Bile salts binding

J. P. Cruse, M. R. Lewin and C. G. Clark, The effects of cholic acid and bile salt binding agents on 1,2-dimethylhydrazine-induced colon carcinogenesis in the rat. Carcinogenesis, 1981, 2, 439. 

PO026 Smith, M. A., and A. A. Aso. Comparison of psyllium hydrophilic mucilloid and bile salt binding resin therapy for hypercholesterolemia. Abstr Endocrine Society 144 Annual Meeting June 1992 62. 

Bile salts bind with soluble fiber and pass out of body. 

Recently the means by which pectin lowers cholesterol levels and even the validity of this effect have been questioned. Upon finding no bile salt binding capacity for soluble pectin, Baig and Cerda (76) proposed that pectin lowered serum cholesterol levels by forming insoluble complexes with the serum low density lipoproteins (LDL) which transport circulating cholesterol. Complexing of LDL by citrus pectin was observed in vitro, but the way in which pectin or some component thereof enters the blood stream to effect such binding in vivo has not been determined. 

Pfeffer et al. (82) have found that bile salt binding activity of commercial citrus pectins was lost if these products were dissolved, filtered, centrifuged, and reprecipitated before testing. Binding activity was concentrated in the residue pellet from centrifugation, which was found to be fine diatomaceous earth. This contaminant was probably introduced during filtration steps in processing and purification of pectin. The authors concluded that any hypocholesterolemic effect of commercial pectin was due solely to its diatomaceous earth contamination. 

Conjugated bile salts are normally absorbed in the terminal ileum. Disease of the terminal ileum (eg, Crohn s disease) or surgical resection leads to malabsorption of bile salts, which may cause colonic secretory diarrhea. The bile salt binding resins cholestyramine or colestipol may decrease diarrhea caused by excess fecal bile acids (see Chapter 35 Agents Used in Hyperlipidemia). The usual dose is 4-5 g one to three times daily before meals. Side effects include bloating, flatulence, constipation, and fecal impaction. In patients with diminished circulating bile acid pools, further removal of bile acids may lead to an exacerbation of fat malabsorption. These agents bind a number... 

About 500 mg cholesterol is converted every day to bile salts. This may be increased if the patient is given bile salt binding resins, such as cholestyramine, which diminishes bile salt resorption, causing increased bile salt excretion in the feces. Cholestyramine and similar substances are given to individuals with high serum cholesterol levels. Most of the cholesterol that enters the small intestine via bile (see earlier) is also excreted. Fecal cholesterol amounts to about 1 g/day and is a major means of removing cholesterol from the organism. 

It has been suggested that carboxyl ester lipase has two different bile-salt-binding sites [34-36], one nonspecific for the bile salt structure and one specific for primary bile salts causing the di(poly)merization. An interesting question is whether the bile salts regulate substrate specificity not only by bile salt-enzyme interactions but also by forming the appropriate substrate surface structure [27]. 

In clinical terms, intraluminal bile salt deficiency such as occurs in various forms of cholestasis, can clearly lead to impaired assimilation of fat-soluble vitamins. When the bile-salt-binding resin cholestyramine is given on a long-term basis in the treatment of hypercholesterolemia there is some risk of malabsorption of fat-soluble vitamins though in clinical practice this is not common. 

Kritchevsky, and G. V. Vahouny, Effect of bile-salt binding resins on the morphology of rat jejunum and colon. Dig.Pis. Sci., 25 504 (1980). 

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