Do bile acids exert a negative feedback control of cholecystokinin release?

Scand J Gastroenterol. 1989 Apr;24(3):315-20. doi: 10.3109/00365528909093053.


The influence of intraduodenal bile deficiency due to chronic bile duct obstruction and acute exogenous administration of bile acids on plasma cholecystokinin (CCK) and pancreatic polypeptide (PP) was investigated. Fourteen patients with tumor-induced bile duct stenosis and five healthy volunteers were given a liquid test meal. Four of the patients had a simultaneous pancreatic duct stenosis. On another day 4 g chenodeoxycholic acid were administered concomitantly with the liquid test meal in six of the patients and all controls. Basal and meal-stimulated plasma CCK did not differ between patients and controls. A pancreatic duct stenosis, which was associated with diminished plasma PP concentrations, had no influence on plasma CCK release. Exogenous bile acids significantly reduced the postprandial CCK response in both groups. Bile-induced inhibition was significantly greater in patients than in controls (75 +/- 7% and 44 +/- 11%, respectively; p less than 0.05). It is concluded that intraduodenal bile is an important modulator of the postprandial secretory activity of the CCK cell. Although chronic intraduodenal bile acid reduction in tumor-induced biliary duct stenosis did not influence plasma CCK levels, a negative feedback control of plasma CCK by acute bile acid administration could be demonstrated.

MeSH terms

  • Adult
  • Aged
  • Bile Acids and Salts / administration & dosage
  • Bile Acids and Salts / physiology*
  • Biliary Tract Neoplasms / complications
  • Cholecystokinin / blood
  • Cholecystokinin / metabolism*
  • Cholestasis / blood
  • Cholestasis / etiology
  • Cholestasis / physiopathology
  • Feedback
  • Gallbladder Neoplasms / complications
  • Humans
  • Middle Aged
  • Pancreatic Neoplasms / complications
  • Pancreatic Polypeptide / blood
  • Pancreatic Polypeptide / metabolism


  • Bile Acids and Salts
  • Pancreatic Polypeptide
  • Cholecystokinin