Intraduodenal conjugated bile salts exert negative feedback control on gall bladder emptying in the fasting state without affecting cholecystokinin release or antroduodenal motility

Abstract

Background: Intraduodenal bile salts exert negative feedback control on postprandial gall bladder emptying. Aims: We wished to examine whether a similar control mechanism occurs in the fasting state. Methods: Intraduodenal bile salt depletion was achieved by 12 g of cholestyramine. Thereafter, in study A (seven subjects), the effects on gall bladder volume (by ultrasound) and antroduodenal motility of intraduodenal infusions of taurocholate egg yolk-phosphatidylcholine micelles were assessed. In study B (nine subjects), the effects on gall bladder volume of infusing mixed micelles composed of taurocholate (100 mM) and low (26 mM) or high (68 mM) amounts of egg yolk-phosphatidylcholine, or low amounts of dipalmitoylphosphatidylcholine were determined. Results: Cholestyramine induced strong and prolonged gall bladder contraction without cholecystokinin release. In study A, micellar infusions increased gall bladder volume without affecting migrating motor complex cycle length. In study B, intraduodenal infusion induced strong increases in gall bladder volume in the case of taurocholate micelles containing low amounts of egg yolk-phosphatidylcholine, moderate increases in micelles containing low amounts of dipalmitoylphosphatidylcholine but no change in micelles containing high amounts of egg yolk-phosphatidylcholine, in all cases without altered plasma cholecystokinin levels. Phosphatidylcholine hydrolysis was significantly higher after infusion of egg yolk-phosphatidylcholine compared with infusion of dipalmitoylphosphatidylcholine containing micelles. Intermixed micellar-vesicular bile salt concentrations (responsible for detergent effects) were higher in egg yolk-phosphatidylcholine than in dipalmitoylphosphatidylcholine containing model biles and if lyso-phosphatidylcholine was included. Conclusions: Intraduodenal bile salts exert negative feedback on fasting gall bladder volume. The modulating effects of various phospholipids may relate to their effects on intermixed micellar-vesicular bile salt concentrations.

Effects of ileal bile salts on fasting small intestinal and gallbladder motility

“…We previously observed a similar gallbladder dilation after duodenal infusion of mixed micelles, as well as gallbladder contraction after cholestyramine‐induced bile salt depletion 5 . Taken together, these findings are consistent with the existence of a negative feedback by bile salts within the intestinal lumen on interdigestive gallbladder motility.…”

“…This composition was chosen because intraduodenal infusion of mixed micelles with the same lipid concentrations (i.e. relatively low phospholipid contents) resulted in the most marked effect on gallbladder motility in our previous study 5 . It should be noted that infusion of taurocholate simple micelles (without micellar phospholipid) is not possible due to the cytotoxic effects of the detergent bile salts 8 .…”

Effect of Intraduodenal Administration of Ursodeoxycholic Acid on Interdigestive Interaction between Gallbladder Motility, Pancreatic Secretion and Endocrine Activity

“…In addition, intraduodenal ingestion of even a very high concentration of bile salts does not affect the CCK release in humans. A recent study by van Ooteghem et al [24]showed that CCK is not involved in the negative feedback control of gallbladder motility. Thus, we do not believe that the enlargement of the gallbladder after intraduodenal UDC application is caused by a decrease in CCK release.…”

“…Negative feedback control by intraduodenal bile salts on postprandial gallbladder emptying and cholecystokinin (CCK) release is well established [21, 22, 23]. A recent study on the interdigestive effect of bile salts in gastrointestinal motility showed a similar negative feedback control on gallbladder motility, which, however, was not mediated by CCK [24]. …”

Effects of Chenodeoxycholic Acid on the Secretion of Gut Peptides and Fibroblast Growth Factors in Healthy Humans

“…In the early 1990s, Miyasaka et al (14) also reported effects of some BAs on cholecystokinin (CCK) release in rats. In humans, Koop et al (15) noted a small increase in CCK levels after chenodeoxycholic acid (CDCA) administration; however, these data were not supported by van Ooteghem et al (16) or Portincasa et al (17).…”