Bile salts excretion

Similarly, dietary fibers are known to interact with bile acids in the intestinal limien and thus increase bile salt excretion in feces, resulting in decreased munbers... 

RJ Leipold. Description and simulation of a tubular, plug-flow model to predict the effect of bile sequestrants on human bile salt excretion. J Pharm Sci 84 670-672, 1995. 

ATP-dependent process, aided by the bile-salt excretion pump (BSEP) expression in the canalicular membrane. Conjugation increases the aqueous solubility of the bile adds, and renders these bile adds largely impermeable to the cell membranes of the intestine and duodenum hence, they are unable to leave the intestinal lumen. This allows bile-add levels to rise in the lumen, ultimately reaching sufficient concentrations to form micelles, which allow lipid emulsification and subsequent absorption. 

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. 

The bile salt-independent pathway depends on osmotically active solutes such as glutathione and bicarbonate to generate water flow into the canaliculi. It has been shown that bile flow continues at zero bile salt excretion, i.e. a bile salt-independent process. 

The ring structure of cholesterol cannot be degraded in the body. The bile salts excreted in the feces are the major form in which the steroid nucleus is excreted. 

Intrahepatic cholestasis of pregnancy is a syndrome of unknown etiology characterized by a 100-fold increase in maternal and fetal blood bile salt levels. Bile salts are produced in both the fetal and maternal liver. The fetus transfers the bile salts across the placenta for disposal. When the function of the maternal gallbladder is slowed, bile salts can accumulate in the liver and bloodstream, ultimately resulting in the classical pruritus symptom. It is believed that pregnancy-related hormones may slow bile salt excretion from the gallbladder. 

Bile binding resin - binds bile salts Excretion... 

Cholestyramine (Questran) Forms insoluble complex with bile salts, excreted in feces. Body compensates by increasing LDL receptors and oxidizing cholesterol to bile acids. LDL > 190 mg/dl (160 with 2 risk factors) provided that 6 month trial of low lipid diet has failed. i Cholesterol, LDL T Triglycerides, VLDL, HDL ... 

Dissociated jaundice (ictere dissociee) refers to a dissociation of bilirubin and bile salt excretion in which bilirubin is retained, leading to jaundice, but bile salts are excreted in a normal manner so that such patients are icteric but do not have pruritus and no bile salts are detected in blood or urine. The concept was held that only the hepatic cell could selectively retain bilirubin but excrete bile salts and that bile ducts or gallbladder cells could not. The observation of dissociated jaundice was therefore regarded as useful in distinguishing jaundice due to hepatitis or cirrhosis from that caused by bile duct obstruction (74-76). 

Most bile salts excreted in the feces are of the secondary type. Their formation is discussed in Section VII. The daily fecal excretion of bile salts in healthy subjects is highly variable and easily influenced by dietary alterations. Values from several studies are given in Table VIII. Bile salts virtually disappear from the stools during prolonged fasting, and turnover nearly ceases (19). Primary bile salts appear in the stools of patients with diarrhea (1). Patients taking cholestyramine excrete the usual pattern of secondary bile salts (57), so that apparently bacterial dehydroxylation of bile salts can occur in the presence of this resin. Patients with total external bile fistulas have no bile salts in the feces (2) this does not exclude transintestinal excretion of bile salts but makes it unlikely. As mentioned earlier, the predominance of chenodeoxycholic acid in blood and bile is often reflected in a predominance of lithocholate over deoxycholate in the feces (27). 

In contrast to many earlier studies using less specific procedures cf, 55), the chemical methods, which apparently give the most reliable results, have shown that the daily bile acid synthesis is normally relatively low in man, being about 250 mg/day (range from about 100 to 400 mg/day), i.e., about one-third of total cholesterol catabolism. Dietary factors, and especially body size and obesity, affect the values sensitively impaired liver function and hypercholesterolemia decrease, and malabsorption, especially ileal dysfunction, increases markedly the fecal bile acid elimination (11,62,63). Determination of the fecal bile salt excretion is a sensitive method for detection of ileal dysfunction (64). 

Intestinal bile salt deficiency associated with impaired gallbladder contraction and slightly augmented fecal bile salt excretion during hypocalcemic steatorrhea of patients with primary hypoparathyroidism (84) will be discussed later (see Section VIIE2a). 

Phytosterols have been reported to reduce semm cholesterol concentrations by competitively blocking cholesterol absorption from the intestinal lumen (Heinemann et al, 1986, 1993), by displacing cholesterol from bile salt micelles (Child and Kuksis, 1986), by increasing bile salt excretion (Salen et al, 1970), or by hindering the cholesterol esterification rate in the intestinal mucosa (Child and Kuksis, 1983 Ikeda and Sugano, 1983). Ikeda et al (1988) also showed that the only site of action was the binding of sterols to micelles. As mentioned above, although many studies have been conducted, the precise mechanism of the inhibitory effect of phytosterols on cholesterol absorption in the intestine is not fully understood. 

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