Miyasaka K, Funakoshi A
Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology, Japan.
Pancreas. 1998 Apr;16(3):277-83. doi: 10.1097/00006676-199804000-00012.
We summarize the discovery of luminal feedback regulation of pancreatic secretion in rats and its history. In rats, removal of proteolytic activity from the intestine produced a significant increase in pancreatic protein (enzyme) output. This increase was confirmed to be mediated by circulating cholecystokinin (CCK). Subsequently, two CCK-releasing peptides, monitor peptide and luminal CCK-releasing factor (LCRF), were purified from the rat pancreatic juice and small intestine, respectively, to elicit CCK release in luminal feedback regulation. Furthermore, we emphasize the important physiologic roles of CCK and CCK receptors by the discovery of disrupted CCK-A-receptor gene in rats. These findings should help to determine the regulation of pancreatic secretion and CCK functions in humans.
我们总结了大鼠胰腺分泌的管腔反馈调节的发现及其历史。在大鼠中，去除肠道中的蛋白水解活性会导致胰腺蛋白质（酶）输出显著增加。这种增加被证实是由循环中的胆囊收缩素（CCK）介导的。随后，分别从大鼠胰液和小肠中纯化出两种CCK释放肽，即监测肽和管腔CCK释放因子（LCRF），以在管腔反馈调节中引发CCK释放。此外，通过在大鼠中发现CCK-A受体基因的破坏，我们强调了CCK和CCK受体的重要生理作用。这些发现应有助于确定人类胰腺分泌和CCK功能的调节。
