We determined the serum concentrations of cholic, chenodeoxycholic and deoxycholic acids in portal and peripheral venous blood in 9 gallstone-free patients and 39 patients with cholesterol gallstones during standardized cholecystectomy . An accurate and specific gas chromatographicmass spectrometric technique was used. The portal venous concentration of total bile acids was similar in gallstone-free and untreated gallstone patients (n = 20); there was no evidence of a reduced hepatic uptake of bile acids in the latter. Treatment with cholic acid (n = 10) was aseociated with a 70% increase in cholic acid and normal concentration of total bile acids. In chenodeoxycholic acid-treated patients (n = 9). the portal venous concentration of this bile acid was increased 3-fold; total bile acids were increased about 60%. The estimated hepatic uptake of cholic acid was slightly decreased during chenodeoxycholic acid treatment. The results indicate that neither bile acid inflow to the liver nor hepatic bile acid uptake is reduced in fasting patients with cholesterol gallstones, and treatment with chenodeoxycholic acid increaees fasting inflow of bile acids to the liver. The latter may contribute to unsaturation of fasting hepatic bile during treatment with chenodeoxycholic acid.
The portal venous (PV) inflow of bile acids regulates formation of bile acids from cholesterol by negative feedback inhibition, is the major determinant of bile flow and is a primary determinant of the secretion of biliary cholesterol and phospholipids (1-4). Changes in PV inflow of bile acids may result in secretion of more or less saturated bile. In some studies, reduced bile acid secretion ( 5 ) and diminished bile acid pool size (5, 6) were demonstrated in normal-weight, normolipidemic patients with cholesterol gallstones during stimulated enterohepatic circulation, after gallbladder contraction. It is not known whether bile acid secretion is reduced in fasting when the gallbladder is filling.
Treatment with the two primary bile acids, cholic acid (CA) and chenodeoxycholic acid (CDCA), affects biliary