Antarctic Krill (Euphausia superba) Protein Hydrolysates Stimulate Cholecystokinin Release in STC-1 Cells and its Signaling Mechanism

Abstract

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, P38-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. Practical Applications Although Antarctic krill (Euphausia superba) has a large biomass and high-quality protein, its consumption by mankind, especially for its protein, is limited. In recent years, krill protein hydrolysates (KPHs) have attracted increasing attention due to their various health benefits. KPH is usually produced by using a proteolysis and centrifugation process, and the protein from muscle and internal tissue is reserved, but the cuticle is removed. The process can produce low-fluoride krill proteins (peptides) because the fluoride in krill is mainly located in the cuticle. The present study showed that KPHs produced by simulated gastrointestinal digestion and by alkaline proteinase hydrolysis were able to highly stimulate CCK secretion in intestinal endocrine STC-1 cells, indicating KPHs have potential application prospect as functional food ingredients for food intake-inhibitory effects.