Nishi T, Hara H, Aoyama Y
Department of Bioscience and Chemistry, Faculty of Agriculture, Hokkaido University, Sapporo, Japan.
Biosci Biotechnol Biochem. 1999 Jun;63(6):1070-4. doi: 10.1271/bbb.63.1070.
We had demonstrated that a peptic hydrolysate of guanidinated casein that is made from casein by the conversion of lysine to homoarginine stimulated pancreatic exocrine secretion in rats with chronic bile-pancreatic juice (BPJ) diversion from the proximal small intestine. This modified protein also stimulated cholecystokinin (CCK) release from dispersed rat intestinal cells. In this study, we found that guanidinated casein hydrolysate stimulates CCK release in chronic BPJ-diverted rats with cholinergic control blocked by atropine. Intraduodenal guanidinated casein hydrolysate increased portal plasma CCK concentration and pancreatic secretion in atropine-treated BPJ-diverted rats. In contrast, the portal plasma CCK concentration was not increased by intact casein hydrolysate. We conclude that guanidinated casein hydrolysate directly stimulates CCK release from the intestine via some cholinergic-independent mechanism, and an increase of the pancreatic exocrine secretion is regulated by CCK released by guanidinated casein hydrolysate. A guanidyl residue is likely to be involved in this control.
我们已经证明,通过将赖氨酸转化为高精氨酸由酪蛋白制成的胍基化酪蛋白的胃蛋白酶水解产物,可刺激慢性胆汁胰液(BPJ)从小肠近端转流的大鼠的胰腺外分泌。这种修饰后的蛋白质还能刺激分散的大鼠肠道细胞释放胆囊收缩素(CCK)。在本研究中,我们发现胍基化酪蛋白水解产物在阿托品阻断胆碱能控制的慢性BPJ转流大鼠中刺激CCK释放。十二指肠内给予胍基化酪蛋白水解产物可增加经阿托品处理的BPJ转流大鼠的门静脉血浆CCK浓度和胰腺分泌。相比之下,完整的酪蛋白水解产物不会增加门静脉血浆CCK浓度。我们得出结论,胍基化酪蛋白水解产物通过某种非胆碱能机制直接刺激肠道释放CCK,胰腺外分泌的增加由胍基化酪蛋白水解产物释放的CCK调节。胍基残基可能参与了这种调控。