Role of Dietary Propionic Acid and Bile Acid Excretion in the Hypocholesterolemic Effects of Oligosaccharides in Rats

Abstract

The aim of this study was to evaluate the influence of dietary propionic acid and bile acid excretion on the hypocholesterolemic effect of fibers. For this purpose, rats were adapted to a diet containing 10 g inulin, 10 g beta-cyclodextrin, or 2.5 g calcium propionate per 100 g diet. Both the inulin and beta-cyclodextrin diets elicited high propionic acid fermentations in the cecum (approximately 45% of total short-chain fatty acids) with relatively low molar proportions of acetic and butyric acids. In rats fed the three experimental diets, 5-7 mumol/min of propionic acid was absorbed in the portal vein, and propionic acid was entirely metabolized by the liver. Plasma cholesterol was more effectively depressed by the beta-cyclodextrin diet than by the inulin diet; the propionic acid-supplemented diet was ineffective in this respect. The inulin diet slightly increased fecal bile acid excretion, compared with the control diet, whereas beta-cyclodextrin markedly enhanced (1.8-fold) bile acid excretion. Microsomal hydroxymethylglutaryl-CoA (HMG-CoA) reductase activity was slightly depressed in rats fed the propionic acid-supplemented diet, whereas it was enhanced by the beta-cyclodextrin diet in parallel to the activity of cholesterol 7 alpha-hydroxylase. The present data suggest that absorption and further hepatic metabolism of large amounts of propionic acid are not sufficient to counteract the induction of HMG-CoA reductase resulting from bile acid fecal losses. The rise of these losses plays a major role in the hypocholesterolemic effect of beta-cyclodextrin.

The bifidogenic effect of inulin and oligofructose and its consequences for gut health

“…Supplementation with inulin has also been shown to increase bile acid secretion in rats (Levrat et al, 1994) and in hamsters (Trautwein et al, 1998).…”

Comparative gastrointestinal and plasma cholesterol responses of rats fed on cholesterol-free diets supplemented with guar gum and sodium alginate

“…Anderson (1985) suggested that increased hepatic propionate supply via the portal vein from large-bowel NSP fermentation may inhibit hydroxymethylglutaryl-CoA reductase, the rate-limiting enzyme for cholesterol biosynthesis (Rodwell et al 1976;Levrat et al 1994), and thus reduce circulating cholesterol concentrations. There is no doubt that increased consumption of fermentable NSP has been associated with increased caecal production of SCFA, and higher concentrations of SCFA, including propionate, in portal blood (Goodlad & Mathers, 1990).…”

Apolipoprotein A-I, Phospholipid Vesicles, and Cyclodextrins as Potential Anti-Atherosclerotic Drugs: Delivery, Pharmacokinetics, and Efficacy

“…While b -CD is not hydrolyzed by the salivary or pancreatic a -amylase (Andersen et al 1983;Suzuki and Sato 1985), it is fermented in mammalian large intestine to glucose and oligosaccharides by resident micro ora (Suzuki and Sato 1985;Levrat et al 1994) and humans (Flourie et al 1993;Antenucci and Palmer 1984). b -CD is negligibly hydrolyzed in and slightly absorbed from the stomach and small intestine (Andersen et al 1983;Antenucci and Palmer 1984;Flourie et al 1993).…”

“…This favors hypocholesterolemia (Riottot et al 1993;Levrat et al 1994). b -CD is fermented mainly to propionate in the large intestine (Levrat et al 1994;Moundras et al 1994).…”

“…This favors hypocholesterolemia (Riottot et al 1993;Levrat et al 1994). b -CD is fermented mainly to propionate in the large intestine (Levrat et al 1994;Moundras et al 1994). The three different forms of CDs (a , b , and c ) have been used to alter the composition of erythrocyte membranes (Klein et al 1995), while b -CD has been noted to selectively extract cholesterol from PMs (Neufeld et al 1996).…”