1. Bile acids were analysed in the bile and lumen samples of rats which received a cholesterol-free or cholesterol-enriched (5 g/kg) diet free from fibre, or containing cellulose or citrus pectin at the level of 100 g/kg.
2. Dietary pectin but not cellulose increased biliary bile acid concentration and excretion. Dietary cholesterol did not affect biliary bile acids quantitatively.
3. Biliary bile acids were almost exclusively conjugated with glycine or taurine in the various experimental situations. The predominant portion of bile acids in rats fed on the cholesterol-free diet was conjugated with taurine when the diet was either free from fibre or contained cellulose; the ratio of bile acids conjugated with glycine: those conjugated with taurine (G:T) was less than 0·2. In contrast, with pectin as a fibre source, the conjugation with glycine increased enormously (G:T increased to approximately 4). Cholesterol enrichment of the diet also increased the glycine conjugation in all groups of rats. Even in this situation, the G:T was highest in rats fed on pectin.
4. Pectin, but not cellulose, increased the bile acid content of the small intestine and caecum, both in rats fed on the cholesterol-free and cholesterol-enriched diets. Cholesterol feeding doubled the bile acid content of the caecum in rats fed on a fibre-free diet or a cellulose diet, but not in those fed on pectin. No such effect of cholesterol was observed in the small intestine, except for the ileal bile acid content in rats fed on cellulose.
5. A considerable portion of the bile acids in the small intestine was deconjugated. The extent of the deconjugation was higher in the ileum than in the jejunum. As in the bile, G:T in rats fed on pectin (3·5·5) were higher than those in the other groups (0·05–1·05) in various situations. Also, cholesterol feeding considerably increased the ratio in all groups of rats.
6. The observed dietary alteration of the partition of bile acids between glycine and taurine may be of physiological significance in regulating bile acid and lipid metabolism in rats.