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Intestinal Bile Acids and Cholesterol Absorption in the Germfree Rat1

B. S. Wostmann

Lobund Laboratory, Department of Microbiology, University of Notre Dame, Notre Dame, Indiana 46556

Germfree rats fed moderate amounts of cholesterol with the diet have a 2 to 3 times higher liver cholesterol content than comparable conventional rats. Since profound differences were known to exist between fecal bile acid patterns of germfree and conventional rodents, the present study was carried out to determine if a change in bile acid pattern related to the absence of an intestinal microflora would enhance the uptake of dietary cholesterol.

The bile of the adult germfree rat fed diets low in cholesterol (0.05% or less) contained approximately three times as much bile acid as found in conventional rat bile. The taurocholic acid content was 1.6 to 1.7 times higher, the tauro-ß-muricholic acid approximately 10 times higher in bile from germfree than from conventional rats. In germfree bile taurocholic acid and tauro-ß-muricholic acid were present in about equal amounts, and together accounted for 98% of the total bile acids. Biliary bile acid composition of the germfree rat was quite similar to the pattern found in its feces, except for a moderate preponderance of tauro-ß-muricholic acid in the feces resulting from preferential reabsorption of taurocholic acid in the ileum of the germfree rat.

Bile acid composition and concentration in the small intestine reflect the hepatic input. Throughout the small intestine bile acid concentrations of germfree rats were approximately three times as high as in conventional rats. The germfree rats also demonstrated a 25% greater absorption of labeled dietary cholesterol. The cholesterol accumulation found in the germfree rat fed cholesterol-containing diets may therefore be caused not only by reduced elimination via bile acids, but also, indirectly, by enhancement of the absorption of dietary lipids.


KEY WORDS: • germfree • cholesterol absorption • bile acids

1 Supported by funds from the Indiana Heart Foundation, from The National Institute of Health (HE 08351), and from the Fannie E. Rippel Foundation, Newark, N. J.

Manuscript received 21 December 1972.





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