Post-prandial and interdigestive return of bile acids to the gallbladder in healthy subjects (original) (raw)

Hepatic uptake of bile acids in man. Fasting and postprandial concentrations of individual bile acids in portal venous and systemic blood serum

Journal of Clinical Investigation

A B S T R A C T This investigation was undertaken in order to (a) characterize the postprandial inflow of individual bile acids to the liver and (b) determine if peripheral venous bile acid levels always adequately reflect the portal venous concentration, or if saturation of hepatic bile acid uptake can occur under physiological conditions. In five patients with uncomplicated cholesterol gallstone disease, the umbilical cord was cannulated during cholecystectomy, and a catheter was left in the left portal branch for 5 to 7 d. The serum concentrations of cholic acid, chenodeoxycholic acid, and deoxycholic acid in portal venous and systemic circulation were then determined at intervals of 15 to 30 min before and after a standardized meal.

Postprandial serum bile acids in healthy man. Evidence for differences in absorptive pattern between individual bile acids

Gut, 1977

The serum concentrations of cholic acid (C), chenodeoxycholic acid (CD), and deoxycholic acid (D) before and after a standardised meal were determined in five healthy female subjects using a highly specific and accurate gas chromatographic-mass spectrometric technique. The C level rose significantly 60 minutes after the meal, reached a peak after 90 minutes, and had returned to the original level after 150 minutes. In contrast, the serum concentrations of CD and D displayed a significant rise by 30 minutes, reached a peak after 90 minutes, but had not returned to fasting levels after 150 minutes. The serum bile acid responses after a meal suggest that there is considerable absorption of dihydroxy bile acids in the proximal small intestine in man.

Enterohepatic circulation of bile acids after cholecystectomy

Gut, 1978

Bile acid metabolism was investigated in 10 patients after cholecystectomy, 10 gallstone patients, and 10 control subjects. Diurnal variations of serum levels of cholic and chenodeoxycholic acid conjugates were not abolished by cholecystectomy. Cholic acid pool size was significantly reduced in cholecystectomised patients and the fractional turnover rate and the rate of intestinal degradation of bile acid showed a significant increase. In cholecystectomised patients fasting bile was supersaturated in cholesterol, though less than in gallstone patients, but, in both, feeding resulted in improvement of cholesterol solubility in bile. These data suggest that after cholecystectomy the small intestine alone acts as a pump in regulating the dynamics of the enterohepatic circulation of bile acids and that the improvement of cholesterol solubility in bile is due to a more rapid circulation of the bile acid pool in fasting cholecystectomised patients.

Effects of artificial depletion of the bile acid pool in man

Gut, 1986

In order to elucidate the relationship between bile acid pool size and cholesterol saturation index of fasting state gall bladder bile, we artifically depleted the bile acid pool in 12 healthy volunteers. Bile acid pool size decreased from 7-6±0*9 to 5 8±0 7 mmol (mean+SEM, p<0.01), and saturation index of fasting state gall bladder bile increased from 0 93±0*07 to 1-18±0-07 (p<0001). There was no alteration in saturation index of basal or stimulated hepatic bile. There was no change in gall bladder storage of basal hepatic bile, nor in the proportion of the bile acid pool stored in the gall bladder. The bile acid mass in the gall bladder fell from 4 9±0-5 to 3-4±0*4 mmol (p<0-05) and phospholipid mass from 1*6±0-3 to 1-2±0-2 mmol (p<O0O5), but there was no change in cholesterol mass. The gall bladder volume fell from 30±4 to 18±2 ml (p<0.01). These results suggest that artificial depletion of the bile acid pool increased saturation index of fasting state gall bladder bile without altering saturation index of basal or stimulated hepatic bile; it probably increased the ratio of basal: stimulated hepatic bile within the gall bladder by decreasing gall bladder storage of stimulated hepatic bile. concept is correct, it implies that the gall bladder

Kinetics of primary bile acids in patients with non-operated Crohn's disease

European Journal of Clinical Investigation, 1982

The metabolism of cholic acid and chenodeoxycholic acid was studied in seventeen patients with non-operated Crohn's disease, eleven ileitis and six ileocolitis patients. The turnover of cholic acid was significantly increased in patients with ileitis (k=2.0+ 1.13 days-'; P<O.OOI) and ileocolitis (k = 0.91 k 0.47 days-I; P < 0.005) as compared to normals (k = 0.35 k 0. I9 days-'). Although chenodeoxycholic acid was better preserved in the enterohepatic circulation than cholic acid its turnover was also significantly faster in ileitis (k = 0.81 f 0.56 days-'; P < 0.005) and ileocolitis patients (k = 0.62 k 0.1 8 days-'; P < 0.01) than in normals (k = 0.20 f 0.09 days-I). The fractional turnover of cholic acid was related to the length of ileal involvement (r = 0.761; P<O.OOl; n= 17). Patients with Crohn's ileitis tended to preserve normal fasting total bile acid pools by increased synthesis of primary bile acids and efficient absorption of deoxycholic acid and ursodeoxycholic acid by the normal colon. Patients with active ileocolitis had decreased total fasting pool sizes (2.62 f 1.83 mmol; P<O.O01) as compared to normals (7.69f 1.61 mmol). In these patients there was no increase in bile acid synthesis as compared to normals and secondary bile acids were absent from bile. It is concluded that the colon has an important role in maintaining the fasting pool size to a normal level in the presence of an interrupted enterohepatic circulation of bile acids due to ileal disease.

Fecal bile acid excretion profile in gallstone patients

Medicina, 1999

Epidemiological studies have shown a positive association between cholesterol gallstones and colonic cancer. These two diseases may be somehow related with bile acids metabolic alterations. The aim of this study was to evaluate the profiles of fecal bile acid in gallstone patients, in order to estimate the quality and amount of fecal bile acids. A fecal bile acid profile of ten gallstone patients and ten controls was compared using high performance liquid chromatography. Total fecal bile acid excretion was significantly increased in gallstone patients compared with controls (692.7 mg/day (302.5-846.2) vs 165.7 mg/day (138.7-221.3), p < 0.01) as was the excretion of secondary free bile acids 562.9 mg/day (253.3-704.9) vs 99.9 mg/day (88.9-154.2), p < 0.01). Lithocholic and glycodeoxycholic acid percentages have also been found to show differences with controls of 55.4 (47.4-73.9) vs 24.6 (22.1-38.4) (p < 0.01) and 29.4 (3.3-41.7) vs 2.8 (1.0-3.8) (p < 0.03), respectively ...

Hepatic Uptake of Bile Acids in Man

Journal of Clinical Investigation, 1982

is the recipient of a research fellowship from the Ernst Klenk Foundation. well as total bile acids were well correlated with those in portal venous serum. The results (a) give a quantitation of postprandial bile acid inflow to the liver and (b) indicate that the hepatic uptake system for bile acids in healthy man cannot be saturated during maximal inflow of endogenous bile acids. Measurement of peripheral serum bile acids can thus give important information on the status of the enterohepatic circulation. ' Abbreviations used in this paper: C, cholic acid; CD, chenodeoxycholic acid; D, deoxycholic acid.

Intragastric bile does not perturb gastric emptying of liquids in humans

Digestive Diseases and Sciences, 1988

Gastric stasis and duodenogastric reflux have each been implicated in the pathogenesis of various upper gastrointestinal disorders. However, the relationship between intragastric bile and gastric emptying has not been explored. In each of nine healthy volunteers (seven men and two women, ages 22--47 years), gastric emptying of 300 ml 10% dextrose labeled with [99mTc]DTPA was measured twice using gamma camera imaging. During one study, 20 min after ingestion of the test meal, 525 mg of freeze-dried, sterilized human T-tube bile dissolved in 20 ml water was introduced into the stomach via a previously sited fine-bore nasogastric tube. Intragastric bile salt concentrations were calculated to be within the range 1.7-2.9 mM. In control studies, 20 ml of water alone was similarly introduced. Emptying at 20 min was comparable for both groups of studies (38 +-3% vs 39 +-4%; mean values +-SEM). For each individual study, emptying from 20 to 60 min was well represented by a single exponential function (r = 0.81-0.99). Half-emptying times for curves fitted over this period were similar in the two groups (bile: Tt/2 = 18.8 +-2.6 min; control T1/2 = 18.8 +-1.9 min). These results indicate that intragastric bile, in concentrations similar to those found in patients with gastric ulcer, has no effect on gastric emptying of dextrose in normal subjects.

Biliary Secretion in Conscious Rabbits: Role of the Enterohepatic Circulation of Bile Salts and of the Gall Bladder

Quarterly Journal of Experimental Physiology, 1981

The role of enterohepatic circulation of bile salts in biliary secretion in conscious rabbits has been investigated before and after cholecystectomy. Bile flow was higher and bile salt concentration lower in cholecystectomized than in intact rabbits: this could have been caused by a negative feedback effect on bile salt synthesis as the circulating bile salt pool increased. The effects of cholecystectomy on flow and bile salt concentration balanced each other. Bile flow and bile salt concentration declined after interruption of the enterohepatic circulation in both cholecystectomized and intact rabbits. Furthermore, the percentage of the flow of bile independent of bile salt secretion increased, while that independent of total analysed solutes decreased after the enterohepatic circulation was broken. These results confirm that the decrease in bile flow after interruption of the enterohepatic circulation is due to loss of bile salts and not of electrolytes. * See Methods.