A complete overview of digestion and absorption of lipids with the suitable diagrams.

1. Digestion and Absorption of lipids
Mohmmad Amil Rahman
S.R.
Department of Biochemistry
Dr. R.P.G.M.College Kangra at Tanda(H.P.)

2. What are lipids???
• Lipid = a compound that is insoluble in water, but soluble in
an organic solvent (e.g., ether, benzene, acetone, chloroform)
• Major source of energy for the body.
• Also provide the hydrophobic barriers that permit partitioning
of aqueous contents of cells and sub cellular structures.
• Fat soluble vitamins have regulatory or coenzyme role in the
body.
• Prostaglandins and steroid hormones play major roles in the
control of body’shomeostasis.
• Give shape and contour to the body and protect internal organs
by providing a cushioning effect.

3. Saturated vs. Unsaturated Fatty Acids ???
• Saturated: the SFA’s of a lipid have no double bonds
between carbons in chain.
• Polyunsaturated: more than one double bond in the
chain most common polyunsaturated fats contain the
polyunsaturated fatty acids (PUFAs) oleic, linoleic and
linolenic acid
• unsaturated fats have lower melting points

4. Types of fats we use
• More than 95% are triglycerides, the other are
• Cholesterol,
• Cholesteryl esters,
• Phospholipids, and
• Unesterified fatty acids.

5. Sources of Lipids
Animal Sources
Dairy products- butter, ghee
Meat and Fish, Pork, eggs
Vegetable Sources
Cooking oils- Sun flower oil,
Mustard oil, Ground nut oil Fats
from other vegetable sources
• Additional lipid is supplied in the form of
phospholipids and cholesterol, mostly arising
from the liver in biliary secretions

6. Digestion of fat in Mouth
Hydrolysis of triacylglycerol is initiated by lingual lipases, which
attack the sn-3 ester bond forming 1,2-diacylglycerols and free fatty
acids
Lingual lipase: Secreted by dorsal surface of tongue
• Active at low pH (pH 2.0 – 7-5), optimum pH 4.0-4.5 and ideal
substrate-Short chain TGS.
• Milk fat contains short chain fatty acids which are esterifies at -
3 position, thus it is the best substrate for lingual lipase.
• Enzymatic action continues in stomach.
• Short chain fatty acids, released are absorbed directly from the
stomach wall and enter the portal vein.

7. Digestion of fat in Stomach
• Gastric Lipase- secreted in small quantities
• More effective at alkaline p H (Average p H 7.8)
• Requires the presence of Ca++
• Less effective in stomach due to acidic p H except
when intestinal contents are regurgitated in to the
gastric lumen
• Not effective for long chain fatty acids, most effective for
short and medium chain fatty acid
• Milk, egg yolk and fats containing short chain fatty
acids are suitable substrates for its action

8. Work of fats in gastric emptying
• Fats delay the rate of emptying of
stomach.
• Action is brought about by secretion of
Enterogastrone.
• Enterogastrone inhibits gastric motility and
retards the discharge of bolus of food from the
stomach.
• Thus fats have a high satiety value.

9. Significance of Lingual and Gastric Lipases
• Free fatty acids produced by lipases initiates secretion of
CCK
• Play an important role in lipid digestion in neonates
since milk is the main source of energy
• Lingual and gastric lipases can degrade triglycerides in
patients with pancreatic disorders despite a near or
complete absence of pancreatic lipase

10. Emulsification & digestion
• Lipids are hydrophobic, and thus are poorly
soluble in the aqueous environment of the
digestive tract.
• The digestive enzyme, lipase, is water
soluble and can only work at the surface of
fat globules.
• Digestion is greatly aided by emulsification,
the breaking up of fat globules into much
smaller emulsion droplets.

11. • Bile salt are responsible for
lowering the surface tension
allowing to formation of emulsion,
•The critical process of
emulsification takes place in the
duodenum.
•This emulsification provide more
site for lipases to act

12. Digestion in small intestine
• Major site of fat digestion is small intestine
• Effective digestion due to the presence of Pancreatic lipase (that is
activated by bile acids)
• cholesterol esterase catalyzes the hydrolysis of cholesterol esters,
esters of fat-soluble vitamins, and phospholipids, as well as
triglycerides.
• Bile salts act as effective emulsifying agents for fats
• Secretion of pancreatic juice is stimulated By secretion of Secretin,
Cholecystokinin

13. Gastro Intestinalhormones
• Secretin-Increases the secretion of electrolytes
and fluid components of pancreatic juice.
• Pancreozymin of CCK -PZ stimulates the secretion of
the pancreatic enzymes
• Cholecystokinin of CCK-PZ- causes the contraction
of the gall bladder and discharges the bile in to the
duodenum.
• Hepatocrinin- Released by intestinal mucosa, stimulates
more bile formation which is relatively poor in bile acid
content

14. Contents of PancreaticJuice
• Pancreatic Lipase- For the digestion of
triglycerides.
• Phospholipase A2- for the digestion of
Phospholipids.
• Cholesterol esterase-For the digestion of
Cholesteryl esters.

15. Role of Bile Salts
• Bile salts help in combination of lipase with two
molecules of a small protein called as Co-lipase.
• This combination enhances the lipase activity.
TG particle
Colipase
lipase

16. • They 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.
• The primary bile acids are cholic acid (found in the
largest amount) and chenodeoxycholic acid .
• The primary bile acids enter the bile as glycine or
taurine conjugates.
• Inthealkalinebile,thebileacidsandtheirconjugatesareassumed
to beinasaltform—hencetheterm "bilesalts.“

17. Synthesis of bilesalts

18. • A portion of the primary bile acids in the intestine
is subjected to further changes by the activity of
the intestinal bacteria.
• These include deconjugation and 7-alpha
dehydroxylation, which produce the secondarybile
acids, deoxycholic acid and lithocholic acid.

19. Enterohepatic circulationof Bilesalts
• The enterohepatic circulation of bile salts is the recycling of
bile salts between the small intestine and the liver.
• The total amount of bile acids in the body, primary or
secondary, conjugated or free, at any time is defined as the
total bile acid pool.
• In healthy people, the bile acid pool ranges from 2-4 g.
• The enterohepatic circulation of bile acids in this pool is
physiologically extremely important. By cycling several times
during a meal, a relatively small bile acid pool can provide the
body with sufficient amounts of bile salts to promote lipid
absorption.

20. In a light eater, the bile
acid pool may circulate
three to five (3-5) times a
day; in a heavy eater, it
may circulate 14 to 16
times a day. - If
enterohepatic circulation is
interrupted (e.g. due to
obstruction or surgical
removal or inflammation of
the terminal ileum), bile
flow is markedly reduced.

21. Triacyl glyceroldegradation by pancreaticlipase
• Pancreatic lipase is specific for the hydrolysis of
primary ester linkages(Fatty acids present at
position 1 and 3)
• It can not hydrolyze the ester linkages of position -2
• Digestion of Triglycerides proceeds by removal of a
terminal fatty acid to produce an α, β diglyceride.
• The other terminal fatty acid is then removed to
produce βmono glyceride.

23. • The last fatty acid is linked by secondary ester group,
hence can not be hydrolyzed by pancreatic lipase.
• β- Mono acyl glycerol can be converted to α- Mono
acyl glycerol by isomerase enzyme and then
hydrolyzed by Pancreatic lipase.
• The primary product of hydrolysis are β- Mono acyl
glycerol (78%), α- Mono acyl glycerol (6%) with free
fatty acids and glycerol (14%)

25. Significance ofPancreatic lipase
The enzyme is present in high concentration in
pancreas. Only very severe pancreatic deficiency suchas
cystic fibrosis results in malabsorption of fats due
to impaired digestion.
Orlistat, an antiobesity drug inhibits , gastric and
pancreatic lipases, there by decreasing fat digestion
and absorption resulting in weight loss.

26. Cholesteryl esterdegradation
• Dietary cholesterol is mainly present in the free
(Non esterified) form
• Only 10-15% is present in the esterified form
Cholesteryl esters are hydrolyzed by pancreatic
Cholesteryl esterase (Cholesterol ester Hydrolase) to
produce cholesterol and free fatty acid
• The enzymatic activity is greatly increased in the
presence of bile salts.

28. Phospholipiddegradation
• The enzyme –Phospholipase A2 requires bile salts
for optimum activity.
• Removes one fatty acid from carbon 2 of
Phospholipid to form lysophospholipid.
• The remaining fatty acid at position 1 can be
removed by lysophospholipase , leaving a
glycerylphosphoryl base that may be excreted in the
feces, further degraded or absorbed.

30. Absorption ofLipids
• Glycerol, short and medium chain fatty acids (Chain
length less than 14 carbons) are directly absorbed from
the intestinal lumen in to the portal vein and taken to
liver for further utilization.
• Their uptake is regulated via the activity of specific
membrane transporters, a microvillus membrane fatty
acid–binding protein (MVM-FABP) provides for the
uptake of long-chain fatty acids across the brush border.
• Long chain fatty acids, free cholesterol and β- acyl
glycerol together with bile salts form mixed micelles.

31. Micelles
• Bile salts are amphipathic , one
surface of the molecule is
hydrophilic because the polar
peptide bond and the carboxyl and
hydroxyl groups are on that
surface, whereas the other surface
is hydrophobic.
• Therefore, the bile acids tend to
form cylindrical disks called
micelles.

32. Micelles formation
• When the concentration of
bile acids in the intestine is
high, as it is after contraction
of the gallbladder, lipids and
bile salts interact
spontaneously to form micelles

33. Micelles
• Micelles are disk shaped
clusters of amphipathic lipids
that unite with their
hydrophobic groups on the inside
and their hydrophilic groups on
the outside of clusters
• Mixed micelles are soluble in the
aqueous environment of the
intestinal lumen
• Thus, the micelles move down
their concentration gradient
through the brush border of the
mucosal cells.

34. • The fate of the fatty acids in enterocytes depends on their size.
• Fatty acids containing less than 10–12 carbon atoms are
water-soluble enough that they pass through the enterocyte
unmodified and are actively transported into the portal blood.
• The fatty acids containing more than 10–12 carbon atoms are
re-esterified to triglycerides in the enterocytes.
• The triglycerides and cholesterol esters are then coated with a
layer of protein,cholesterol, and phospholipid to form
chylomicrons
Fate of fatty acids

35. Fate of lipids inside enterocytes
• These leave the cell and
enter the lymphatics, by
exocytosis
• because they are too large to
pass through the junctions
between capillary
endothelial cells

36. Once again , inside the enterocyte, monoglycerides and fatty
acids are re-synthesized into TG.
Chylomicrons are lipoproteins, special particles that are
designed for the transport of lipids in the circulation.
Chylomicrons are released by exocytosis at the basolateral
surface of the enterocytes. Because they are particles, they
are too large to enter typical capillaries.
Chylomicrons then flow into the circulation via lymphatic
vessels.
Chylomicrons

37. Structure ofChylomicron
 Size: 0.1–1 µm
 Average
compositi
on
o TG (84%)
o Cholesterol(2%)
o Ester Cholesterol
(4%)
o Phospholipid (8%)
o Apo lipoproteins
(2%)

38. Formation and Transportation of Chylomicrons

40. Clinical significance ofChylomicron synthesis and
utilization
Defective synthesis- Due to deficiency of apo-B 48 protein.
The triglyceride may accumulate in intestinal cells.
Chyluria- Due to an abnormal connection between urinary
tract and lymphatic drainage system of the intestines, forming
Chylous fistula. Characterized by passage of Milky urine.
Chylothorax- There is an abnormal connection between
pleural space and the lymphatic drainage of small intestine
resulting in accumulation of lymph in pleural cavity giving
Milky pleural effusion

41. Summary oflipid digestion and Absorption

42. ENZYMES SITE TARGET PRODUCT
Lingual /acid
stable lipase
Mouth , stomach TAGS with
medium chain
FAS
FFA+DAG
Pancreatic lipase
+co-lipase
Small intestine TAGSwith long
chain FAS
FFA+2MAG
Intestinal lipase
with bileacids
Small intestine TAGSwith
mediumchain
FAS
2FFA+glycerol
PhospholipaseA2
+bileacids
Small intestine PLswith unsat.
FAat position 2
Unsat FFA
lysolecithin
Lipoprotein lipase
insulin (+)
Capillarywalls TAGsin
chylomicronor
VLDL
FFA+glycerol
Hormone
sensitive lipase
Adipose cell TAGstored in
adipose cells
FFA+glycerol