The aim of this study was to elucidate the importance of biliary output for the regulation of migrating motor complex and the release of plasma motilin. Gallbladder emptying was monitored by hepatobiliary scintigraphy, plasma motilin concentration by radioimmunoassay and gastrointestinal motility by a perfused catheter system. During a total recording time of 46 h and 20 min in 16 volunteers, we observed 29 episodes of gallbladder emptying, 27 plasma motilin peaks and 23 activity fronts (phase 3 activity) of the migrating motor complex (MMC). Twelve episodes of gallbladder emptying started in phase 1 and continued into phase 2 of the MMC. The remaining 17 episodes of gallbladder emptying started in phase 2, and three of these continued into phase 3 of the MMC. Biliary output was associated with a significant rise in plasma motilin concentration, whereas plasma motilin significantly decreased after the activity fronts. These observations may explain the well-known fluctuations of plasma motilin concentration in the fasted state. Motilin is released into the circulation as a result of biliary output, while the ensuing activity front of the MMC removes this stimulant from the proximal small bowel, resulting in a fall in plasma motilin. In conclusion, we have confirmed a temporal relationship between biliary output into the duodenum and the release of plasma motilin. The observed transition from phase 1 to phase 2 and from phase 2 to phase 3 of the MMC during gallbladder emptying episodes suggests that biliary output stimulates gastrointestinal motility in the fasted state.
The serum levels of conjugated cholic and chenodeoxycholic acid have been studied before and during a 4 h period after the intake of a liquid test meal in seven control subjects and in fourteen patients with Crohn's disease. The concentrations of serum bile acids were determined by radioimmunoassay. The control group showed a postprandial increase of both conjugates with a return to the fasting level for cholic acid within 4 h. The chenodeoxycholic acid conjugate did not return to the fasting level within the test period. The serum bile acid concentration in Crohn's disease divided the patients in two groups; one group with decreased or normal fasting levels and low postprandial increase and another group with elevated fasting levels and a postprandial increase without return to the fasting levels within the test period.
The fasting serum concentrations of primary bile acids were determined in 30 patients with cystic fibrosis, aged 1 to 27 years, and correlated to liver disease. Cholic (fs-C) and chenodeoxycholic (fS-CDC) acids were determined by radioimmunoassays. Two patients had biopsy-proven liver cirrhosis, 13 had portal fibrosis. 8 had minor different pathological changes, and 7 had normal liver morphology. Standard liver function tests were of no help in evaluating liver disease in these patients. Eight patients had increased fS-C and 15 had increased fS-CDC, not correlated to liver morphology. Serum bile acid determination seems to be of no value in evaluating the extent of liver disease in cystic fibrosis. The more frequent and more marked increase of fS-CDC than of fS-C suggests that there is another hepatic clearance of bile acids in CF and/or that intestinal factors have a greater influence on the serum bile acid concentrations in this disease.
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