Soluble fibre has been shown to possess the ability to lower blood lipids in both normal and hypercholesterolaemic subjects, with effects being seen generally in the low density lipoprotein (LDL) fraction. However, insoluble fibre does not share the same lipidaemic effect. It is not known how fibre is able to lower blood lipids but it has been suggested that it may result from increased transit time during digestion that may result in reduced nutrient absorption rates. The downstream effect of this is a slower and more controlled metabolism of substrates by hepatic tissues. However, this does not explain the ineffectiveness of insoluble fibre to affect blood lipids. Another mechanism that has been suggested in the upregulation of hepatic bile acid synthesis which would require cholesterol as a substrate. However, soluble fibre is particularly susceptible to bacterial degradation that produces a range of short-chain fatty acids (SCFA). These fatty acids may be pivotal in providing the cholesterol modifying effects of soluble fibre.
Research has compared the effects of insoluble wheat fibre and soluble oat fibre to increase serum levels of SCFA in 20 hypercholesterolaemic men1. Subjects received control diets for one week, followed by either a wheat bran or oat bran diet for the following 3 weeks. The oat bran diet provided 110 gram of oat bran per day as a bowl of hot cereal and oat bran muffins (34 grams total fibre and 13.4 grams of soluble fibre), whereas the wheat bran diet provided 40 grams of wheat bran (34 grams total fibre and 7.8 grams soluble fibre) as wheat bran muffins and a bowl of cereal, both served at breakfast. Subjects on the oat bran diet had a 12.8 % reduction in serum cholesterol whereas those following the wheat bran diet showed no change to blood lipids. Serum acetate values in the oat bran group and were significantly higher than the wheat bran group. Other SCFA were barely detectable in the peripheral circulation, although serum levels of propionate did rise in the oat bran subjects, but the change was not significant.
These results suggest that acetate is the main product of the fermentation of soluble oat fibre in the colon. Acetate has been shown to inhibit cholesterol synthesis in rat hepatocytes, but it is unclear if this mechanism is responsible for the cholesterol reducing effect of soluble fibre in humans. Increases in SCFA have been demonstrated in previous studies using various degradable fibers such as pectins and gums. The wheat bran fibre used in this study is partially degradable in the colon by bacteria, and this explains the smaller rise in acetate seen with this group compared to the oat fibre group. Therefore rises in acetate following fibre ingestion may explain the hypocholesterolaemic effects of fibre. Because many early studies investigating the effects of dietary cholesterol on plasma cholesterol levels did not control for SCFA production from varying fibre intakes, their results should be treated with caution. These results also demonstrate that fibre is a source of energy in humans, as SCFA are oxidised hepatically.
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