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For weak acids that associate and disassociate depending on the pH of the
solution they are in the terms salt and acid are often used interchangably.
The pK is the pH at which 50% of the molecule is in the acid form (proton
attached) and 50% is in the salt form (proton detached). When reading about
bile salts don't get confused by seeing the term acid used.
Figure 1:
Bile salt schema, 1 source of bile
salts, 2 small bowel, 3 large bowel. Bile salts may be carcinogenic in the stomach and esophagus
6cm
|
Bile salts are made in the liver from cholesterol. They thus share the steroid
nucleus (cyclo-pertano-penhydro-phenantherene). To increase their solubility
they have hydroxyl groups and are conjugated with the amino acids glycine and
taurine. 75% is conjugated with glycine and the remaining 25% with taurine.
These are the primary bile acids/salts; cholic acid (glycine or taurine
conjugate) chenodeoxycholic acid (glycine or taurine conjugate). The primary
bile acids/salts are released into the intestine in bile.
In the small bowel the primary bile salts are reabsorbed in the terminal
ileum, (enterohepatic circulation).
About 99% of the bile salts are in the
enterohepatic circulation. In all there is about 3-5 g of bile salts in a
person. These are turned over 6 times a day. In the presence of ileal
disease, too much bile salt reaches the colon and causes diarrhoea. A small
amount of bile salt enters the colon.
Bacterial metabolism of the primary bile salts occurs in the colon; cholic
acid is metabolised to deoxycholic acid and chenodeoxycholic acid is
metabolised to lithocolic acid. Deoxycholic acid is reabsorbed and has an
enterohepatic circulation.
With increasing loss of the ileum there are three different scenarios
- Asymptomatic
- This occurs when the remaining ileum can absorb sufficient
bile salts to maintain the bile salt pool and prevent excess bile salts
reaching the colon.
- Choleriform (cholerrheic) diarrhoea
- (Less than 100 cm ileum resected) Enough bile salts are reabsorbed to
maintain the bile salt pool, lost bile salts are replaced by increased
hepatic synthesis, but sufficient bile salts reach the colon to cause
diarrhoea.
- Steatorrhoea
- (More than 100 cm of ileum resected) The bile salt pool is
severly diminished. Too little bile salts reach the colon to cause diarrhoea,
but the lack of bile salts results in decreased absorbtion of fat and fat
soluble vitamins. Fatty meals are followed by steatorrhoea.
A compounding factor following bowel resection is the colonisation of the
remaining bowel with organisms that can break down conjugated bile salts such
that they loose their ability to form micells.
Next: Nutrients
Up: Physiology relevant to short
Previous: Ileal brake
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Adrian P. Ireland
2004-02-02