Soybean β-conglycinin peptone suppresses food intake and gastric emptying by increasing plasma cholecystokinin levels in rats

Abstract

Cholecystokinin (CCK) is an important physiologic mediator that regulates satiety and gastric emptying. We demonstrated previously that soybean peptone acts directly on rat small intestinal mucosal cells to stimulate CCK release. In the present study, we examined the effects of β-conglycinin, a major component of soy protein, and its peptone on food intake and gastric emptying after an intraduodenal infusion of β-conglycinin peptone in relation to CCK release and interaction with the mucosal cell membrane. Intraduodenal infusion of β-conglycinin peptone inhibited food intake in a dose-dependent manner, but that of whole soy peptone or camostat did not. The suppression of food intake by β-conglycinin peptone was abolished by an intravenous injection of devazepide, a selective peripheral CCK receptor antagonist. The β-conglycinin peptone infusion strongly suppressed gastric emptying with marked increases in portal CCK levels. We also observed that the β-conglycinin peptone dose dependently and more potently stimulated CCK release from isolated dispersed mucosal cells of the rat jejunum than did β-conglycinin itself. This stimulation corresponded to the binding activity of the peptide or protein to solubilized components of the rat jejunum membrane as evaluated by surface plasmon biosensor. These results indicate that β-conglycinin peptone suppresses food intake, and this effect may be due to β-conglycinin peptone in the lumen stimulating endogenous CCK release with direct acceptance to the intestinal cells.