Bile functions as the body’s emulsifying
agent, critical for fat digestion and assimilation.
Bile is produced by the liver, and it is
temporarily stored in the gall bladder. Bile is
released into the small intestine in response
to hormones, such as cholecystokinin, when
fat enters the intestine.
Bile consists of a mixture of bile salts and
bile acids, cholesterol, bilirubin and phospholipids,
Electroplytes are present at levels found in
serum. The ratios of in-dividual lipids are
critical to maintain a stable micellar liquid.
The molar ratios are typically 5:15:80 for
If the bile concentration becomes too high,
cholesterol will precipitate and gallstones
will form in the gall bladder, a condition
known as cholelithiasis (1).
Bile salts and acids represent oxidized
derivatives of cholesterol. About 80% of the
cholesterol in the body will eventually be
disposed of as cholic acid. The primary bile
acids, cholic acid and chenodeoxycholic
acid, possess a carboxylic acid side chain,
which confers hydrophilic properties to the
lipophilic sterol ring and creates detergentlike
molecules. The liver attaches taurine
and glycine to bile acids to create bile salts
(taurocholate or taurochenodeoxycholate,
and glycocholate or glycodeoxycholate,
respectively). Bacterial enzymes in the
colon can convert these to secondary bile
acids, deoxycholate and lithocholate.
Bile and digestion
Bile is needed for efficient uptake of oily
nutrients. When bile acids and bile salts first
encounter ingested fats, they act as emulsifiers
to create suspensions which can be
broken down enzymatically. The process
involves several important steps:
1. The combined action of bile salts and
pancreatic lipase initiates hydrolysis of
triglycerides to free fatty acids and
diglycerides with the formation of emulsions
containing other lipid-soluble nutrients,
including vitamins and carotenoids. The
particle size of these emulsions ranges from
200 to 5000 nm in diameter.
2. Lipase is then able to hydrolyze di-and
triglycerides to monoglycerides and free
fatty acids. Lipase requires a smaller protein
called colipase, another pancreatic product,
in order to bind to triglycerides and activate
3. Upon further release of bile salts, the lipid
aggregates become smaller, from 3 to 10
nm in diameter. The normal endpoint of
triglyceride digestion is a product containing
70% free fatty acid anions, and 25% beta
monoglycerides, together with cholesterol.
The micelles are taken up by epithelial cells
of the brush border by passive
diffusion. After absorption, the fate of fatty
acids depends upon their sizes. Medium
chain fatty acids, with less than 10-12
carbons, pass directly from the mucosal
cells into the portal blood and bind to serum
albumin. Longer chain fatty acid anions are
re-esterified with beta monoglycerides
in the smooth endoplasmic reticulum to
reform triglycerides. The newly synthesized
triglycerides are then complexed with
apoproteins, cholesterol and phospholipids,
to produce particles called chylomicrons.
These particles are released from mucosal
cells by exocytosis and enter the lymph,
rather than entering the bloodstream directly.
Bile salts do not cross the mucosal barrier
into the lymphatic system, but rather they
are reabsorbed as micelles in the lower
region of the small intestine. Most of the bile
salts released into the intestine are reabsorbed
in the lower ileum where
bacteria can reduce free bile acids to lithocholate
and deoxycholate. The absorbed
bile acids and salts are transported via the
portal vein to the liver as complexes with
serum albumin. The liver efficiently extracts
them, conjugates them with amino acids,
and again secretes them as bile, which is
returned to the gall bladder to continue to
aid digestion. Bile salts recirculate
2-3 times through the liver with each meal.
Beets contain high amounts of Betaine
which is used to add a methyl group
to Homocysteine and thus form Methionine
and Dimethylglycine. Dimethylglycines is a
methyl-donor that helps in the detoxification
and immune system pathways. In one study,
after exposure to carbon tetrachloride
(CC14), there was a reduction in liver necrosis
and a significant reduction in liver damage
after oral treatment of betaine (2).
Another study showed that after injection of
CC14 to test animals, supplemental betaine
reduced triglyceride in the liver and centrilobular
hepatic lipidosis induced by the
CC14 injections (3).
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