Hypocholesterolaemic Effects of Dietary Propionate: Studies in Whole Animals and Perfused Rat Liver

Abstract

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.

Effects of Dietary Addition of a Low-Pectin Apple Fibre Preparation on Rats

“…[Fung et al, 2012]. Moreover, acetate and propionate which are also signifi cantly increased in the present study can differentially infl uence fat metabolism; acetate seems to promote lipogenesis in the liver, whereas propionate has been reported to inhibit this process [Nishina & Freedland, 1990;Demigné et al, 1995], however, there are strong evidences suggesting that the inhibitory effect of propionate is rather unlikely [Illman et al, 1988]. In the present study, the intensifi cation of SCFA synthesis in group A resulted in just slightly lowered pH value of the caecal digesta and signifi cantly lowered pH of the colon digesta.…”

Effect of White Wheat Bread Containing Sugar Beet Fiber on Serum Lipids and Hepatic mRNA in Rats Fed on a Cholesterol-Free Diet

“…Illman et al have also reported that white wheat flour lowered the plasma cholesterol concentration in rats. 23) We found that the bile acid concentration in the fecal excretion and SCFA in the cecum of the BBP group were both higher than in the other two groups. These results show that the sugar beet fiber might have influenced the cholesterol metabolism in the large intestine.…”

Glycemic index in chronic disease: a review

“…The proposed mechanisms for lipid modulation by low-GI foods compared to high GI foods may include: (1) lower insulin-stimulated HMG-CoA reductase activity (the ratelimiting enzyme in cholesterol synthesis; Rodwell et al, 1976), as a result of a reduced rate of carbohydrate absorption; (2) impaired bile acid and cholesterol reabsorption from the ileum due to the typically high fibre content of low-GI foods (Kritchevsky & Story 1974;Jenkins et al, 1993); (3) inhibition of hepatic cholesterol synthesis by the short chain fatty acid propionate, a by-product of colonic fermentation (Illman et al, 1988;Wolever et al, 1988;Wright et al, 1990); (4) reduced inflammatory response. Some evidence suggests a possible role of insulin in stimulating acute-phase proteins (O'Riordain et al, 1995;Thompson et al, 1991) which have been directly related to intra-abdominal fat and inversely related to insulin-stimulated glucose disposal (Sites et al, 2002).…”