Stimulation of secretion of CCK and GLP-1 in STC-1 cells by casein and whey protein digests

Abstract

Protein is the macronutrient with greater satiating effect. Among others, this effect is mediated by different postprandial hormonal signals originated in the gastrointestinal tract, like cholecystokinin (CCK) and glucagon-like peptide 1 (GLP-1). Casein and whey differ in the way they are digested and absorbed. Caseins coagulate in the acidic environment in the stomach delaying its gastric emptying; whereas whey proteins rema in soluble and pass rapidly through the stomach. lt has been proposed that the rate of digestion, absorption and the released digestion products may play a role in their satiating effects. The aim of this research is to evaluate the effect of gastrointestinal digests from casein and whey proteins, obtained by in vitro gastrointestinal digestion, on the secretion of CCK and GLP-1 in STC-1 cells. Human jejunal aspirates after oral administration of the same substrates were al so tested in this cellline. Gastric and gastrointestinal digests from casein and whey proteins induced CCK secretion. However, intestinal digests containing small size peptides (< 20 a mino acids) and free amino acids stimulated CCK release in greater proportion than gastric digests. In contrast, secretion of GLP-1 was induced by casein gastric digests and by digests obtained after 120 min gastrointestinal digestion of whey proteins. The digestion products found in human jejunum of both, case in and whey proteins, stimulated CCK and GLP-1 release. In general, they confirmed the in vitro results, although sorne differences in GLP-1 release were found. The results support the rapid satiating effect of whey proteins against the more sustained effect of caseins over time, dueto the different gastric emptying rates and demonstrate that digestion products affect differently the release of anorexigenic hormones. In view ofthese results, we can suggest that stimulation of GLP-1 is produced by longer peptides while small peptides and a mino acids act as CCK inducers.