2. DIETARY
LIPIDS
Dietary lipids derived from plants and
animals
Essential for growth and development
They are oxidized for energy or stored as
reserve fat in adipose tissue.
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5. DIGESTION
OF LIPIDS
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An emulsion is a mixture of two or more liquids that are
normally immiscible owing to liquid-liquid phase
separation.
Emulsions are created when one liquid is dispersed in
another and held together by small amounts of a third
liquid known as the emulsifier.
7. DIGESTION
OF LIPIDS
IN MOUTH
Lingual lipase – secreted by dorsal
surface of the tongue
But this enzyme is not significant in
humans
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LITTLE OR NO DIGESTION OF LIPIDS IN MOUTH
9. DIGESTION
OF LIPIDS
IN
STOMACH
Lipids delay the rate of emptying the
stomach by ENTEROGASTRONES
Enterogastrone is any substance in the lower
gastrointestinal tract which opposes the caudal
(or "forward, analward") motion of the contents
of chyme when exposed to lipids.
Examples include: Secretin, Cholecystokinin
Inhibit gastric motility
Retard discharge of food from stomach
FATS HAVE SATIETY(feeling of fullness)
feature
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10. DIGESTION
OF LIPIDS
IN
STOMACH
Heat of the stomach –liquidising dietary
lipids
Peristaltic movements of the stomach –
emulsification of lipids
Gastric lipase and lingual lipase
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11. DIGESTION
OF LIPIDS
IN
STOMACH
Both enzymes are relatively acid-stable
Play a particularly important role in
lipid digestion in neonates
in individuals with pancreatic
insufficiency - cystic fibrosis
Hydrolyse TAG molecules especially
those with short- to medium-chain
fatty acids
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GASTRIC LIPASE AND LINGUAL LIPASE - “ACID LIPASES”
20. DIGESTION
OF LIPIDS
IN SMALL
INTESTINE
ACIDIC CHYME
STIMULATES DUDENAL
MUCOSATO RELEASE
• SECRETINS (secreted by
S-cells in the duodenum)
• CHOLECYSTOKININ
(produced by I-cells in the
lining of the duodenum)
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The chyme which enters the duodenum is acidic in nature due to the
action of hydrochloric acid in the stomach. But since the pancreatic
enzymes work in an alkaline medium, chyme is transformed into an
alkaline medium by the bile secreted into the small intestine
29. ABSORPTION
OF LIPIDS
The products of digestion are incorporated into
molecular aggregates to form mixed micelle
Micellar formation is essential for the
absorption of fat soluble vitamins A, D, E and K
Site of absorption is jejunal mucosa
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34. ABSORPTION
OF LIPIDS BY
INTESTINAL
MUCOSAL
CELLS
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2-MAG
FA
C
LysoPL
Vitamin
A,D,E,K
2-MAG
FA
C
LysoPL
Vitamin
A,D,E,K
CoA-SH
Fatty acyl-CoA
TG
CE
PL
Vitamin
A,D,E,K
APOLIPOPROTEIN
B-48
Free CHOLASTEROL
MIXED
MICELLES
35. ABSORPTION
OF LIPIDS
CHYLOMICRONS
from intestinal
mucosal cells are
absorbed into
lymphatic system
then into systemic
circulation via
thoracic duct
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36. ABSORPTION
OFSHORT &
MEDIUM
CHAIN FATTY
ACIDS
Short and medium chain fatty acids do not
need re-esterification
They can directly enter into blood vessels
So they are better absorbed than long chain
fatty acids
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39. Triacylglycerols contained in food are first acted upon by
pancreatic lipases and are absorbed as monoacylglycerols,
free fatty acids, and free glycerol.
In the intestinal cells (enterocytes), triacylglycerols are
resynthesized and, together with phospholipids, cholesterol
and apoB48, are reassembled into chylomicrons.
These are secreted into the lymph and reach plasma through
the thoracic duct.
Chylomicron TAGs normally appear in plasma only after
fat-containing meals, giving plasma a milky appearance.
In the peripheral tissues, such as muscle and adipose
tissue, chylomicron triacylglycerols are hydrolyzed by LPL
(Lipoprotein lipase). The remaining smaller particles are the
chylomicron remnants.
The remnants of chylomicrons travel to the liver, where they
bind to the LDL receptor and the LRP (LDL Receptor related
Protein).
The half- life of chylomicrons in plasma is less than 1 h
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40. Stages of Lipoprotein metabolism:
1. Assembly of lipoprotein particles. Chylomicrons are
assembled in the intestine, and VLDL in the liver;
2. Transfer of fatty acids via lipoproteins to cells. This is
facilitated by enzymes, LPL and HTGL hepatic triglyceride
lipase and transforms chylomicrons and VLDL into the
relevant remnant particles (remnants);
3. Binding of the remnant particles to membrane receptors and
their cellular uptake;
4. Transformation of some remnants into LDL, their subsequent
receptor binding and cellular uptake.
5. Reverse cholesterol transport, i.e. removal of cholesterol
from cells by HDL particles, its esterification by LCAT and
either transport back to the liver, or CETP-mediated transfer
to other lipoproteins by which they re-enter the VLDL-IDL-
LDL pathway.
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41. Lipoprotein Metabolism
Chylomicrons transport triglyceride TAGs to
periphery, and their remnants are metabolized in
the liver.
VLDL transport fuel from the liver toperipheral
tissues, and the remnants also return to the liver.
Part of VLDL remnants and IDL are further
converted into LDL, which enter the overflow
pathway.
The overflow pathway: LDL travel in blood from
the liver through the peripheral tissues and back to
the liver. On its way it may enter the arterial wall.
The amount of lipids deposited in the arteries is
proportional to their plasma concentration.
Cholesterol is PICKED from cells and transported
back to liver by HDL particles.
LPL: lipoprotein lipase, LRP: LDL-receptor-related
protein HTGL; hepatic triglyceride lipase
42. INTERNALLY
SYNTHESIZED
TAGSARE
TRANSPORTED
BYVLDL
1. Endogenously synthesized triacylglycerols are transported by
VLDL, which are assembled in the liver.
2. There, VLDL are 'built up' around apoB100 molecules.
3. The binding of triacylglycerols to apoB is facilitated by the
microsomal triglyceride transfer protein (MTP).
4. Unused ApoB100 is degraded by ubiquitin-dependent
protease (Protein breakdown pathway).
5. Once made, the VLDL goes Into plasma and acquires cholesteryl
esters and other apoproteins (including apoE) from HDL.
6. Its triacylglycerols are hydrolyzed by LPL in a way analogous to
chylomicrons, and this yields VLDL remnants.
7. At this stage apoE assumes its receptor-binding conformation
and it binds to the apoB/E receptor.
8. Most of the remnants are taken up by the liver. The remaining
ones are further hydrolyzed by HTGL hepatic triglyceride lipase
to yield IDL, which in turn, by losing still more triacylglycerol,
transform into LDL. By this stage, all apoproteins except for
the apoB100 had been shed off from the particle.
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