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Fat digestion in patients with bile acid malabsorption but minimal steatorrhea.

Abstract
Patients with an interrupted enterohepatic circulation of bile acids and minimal or no steatorrhea were studied to determine if their fat absorption was aided by compensatory mechanisms which delivered increased amounts of lipid to the aqueous phase of post-prandial duodenal fluid. The data suggested that the molar stoichiometry of association of fatty acid and bile acid in an aggregated (micelle) form was reduced in the patients (0.8) as compared to normals (1.4). Each patient had either normal sized or undetectable micelles; one patient had a large fatty acid-rich aggregated species. The bile acid composition of the whole duodenal fluid was found to have an increased proportion of dihydroxy bile acids which were conjugated with glycine. There was a selective precipitation of dihydroxybile acids from the aqueous phase, such that the patients had a normal proportion of these bile acids in the aqueous phase. We were unable to identify a consistent compensatory mechanism whereby these patients could increase the concentration of lipid in the aqueous phase which would have led to a better understanding of their minimal steatorrhea. We believe that the reduced stoichiometry of aggregated fatty acid to aggregated bile acid is in part due to the altered bile acid pool composition of these patients.
AuthorsC M Mansbach 2nd, D Newton, R D Stevens
JournalDigestive diseases and sciences (Dig Dis Sci) Vol. 25 Issue 5 Pg. 353-62 (May 1980) ISSN: 0163-2116 [Print] United States
PMID7371473 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Bile Acids and Salts
  • Dietary Fats
  • Fatty Acids, Nonesterified
  • Phosphatidylcholines
  • Cholesterol
Topics
  • Bile Acids and Salts (metabolism)
  • Celiac Disease (metabolism)
  • Cholesterol (metabolism)
  • Chromatography, Gel
  • Crohn Disease (complications)
  • Dietary Fats (metabolism)
  • Digestion
  • Fatty Acids, Nonesterified (metabolism)
  • Humans
  • Malabsorption Syndromes (etiology, metabolism)
  • Male
  • Phosphatidylcholines (metabolism)

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