Role of bile acids in the control of pancreatic secretion and CCK release

Abstract

In most species stimulated pancreatic enzyme secretion and CCK release are increased in the absence and inhibited in the presence of luminal bile acids. Changes in CCK release are almost unequivocal in all investigated species. With respect to enzyme secretion, physiological bile acid concentrations seem to be necessary to exert an inhibitory effect on stimulated enzyme output in humans. Bile acids administered in higher concentrations may enhance basal and stimulated pancreatic secretion. Furthermore, the chemical properties of different bile acids (i.e., hydroxylation, conjugation) seem to contribute to their stimulating effect on enzyme secretion as was observed in several species. The rank order of bile acids inhibiting stimulated enzyme secretion in humans is taurocholate greater than taurodeoxycholate greater than taurochenodeoxycholate. On the other hand, chenodeoxycholic acid exerts the strongest stimulating effect on secretion release, which may account for the stimulating effect of this bile acid on exocrine pancreatic secretion. The strongest candidate for the mediator role in bile-acid-induced changes of exocrine pancreatic secretion is CCK (at least in dogs and rats). The CCK cell may be influenced either directly or indirectly. In conclusion, bile acids modulate pancreatic enzyme secretion and CCK release. CCK is a major candidate for this regulatory role under physiological conditions.