Lipids are digested and absorbed through a multi-step process. They are emulsified in the small intestine by bile salts to increase surface area for pancreatic lipase. Pancreatic lipase breaks triglycerides into fatty acids and monoglycerols. These products and other lipids form micelles which transport the lipids across the intestinal wall. Inside cells, lipids reassemble into triglycerides and combine with proteins to form chylomicrons, which transport the absorbed lipids into the lymphatic system and bloodstream.

1. Lipids digestion and absorption
• Lipids are large molecules and generally are not water-soluble. Like
carbohydrates and protein, lipids are also broken into small components for
absorption
• There is considerable variation in the daily consumption of lipids which
mostly depends on the economic status and dietary habits.
• The intake of lipids is much less (often < 60g/day) in poorer sections of the
society, particularly in the less developed countries.
• In the developed countries, an adult ingests about 60-150 g of Iipids per day,
of this, more than 90% is fat (triacylglycerol). The rest of the dietary lipid is
made up of phospholipids, cholesterol, cholesteryl esters and free fatty
acids

2. A. Processing of dietary lipid in the stomach
• The digestion of lipids begins in the stomach, catalyzed by an acid
stable lipase (lingual lipase) that originates from serous glands at the
back of the tongue.
• TAG molecules, particularly those containing fatty acids of short- or
medium-chain length (fewer than 12 carbons, such as are found in
milk fat), and is found to be more specific for ester linkage at 3-
position rather than position-1 are the primary target of this enzyme
• The ester linkage is a very high-energy bond releasing a tremendous
amount of energy upon hydrolysis. it is broken down by incorporating
a water molecule. The hydrolysis of the ester linkage yields 9 Kcal/g
energy.

3. • These same TAGs are also degraded by a separate gastric lipase,
secreted by the gastric mucosa. Both enzymes are relatively acid
stable, with pH optimums of pH 4 to pH 6.
• These “acid lipases” play a particularly important role in lipid
digestion in neonates, for whom milk fat is the primary source of
calories.
• They also become important digestive enzymes in individuals with
pancreatic insufficiency, such as those with cystic fibrosis. Lingual and
gastric lipases aid these patients in degrading TAG molecules
(especially those with short- to medium-chain fatty acids) despite a
near or complete absence of pancreatic lipase

4. B. Emulsification of dietary lipid in the small intestine
• The major site of fat digestion is the small intestine. This is due to the
presence of a powerful lipase in the pancreatic juice and presence of
bile salts, which acts as an effective emulsifying agent for fats
• Pancreatic juice and bile enter the upper small intestine, the
duodenum, by way of the pancreatic and bile ducts respectively
• The critical process of emulsification of dietary lipids occurs in the
duodenum by the help of bile salts
• Bile salts act as detergents, emulsifying large fat droplets into small
ones. This action creates a much larger surface area for the action
of lipase in the small intestine, thereby increasing lipid absorption.

5. • Emulsification is accomplished by two complementary mechanisms,
namely,
• use of the detergent properties of the bile salts,
• and mechanical mixing due to peristalsis.
• Bile salts, made in the liver and stored in the gallbladder, are
derivatives of cholesterol. They consist of a sterol ring structure with
a side chain to which a molecule of glycine or taurine is covalently
attached by an amide linkage .
• These emulsifying agents interact with the dietary lipid particles and
the aqueous duodenal contents, thereby stabilizing the particles as
they become smaller, and preventing them from coalescing.

6. C. Degradation of dietary lipids by pancreatic enzymes
The dietary TAG, cholesteryl esters, and phospholipids are enzymatically
degraded (“digested”) by pancreatic enzymes, whose secretion is hormonally
controlled
1. TAG degradation: TAG molecules are too large to be taken up efficiently by
the mucosal cells of the intestinal villi. They are, therefore, acted upon by an
esterase, pancreatic lipase, which preferentially removes the fatty acids at
carbons 1 and 3. The primary products of hydrolysis are thus a mixture of 2-
monoacylglycerol and free fatty acids
• This enzyme Estrase is found in high concentrations in pancreatic secretions
(2–3% of the total protein present), and it is highly efficient catalytically, thus
insuring that only severe pancreatic deficiency, such as that seen in cystic
fibrosis, results in significant malabsorption of fat.]
• A second protein, colipase, also secreted by the pancreas, Colipase is secreted
as the zymogen, procolipase, which is activated in the intestine by trypsin.]

7. • 2. Cholesteryl ester degradation: Most dietary cholesterol is present
in the free (nonesterified) form, with 10–15% present in the esterified
form. Cholesteryl esters are hydrolyzed by pancreatic cholesteryl ester
hydrolase (cholesterol esterase), which produces cholesterol plus free
fatty acids. Cholesteryl ester hydrolase activity is greatly increased in
the presence of bile salts
• 3. Phospholipid degradation: Pancreatic juice is rich in the proenzyme
of phospholipase A2 that, like procolipase, is activated by trypsin and,
like cholesteryl ester hydrolase, requires bile salts for optimum activity.

8. • Phospholipase A2 removes one fatty acid from carbon 2 of a
phospholipid, leaving a lysophospholipid. For example,
phosphatidylcholine (the predominant phospholipid during digestion)
becomes lysophosphatidylcholine.
• The remaining fatty acid at carbon 1 can be removed by
lysophospholipase, leaving a glycerylphosphoryl base (for example,
glycerylphosphorylcholine, that may be excreted in the feces, further
degraded, or absorbed.

9. Control of lipid digestion:
• Pancreatic secretion of the hydrolytic enzymes that degrade dietary
lipids in the small intestine is hormonally controlled. Cells in the
mucosa of the lower duodenum and jejunum produce a small peptide
hormone, cholecystokinin (CCK), in response to the presence of lipids
and partially digested proteins entering these regions of the upper
small intestine.
• CCK acts on the gallbladder (causing it to contract and release bile—a
mixture of bile salts, phospholipids, and free cholesterol), and on the
exocrine cells of the pancreas (causing them to release digestive
enzymes).
• It also decreases gastric motility, resulting in a slower release of gastric
contents into the small intestine.

10. • Other intestinal cells produce
another small peptide
hormone, secretin, in
response to the low pH of
the chyme entering the
intestine. Secretin causes the
pancreas and the liver to
release a solution rich in
bicarbonate that helps
neutralize the pH of the
intestinal contents, bringing
them to the appropriate pH
for digestive activity by
pancreatic enzymes

11. • Once the stomach contents have been emulsified, fat-breaking enzymes
work on the triacylglycerols and diglycerides to sever fatty acids from their
glycerol foundations. As pancreatic lipase enters the small intestine, it
breaks down the fats into free fatty acids and monoglycerides
• Yet again, another hurdle presents itself. How will the fats pass through
the watery layer of mucous that coats the absorptive lining of the digestive
tract? As before, the answer is bile
• Bile salts envelop the fatty acids and monoglycerides to form micelles.
Micelles have a fatty acid core with a water-soluble exterior. This allows
efficient transportation to the intestinal microvillus. Here, the fat
components are released and disseminated into the cells of the digestive
tract lining

12. Absorption of lipids by intestinal mucosal cells
(enterocytes)
• Free fatty acids, free cholesterol, and monoacylglycerol are the
primary products of lipid digestion in the jejunum. These, plus bile
salts and fat-soluble vitamins (A, D, E, and K), form mixed micelles
• Bile salts envelop the fatty acids and monoglycerides to form micelles.
Micelles have a fatty acid core with a water-soluble exterior.
• This allows efficient transportation to the intestinal microvillus. Here,
the fat components are released and disseminated into the cells of
the digestive tract lining.
• Bile salts are absorbed in the ileum

13. Micelle Formation

14. • Inside the intestinal cells, the monoglycerides and fatty acids reassemble
themselves into triglycerides. Triglycerides, cholesterol, and phospholipids
form lipoproteins when joined with a protein carrier.
• Lipoproteins have an inner core that is primarily made up of triglycerides
and cholesterol esters (a cholesterol ester is a cholesterol linked to a fatty
acid).
• The outer envelope is made of phospholipids interspersed with proteins and
cholesterol. Together they form a chylomicron, which is a large lipoprotein
that now enters the lymphatic system and will soon be released into the
bloodstream via the jugular vein in the neck.
• Chylomicrons transport food fats perfectly through the body’s water-based
environment to specific destinations such as the liver and other
body tissues.

16. Structure of a chylomicron.
Cholesterol is not shown in this
figure, but chylomicrons
contain cholesterol in both the
lipid core and embedded on
the surface of the structure.