测定了分离的胃腺对几种促分泌素的胃蛋白酶原分泌情况。与营养良好的动物相比，营养不良的19日龄幼崽对卡巴胆碱、CCK-8、胃泌素、促胰液素和离子载体A23187无反应，但在用二丁酰环磷腺苷（DiBcAMP）刺激后，胃蛋白酶原分泌情况相当。对产后营养不良幼崽分离的胃腺进行48小时的氢化可的松处理，导致胃蛋白酶原积累增加，对卡巴胆碱和促胰液素的胃蛋白酶原分泌反应性升高。我们的结果表明，从营养良好的大鼠分离的胃腺具有两种功能不同的胃泌素和CCK C末端片段受体。我们的研究支持这样的概念，即营养不良大鼠中结合位点数量减少和/或存在一些受体后缺陷。胃蛋白酶原释放机制未受影响。
