摘要

Antarctic krill (Euphausia superba) protein hydrolysates were produced by simulated gastrointestinal digestion (KPHSD) and alkaline proteinase hydrolysis (KPHAP), respectively. The effects of the hydrolysates on cholecystokinin (CCK) secretion and cAMP response element-binding protein (CREB) activation were tested in murine enteroendocrine cell line STC-1. Meanwhile, the signaling mechanism by which the hydrolysates induce CCK secretion was investigated by using inhibitors of signaling proteins. Results indicated that KPHSD and KPHAP both could significantly stimulate CCK secretion and CREB activation. The stimulating effects on CCK release showed a positive correlation with the relative content of peptides with molecular weight ranging from 1,000 to 3,000 Da, indicating this component may mainly account for the ability. The inhibitors on calcium-sensing receptor, PKA, Ca2+/CaMKII, P-38-MAPK, and an intracellular calcium chelator all inhibited krill protein hydrolysates-induced CCK secretion and CREB activation, indicating the involvement of the Ca2+/CaM/CaMK, cAMP/PKA and MAPK pathways in the stimulation of CCK secretion.