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In adult male rats fed a non-purified diet supplemented with 5 % sodium propionate, plasma cholesterol concentrations were significantly depressed. Although liver cholesterol was increased by feeding propionate, rates of hepatic cholesterol and fatty acid synthesis were unchanged. Tissue concentrations and rates of synthesis of cholesterol were also unaffected by dietary propionate in stomach, small intestine and caecum. Concentrations of propionate in hepatic portal venous plasma were raised by feeding the supplemented diet but the increase was low in comparison to the dietary intake. Examination of the gut contents revealed concentrations of total volatile fatty acids (VFA) of 19 µmol/ml in the stomach contents of control rats and 148 µmol/ml (of which propionate contributed 116 µmol/ml) in those fed the supplemented diet. Duodenal and ileal concentrations of VFA were very low and were only slightly raised in the propionate-fed rats while caecal VFA were the same in both groups with a combined mean of 159 µmol/ml. These data indicate that in the rat, the absorption of dietary propionate appears to occur in the stomach. In pigs fed a standard ration hepatic portal venous VFA remained low for the first 4 h after feeding but then rose with the onset of large bowel fermentation. Feeding the diet supplemented with propionate caused hepatic portal venous plasma concentrations to rise by approximately 0.4 µmol/ml. This increase was apparent 30 min after feeding and was sustained for 3 h but subsequently there was no difference to controls. As in the rat, the absorption of dietary propionate appeared to occur in the upper gastrointestinal tract. The transport of propionate via the porcine hepatic portal vein also appeared insufficient to account for the dietary intake and suggests metabolism of the acid by the upper gastrointestinal tract. Further studies with perfused livers from fed rats indicated that propionate at a concentration of 1 µmol/ml did not alter cholesterol synthesis but that inhibition occurred at 18 µmol of propionate/ml. It appears that a redistribution of cholesterol from the plasma to the liver, rather than inhibition of hepatic and intestinal cholesterol synthesis, is responsible for the hypocholesterolaemic effects of dietary propionate. Because the absorption and transport of dietary propionate appears to follow a time course which differs considerably to that of the acid produced by the large bowel microflora, we conclude also that VFA produced by such fermentation would not seem to be responsible for the hypocholesterolaemic effects of certain water-soluble plant fibres.

1. The effects of feeding isolated saponins on plasma lipid concentrations and on concentrations of biliary and faecal bile acids and neutral sterols were studied in the rat.2. The animals were given one of four diets, i.e. a standard low-cholesterol synthetic diet, the diet+10 g saponins/kg, the diet+10 g cholesterol/kg, the diet+10 g cholesterol+10 g saponins/kg.3. Saponins partially reversed the hypercholesterolaemia caused by the high-cholesterol diet and increased both the rate of bile acid secretion and the faecal excretion of bile acids and neutral sterols. The proportionate contribution of the primary bile acids (particularly chenodeoxycholic) to faecal excretion was also increased by saponins.4. The results are discussed in relation to the hypothesis that saponins act by inducing the adsorption of bile acids by dietary fibre.

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Four young mature male pigs, 110 to 120 kg of body weight, were maintained on a low (0.01%) cholesterol diet. A double changeover design was used so that at any time two pigs received additionally 20 g/day of saponins as a 0.33% solution in drinking water. Saponins raised concentrations of fecal bile acids and neutral sterols and increased the contribution of primary acids to excretion. Neither the concentration of total plasma cholesterol nor low-density and high-density lipoprotein cholesterol were affected by saponins. There was also no change in either absolute or fractional catabolic rate of low-density or high-density lipiproteins. The data are discussed in relation to the effects of cholestyramine on plasma cholesterol and bile acid excretion in the pig and to the possible role of saponin-containing foods in the control of plasma cholesterol in man.