Source of dietary fibre
Pectin is sourced from plant cell walls and is analysed as a soluble and insoluble fraction as galacturonic acid after hydrolysis. The fruits and vegetables which are especially rich in pectins have dietary fibre contents in the range of 1-2%. In order to increase societal intake in fibre it is therefore preferable to add products concentrated in fibres. Pectin fibres exhibit higher hydration properties than other fibres and this property is exploited in its use as a structural component in foods, for example in bakery products. Studies have shown that substitution of flour with citrus fibres, apple flakes and concentrates in bakery and confectionery products had a positive sensory effect. Pectin’s adsorbent and bulk-forming properties have promoted its use in some multi-ingredient anti constipation and anti diarrhoeal preparations.
Another functionality of dietary fibre is in mineral and ion absorption and exchange. Pectin has the ability to associate ions due to a high content of negative charges and calcium binding is an example of binding strength and specificity. Pectin rich fibres can behave as weak cation exchange resins and are reversible depending on pH conditions.
Following ingestion of pectin, very little of it gets digested in the small intestine. Some fermentation of pectin takes place in the large intestine via the action of bacteria. Pectin substituents (homogalacturonans) are fermented in the colon with the formation of short chain fatty acids. It has been shown that non-methyl-esterified pectins were more rapidly fermented than methyl-esterified pectins. The final products of fermentation of pectin are the short-chain fatty acids, acetate, propionate and butyrate, as well as hydrogen and carbon dioxide. The short-chain fatty acids that escape colonic metabolism are transported via the portal circulation to the liver where they undergo metabolism. The short-chain fatty acids that are not metabolised in the liver enter the systemic circulation and are distributed to the various tissues of the body. Acetate appears to be the principal short-chain fatty acid to reach the systemic circulation from the liver. Pectins are therefore beginning to gain interest as prebiotics. Studies on the metabolising of pectin chains has shown that many bacteria can degrade certain regions of the polymers, generally the HG regions. This use of a plentiful polysaccharide in maintaining and encouraging digestive flora is of advantage in assessing pectin uses in the future.
The mechanism of the possible hypocholesterolemic activity of pectin is not well understood. It appears that the viscosity of pectin is related to its possible hypocholesterolemic activity. Pectin preparations with high viscosity appear to be more effective in lowering cholesterol than are pectin preparations with lower viscosity. High-viscosity pectin is thought to lower cholesterol levels by raising the excretion of fecal bile acids and neutral sterols. High-viscosity pectin may interfere with the formation of micelles and/or lower the diffusion rate of bile acid and cholesterol-containing micelles through the bolus, consequently diminishing the uptake of cholesterol and bile acids. Numerous studies have demonstrated that pectin has favourable effects on lipids. In a small early study, administration of 15 grams of pectin daily for three weeks resulted in a mean 13% reduction in plasma cholesterol levels. There was no effect on plasma triglyceride concentrations. Subsequently, giving 40 to 50 grams of pectin daily significantly lowered cholesterol levels in both normolipidemic and hyperlipidemic subjects. In another study, a pectin-supplemented diet (without other dietary or lifestyle changes), significantly reduced plasma cholesterol in volunteers evaluated to be at medium to high risk for coronary heart disease due to hypercholesterolemia. This was a double-blind, placebo-controlled trial. Treatment continued for 16 weeks. The pectin was credited with decreasing plasma cholesterol 7.6% and LDL-cholesterol 10.8%.
Modified citrus pectin, when administered orally to rats, was found to inhibit spontaneous prostate carcinoma metastasis. It had no effect on the growth of the primary tumour. Injected modified citrus pectin was found to inhibit metastasis of melanoma cells in mice. The mechanism of these anticarcinogenic effects is not clear.
Galectins comprise a family of galactoside-binding mammalian lectins. Lectins themselves comprise a group of hemagglutinating proteins found in plant seeds, which bind the branching carbohydrate molecules of glycoproteins and glycolipids on cell surfaces, resulting in agglutination or proliferation, among other things. Galectins are proteins that can bind to carbohydrates via carbohydrate recognition domains (CRDs). At present, the galactin family includes 10 members. Apparently, galectins are secreted from cells via nonclassical secretory pathways. Galectin-3, one of the members of the family, is thought to be involved in mitosis and proliferation. On the cell surface, galectin-3 mediates cell-cell adhesion and cell-matrix interaction via binding to its complementary glycoconjugates, such as laminin and fibronectin, and thereby is thought to play an important role in the pathogenesis of cancer metastasis.
Some metastic events may involve cellular interactions that are mediated by cell surface components, including galectins. The galactose-containing carbohydrate side chains of modified citrus pectin may interfere with these cellular interactions by competing with the natural ligands of the galectins and by doing so, inhibit the metastatic process. It is thought that galectins may play a role in human prostate cancer, and in particular, human prostate cancer metastasis.