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Research Article Free access | 10.1172/JCI107400

Interactions between Intraluminal Bile Acids and Digestive Products on Pancreatic and Gallbladder Function

Juan R. Malagelada, Vay L. W. Go, Eugene P. DiMagno, and W. H. J. Summerskill

Gastroenterology Unit, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55901

Find articles by Malagelada, J. in: PubMed | Google Scholar

Gastroenterology Unit, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55901

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Gastroenterology Unit, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55901

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Gastroenterology Unit, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55901

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Published September 1, 1973 - More info

Published in Volume 52, Issue 9 on September 1, 1973
J Clin Invest. 1973;52(9):2160–2165. https://doi.org/10.1172/JCI107400.
© 1973 The American Society for Clinical Investigation
Published September 1, 1973 - Version history
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Abstract

Interactions between bile acids (taurocholate, TC; taurochenodeoxycholate, TCDC; or taurodeoxycholate, TDC) and digestive products (essential amino acids, EAA or monoolein, MO) in the lumen of the proximal small bowel, affecting pancreatic enzyme secretion and gallbladder contraction, were studied in 77 healthy volunteers by a perfusion method. Perfusion of EAA or MO caused significant increases in pancreatic enzyme output together with gallbladder contraction; MO was more potent and induced enzyme outputs comparable to the maximal response attained with intravenous cholecystokinin-pancreozymin (CCK-PZ). Perfusion of TC alone had no effect, but addition of 10 mM of either TC, TCDC, or TDC to perfusates containing EAA, or 10 mM TC to MO, or both significantly reduced pancreatic enzyme output and prevented gallbladder contraction. A lower concentration of TC (5 mM) added to EAA also produced a significant inhibitory effect. Inhibition of the stimulatory action of digestive products occurred in the jejunum as well as in the duodenum. The inhibitory action of bile acid was considered to be intraluminal since (a) bile acid did not modify the effects of CCK-PZ given intravenously; and (b) the stimulatory effect of digestive products perfused in the duodenum on pancreatic and gallbladder function was not influenced by simultaneous perfusion of bile acid in the jejunum.

It is proposed that this inhibitory effect of bile acid is mediated through inhibition of CCK-PZ secretion by high intraluminal concentrations of bile acid. Inhibition of CCK-PZ secretion by bile acid may contribute to the regulation of pancreatic and gallbladder function during digestion by reducing pancreatic enzyme secretion and permitting the gallbladder to refill after evacuation of its contents.

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