Download MBBS (Bachelor of Medicine, Bachelor of Surgery) 1st year (First Year) Biochemistry ppt lectures Topic 67 Lipid Absorption And Transport Uptake Notes. - biochemistry notes pdf, biochemistry mbbs 1st year notes pdf, biochemistry mbbs notes pdf, biochemistry lecture notes, paramedical biochemistry notes, medical biochemistry pdf, biochemistry lecture notes 2022 ppt, biochemistry pdf.
Digestion Of Lipids
Action Of Specific
Lipid Digesting Enzymes
in Smal Intestine
?Digestion of Lipids is
cleavage of Ester
bonds present in their
structures.
? Dietary forms of Lipids are
digested:
?By action of specific Lipid
digesting enzymes of
?Pancreatic and intestinal juice
Digestion Of Triacylglycerol
(TAG)
By Enzyme Pancreatic Lipase
? Dietary Fat/Oil which is chemically
TAG is predominant ingested Lipid
form.
? TAG is significantly digested in
smal intestine
? After process of Emulsification.
Action of Pancreatic Lipase
? Pancreatic Lipase specifical y
Digests Triacylglycerol by cleaving
ester bonds present in its structure.
Colipase Facilitates
Pancreatic Lipase Activity
Role Of Pancreatic Colipase
? Procolipase secreted from
Pancreas as
? Activated to Colipase by
Trypsin
? Colipase anchors Lipase to
an Emulsion.
? One Colipase to one Lipase
(i.e., 1:1 ratio)
? Pancreatic Colipase
?Colipase interacts with Pancreatic
Lipase to:
?Displace Bile to al ow recycling
?Improve activity of Pancreatic Lipase
?Interact PL with Triacylglycerol
? Pancreatic Lipase attack TAG at 1 and 3 positions of
Ester bonds.
G Fatty Acid1
G
l
l
y
Lipase
y
Fatty Acid1
c
c Fatty Acid
2 H
+
e Fatty Acid
2
2
20
e
r
r
Fatty Acid3
ol
ol
Fatty Acid3
Triacylglycerol
2-Monoacylglycerol
2 Free Fatty Acids
Triacylglycerol
Colipase Pancreatic Lipase
Optimum PH 8 Cleaves 1st and 3 rd ester
bond of TAG
Free Fatty acids + 2-Monoacylglycerol
(Fatty acid esterified at C2 of Glycerol)
?Pancreatic Lipase digest
TAG
?By specifical y cleaving first
and third ester bonds of
TAG structure.
Bile Salts
Dietary Fat
Lipase 2-Monoacylglycerol
(large TG droplet)
+ 2 FFA
Lipid emulsion
? The products of TAG digestion
? By Pancreatic Lipase activity
are:
?Free Fatty acids
?Monoacylglycerol (2-MAG)
Action of
Non Specific Lipid Esterases
Of Intestinal Juice
2-Monoacylglycerol
Non Specific Esterase
Cleaves Ester bond at C2
Free Fatty acid + Glycerol
? Non specific Lipid Esterases act
on 2-MAG /Retinol Ester.
? It cleaves ester bonds and
releases Free Fatty acid and
Glycerol/Retinol respectively.
Digestion Of Phospholipids
by Pancreatic Enzymes
Action of Phospholipase A2
and
Lysophospholipase
Phospholipid
Phospholipase A2
Cleaves Ester bond at C2 of PL
Lysophospholipid+ Free Fatty acid
Lysophospholipid
Lysophospholipase
Cleaves Ester bond at C1
Glycerophosphorylcholine+ Free Fatty
acid
? Pancreatic juice enzymes
Phospholipase A2 and
Lysophospholipase digests
dietary Phospholipids.
? Phospholipase A2 cleaves second
position ester bond of Phospholipid to
form Lysophospholipid and Free Fatty
acid.
? Lysophospholipid is then acted by
Lysophospholipase which cleaves ester
bond at C1 to generate:
Glycerophosphorylcholine and Free
Fatty acids.
Digestion Of Cholesterol Ester
By
Cholesterol Esterase
Cholesterol Ester
Cholesterol Esterase
Cleaves Ester bond at C3
Free Cholesterol+ Free Fatty acid
End Products Of Lipid Digestion
? 5 Simple Forms as End products of Lipid Digestion
1. Free Fatty acids
2. Glycerol
3. 2-Monoacylglycerol (2-MAG)
4. Glycerophosphoryl-Choline
5. Free Cholesterol
Absorption
of
Dietary End Products
Of Lipid Digestion
Absorption of Dietary Lipids
? End products of Lipid digestion
simple and absorbable forms
? Get absorbed In smal
intestine
? Rate of absorption of different
types of Lipids differ.
?Pork fat is almost absorbed
completely.
?Castor oil is not at al absorbed.
Theories Of Lipid Absorption
? Absorption of Lipids is a complex
mechanism and various theories are
proposed to explain its mechanism.
?Lipolytic Theory
?Partition Theory
?Bergstorm Theory
(Most Recent and accepted one)
Important Role Of Bile Salts
In Both
Lipid Digestion and Absorption
? Bile Salts in intestine helps in
Emulsification of dietary Lipids to
form Emulsions and Facilitates Lipid
Digestion.
? Later Bile Salts form Mixed Micel es
and facilitates the absorption of
digestive end products Lipids.
Role Of Bile Salts In Lipid Absorption
Mechanism Of Lipid Absorption
? Bile Salts play an important role
in absorption of digestive end
products of dietary Lipids.
? Bile salts help in formation of
Mixed micel es.
?Mixed Micelle is aggregation
of
?digestive end products of
dietary Lipids with a
peripheral layer of Bile Salts.
?An efficiency of Lipid
absorption depends upon:
?Quantity of Bile salts
?Which solubilizes and
form Mixed Micelles.
Mixed Micel e Formation
? Mixed Micel e is a complex of Lipid
materials and Bile salts soluble in water
?It contains Bile salts, end products of
Phospholipids & Cholesterol at periphery
of a Mixed Micel es.
?2-Monoacylglycerol, Free fatty acids and
fat-soluble Vitamins in center of Mixed
Micel es.
Mixed Micel e Formation
? In Mixed Micel e non polar
long chain fatty acids are at
the center
? At periphery are Amphipathic
Lipid moieties and Bile salts.
? Bile salts and Amphipathic
Lipids of Mixed Micelle
? Exert a solubilizing effect on
non polar Lipid moieties and
help in their absorption.
? Mixed Micel es then get attached
to an Enterocytes cel membrane.
? This help Lipid end products to
slowly cross the mucosal
membrane and get internalized.
? Bile salts of Mixed Micel es do
not cross intestinal mucosal cel
membrane.
? They get retained in intestinal
lumen and later get recycled.
?Bile salts are reabsorbed
further down the
Gastrointestinal tract
( In ileum)
? Bile salts are transported
back to the Liver through
enterohepatic circulation
? Final y recycled and secreted
back into the digestive tract
Re-Esterification of Simple Lipids
OR
Resynthesis Of Complex
Forms Of Lipids
In Intestinal Mucosal Cells
? Once simpler forms of Lipids
enter the intestinal mucosal
cel s/Enterocytes
? They are resynthesized into
complex forms of Lipids inside
intestinal mucosal cel s.
Resynthesis Of Complex Lipids
In Enterocytes
? Free Fatty acid (FFA) + Glycerol Monoacylglycerol
? MAG +FFA Diacylglycerol
? Diacylglycerol + FFA
Triacylglycerol
? Glycerophosphorylcholine + FFAs
Phospholipid
? Cholesterol +FFA Cholesterol Ester
? Note resynthesized
complex Lipids in intestinal
mucosal cel s
? Are usual y different from
those ingested through diet.
?Dietary absorbed Lipids in
intestinal mucosal
cells/Enterocytes are then
mobilized out as
Lipoproteins.
Formation Of Lipoprotein
Chylomicrons
In Intestinal Mucosal Cells
For
Transportation Of
Dietary Lipids
?Lipids of dietary origin
present in intestinal
mucosal cells are mostly
non polar (TAG) and
hydrophobic in nature.
? Transport of these dietary Lipids
through aqueous phase of lymph
and blood is
? Facilitated through formation of
a Lipoprotein -Chylomicron in
intestinal mucosal cells.
? Lipoprotein Chylomicron is
synthesized in intestinal
mucosal cells/Enterocytes by
? Aggregation of dietary
ingested, digested and
absorbed Lipids and
Apoprotein (ApoB48).
? Chylomicron structure has the
non polar Lipids aggregated at
center, the Amphipathic Lipids
and Apoproteins at periphery.
?Chylomicron has 98% of
TAG (dietary origin)
?1% other Lipids and
?1% Proteins.
? Chylomicrons from intestinal
mucosal cells are first released in
Lacteals (Lymph vessels) of
Lymphatic system
? Which then enters the systemic
blood circulation via Thoracic
duct (Lymphatic duct).
? Thus Chylomicron serve as a
vehicle for transporting the
exogenous forms of dietary Lipids
? From Smal intestine to Liver via
aqueous phase of Lymph and
Blood.
Lipid Digestion Absorption and
Transport
Mechanism Of
Lipid Absorption
Simple diffusion
Exocytosis
Short and
medium
chain fatty
acids
Overview
of Lipid
Digestion
and
Absorption
Transportation Of
Chylomicrons
Through Blood Circulation
Action OF Enzyme Lipoprotein Lipase
On Lipoproteins
(Chylomicrons and VLDL)
Unlike
Plasma Lipid Clearance
OR
Role Of Clearing Factor
? Most of absorbed Lipids from
GIT mucosal cel s do not
directly enter the blood
stream.
? Instead, they are packaged
into Chylomicrons and first
released into the lymph.
? Lymph dumps into Aortic arch (via Thoracic
duct connection with left Sub Clavian vein
enter systemic blood circulation) .
LPL Clears Chylomicrons from Blood
? Chylomicrons transported through
blood stream are cleared by LPL
activity and taken up by:
?Adipocytes (Store House Of TAG)
?Muscle
?Liver
Lipids are Not Carried through
Enterohepatic Circulation
?Since Liver is not the
store house of Lipids.
Liver is not a Storage house for TAG
? Unlike Carbohydrates (Glucose) and Protein
(Amino acids) who use enterohepatic circulation
to reach first to Liver.
? Most Lipids carried through lymphatic and
systemic circulatory system to reach Liver lastly.
? This allows Lipids to be cleared by the whole
body and avoids overwhelming of Lipids to Liver .
? Clearance of Lipoproteins
from circulation
? Is mediated by an enzyme
Lipoprotein Lipase (LPL)
acting upon TAG of
Lipoproteins.
? Nascent (New) Chylomicrons released
from intestinal mucosal cells are
circulated first through lymph and
then in systemic blood circulation.
? Nascent Chylomicrons in
blood circulation get matured
? After the receipt of Apo C I
and ApoE from HDL.
? Apo C I of Mature Chylomicron then
stimulates an enzyme Lipoprotein Lipase
(LPL)
? LPL associated in endothelial lining of
Blood vessels, of Adipose, Heart, Skeletal
Muscles as well as in Lactating Mammary
glands.
? Stimulated Lipoprotein Lipase then
acts upon the TAG of Lipoproteins
(Chylomicron and VLDL).
? Lipoprotein Lipase hydrolyze the TAG
of Lipoproteins to Free Fatty acids and
Glycerol.
? Released Glycerol and Free Fatty acids
enter the adjacent Adiposecytes.
? Glycerol and FFAs entered
in Adipocytes are
transformed into TAG.
?TAG is storage form of Fatty
acids
?TAG serve as a reserve
source of energy.
Liver Internalizes
Only
Chylomicron Remnants
?LPL by its activity on
Chylomicrons reduces
its content of TAG.
? Chylomicrons with
Maximal y reduced TAG
content and now termed as
Chylomicron Remnant.
? Chylomicron remnant in
comparison to Nascent
Chylomicron is
? Smal er in size, and has very
less percentage of dietary
TAG, associated to it.
? Chylomicron remnants get fixed
to their specific receptors
present on Hepatocytes and get
internalized.
? The internalized Chylomicron
remnants inside the Liver gets
further metabolized.
? Thus Lipoprotein Lipase is
also termed as Clearing
Factor
? Since Lipoprotein Lipase clears
Lipaemic sera(Chylomicrons)
in post absorptive phase.
LPL Activity On Chylomicrons
? In Post absorptive phase most of the
blood Chylomicrons are transformed to
Chylomicron remnants
? By the Lipoprotein Lipase activity,
? The released moieties from Chylomicrons
are internalized by Adiposecytes and
Hepatocytes
? This clears the circulating Chylomicrons
from blood.
v Defect In Lipoprotein Lipase
Do not clear blood
Lipoproteins
Accumulates Chylomicrons
and VLDL in blood circulation
Heparin Is a Coenzyme For
Lipoprotein Lipase
? MI patients are administered
with Heparin injections
? Which may stimulate
Lipoprotein Lipase activity
? And clear blood with elevated
Chylomicrons and VLDL.
Transport of Short Chain Fatty Acids
And
Medium Chain Fatty Acids
Is Different From
Long Chain Fatty Acids
? Transport of Short and Medium chain
Fatty acids
?These enter portal blood directly
from enterocytes
?Transported after bound to Albumin
in blood
?Albumin?FFA complex
?FFA are then internalized in Liver
?Oxidized to liberate ATPs
OR
?Elongated and used for TAG
formation
? Long-chain Fatty acids
?Transported in form of Chylomicrons
?Drain into Lymphatics via Lacteals
?Enter blood stream at Thoracic duct
Defective Lipid
Digestion and Absorption
Leads To
Steatorrhoea
Steatorrhoea
? Steatorrhoea is a Lipid Malabsorption
condition
? Where there is no digestion and no
absorption of dietary Lipids from GIT
? Dietary ingested Lipids are excreted out
through feces as it is.
? Steatorrhoea leads to Fatty stools
? Characteristic whitish/greyish,greasy Stool
Causes Of Steatorrhoea
? The basic cause to suffer from
Steatorrhoea is:
?Absence of emulsifying
agents- Bile salts in smal
intestine.
?Absence of specific Enzymes
for Lipid digestion.
Any Condition Affecting,
Synthesis, Secretion and
Transport of Bile to Intestine
Biliary Insufficiency
leads to Steatorrhoea
? Extensive Liver damage
affects Bile Synthesis.
? Celiac Diseases:
?Sprue (Intestinal Disorder)
?Crohn's Disease (Inflammatory
Bowl Disease)
? Surgical removal of intestine
? Obstructive Jaundice
?Obstruction due to narrowing
of bile duct after surgeries
?Obstruction of CBD due to Gal
Stones
? Chronic Pancreatic Diseases
Biochemical Alterations in
Steatorrhea
Excretes Lipids > 6gm/day
? No/Less Bile and Bile Salts in
small intestine
? No/Less Emulsification of
dietary Lipids
? No/Less Emulsions formed
? No/Less Contact of Lipids with
Lipases
? No/Less digestion of dietary Lipids
? No/Less formation of Mixed
Micel es
? No/Less absorption of dietary
Lipids
? More excretion of dietary Lipids
through feces.
? Whitish and greasy stools.
Consequences Of Steatorrhea
? In Steatorrhoea person suffers from
deficiency of essential Fatty acids
and Fat Soluble Vitamins.
? Body lacks exogenous TAG as
secondary source of Energy.
? Body lacks from Exogenous source of
Phospholipids and Cholesterol.
Diagnosis OF Steatorrhoea
? Determination Of Fecal Fat
? Microscopical y (Fat Globules present)
? Quantitatively (Gravimetric Method)
Chyluria
? Chylomicrons in Urine is termed as
Chyluria.
? Abnormal condition where
lymphatic drainage system opens
in urinary tract.
? Urine appears milky
? Chyluria occurs in Filariasis.
Chylothorax
? Chylomicrons in Pleural fluid
is termed as Chylothorax.
? Abnormal y Thoracic duct
opens in pleural cavity.
Overview Of Lipid Metabolism
vLipid metabolism involves:
vLipolysis
vLipogenesis
vLiver and Adipose tissue play a
central role in Lipid metabolism.
vAdipose tissue is main store house
of Triacylglycerol in the body.
Major Tissues In Lipid Metabolism
? Adipocytes----- Lipolysis
? Liver------------------ Lipogenesis
vFatty acids are highly reduced
compounds oxidized/catabolized
to Acetyl CoA
vFatty acids are biosynthesized
using Acetyl CoA as a precursor.
Lipid Metabolism
What Is Lipolysis?
OR
Role Of Hormone Sensitive Lipase
(HSL)
Fat Storage in White Adipose Tissue
?In a well fed condition
TAG is stored as reserve
source of energy in
Adiposecytes.
? Lipolysis occurs in an
emergency conditions
?Fasting Phase
?Between Meals
?When Blood Glucose Lowers
?Low Insulin High Glucagon
Lipolysis
? Lipolysis is break down of
Depot Fat-Triacylglycerol(TAG)
? Into Free Fatty acids and
Glycerol
? By enzyme activity of
Hormone sensitive Lipase
Triacylglycerol
In Adipocytes Hormone Sensitive Lipase
Triacylglycerol Lipase
Cleaves Ester bonds
Glycerol+ Free Fatty acid
Diagrammatic View Of Lipolysis
Significance Of Lipolysis
?During Lipolysis secondary
source of energy TAG
?Stored as depot Fat gets
catabolized and utilized.
Conditions Of Lipolysis
? Lipolysis significantly and efficiently occurs :
?In emergency fasting condition
?In between long hours after meals
?When primary source of energy Glucose
go below normal range in blood
?Low Insulin and high Glucagon or
Epinephrine
?By activity of Hormone Sensitive Lipase
? Enzyme Hormone Sensitive Lipase
of Adipocytes is stimulated By
Hormones:
? Glucagon and Epinephrine
mediated via cAMP cascade
activity of enzymes.
?On Lipolysis the Free Fatty
acids and Glycerol are
mobilized out of
adipocytes in blood
circulation.
End Products Of Lipolysis
?Free Fatty Acids
?Glycerol
Fate Of Glycerol After Lipolysis
? Glycerol (polar moiety)released in
emergency condition during
Lipolysis
? Is carried through blood and
enters in Liver and Muscles.
Fate Of Glycerol In Muscles
(In Muscles)
Glycerol Enter into
Glycolytic Pathway
Glycerol
Glycerol Kinase
Glycerol-3-Phosphate
Glyceraldehyde-3-PO4
?Glycerol of Lipolysis is
metabolized via Glycolysis
in Muscles
? Glycerol in muscles is
Phosphorylated to Glycerol-3-PO4
? Glycerol-3-PO4 is further oxidized
to Glyceraldehyde-3-PO4
? Thus Glyceraldehyde-3-PO4 in
Muscles make its entry in
Glycolysis
? Further gets metabolized to
generate energy (ATP) for
muscle activity.
Fate Of Glycerol In Liver
(In Liver)
Glycerol Of Lipolysis
Is a Precursor For Gluconeogenesis
Glycerol Is Used For Glucose
Biosynthesis In Liver
? Glycerol of Lipolysis is metabolized
via Gluconeogenesis in Liver
? Glycerol in Liver is Phosphorylated
to Glycerol-3-PO4 by Glycerol
Kinase
? Glycerol-3-PO4 is further oxidized to
? Glyceraldehyde-3-PO4 and isomerized
to DHAP
? This then is converted to Glucose.
? Thus Glyceraldehyde-3-PO4
in Liver make its entry in
Gluconeogenesis and
? Further gets metabolized to
produce Glucose.
?Glucose formed in Liver is
mobilized out into blood
and Correct Hypoglycemia.
?Glucose supplied to Brain
and Hepatocytes in fasting
condition.
Fate Of Free Fatty Acids
After Lipolysis
? Non polar Long Chain Free Fatty
acids released in blood
circulation after Lipolysis are not
transported on its own.
? Needs the help of a polar moiety.
Polar Moiety Albumin
Transports
Long Chain Free Fatty Acids
In Blood
Released After Lipolysis
? Long chain Free Fatty acids are
uncharged/nonpolar/hydrophobic
? They are linked with polar Protein
moiety Albumin
? FFA-Albumin complex get transported
through blood circulation.
? Albumin remain in the blood
circulation
? Free Fatty acids make its
entry in Muscle cel s.
Fatty Acids In Muscles
Oxidized To Liberate Energy
(ATP)
? Free Fatty acids are highly reduced
compounds.
? Free Fatty acids entered in Muscles
during emergency condition
? After Lipolysis, are oxidized to
liberate chemical form of energy
ATP.
?Thus after Glucose Free
Fatty acid serve as
secondary source of
energy to body tissues.
170
Oxidation Of Fatty Acids
OR
Catabolism/Degradation
Of Fatty Acids
How Fatty Acid Oxidation
Serve As
Energy Source?
? Fatty acids are an important
secondary source of energy to
body.
?As Fatty acids are reduced compounds
?Possess CH2-CH2 hydrocarbon bonds
with bond energy within it .
? Oxidation of Fatty acid /Catabolism or
breakdown of Fatty acid is by:
?Removal of Hydrogen from hydrocarbon
chain (CH2-CH2).
?Which are temporarily accepted by
oxidized form of Coenzymes
?With formation of reduced Coenzymes
?Reoxidation of these reduced Coenzymes
by entry in ETC /Oxidative Phosphorylation
generates ATP.
?Oxidation of the Hydrocarbon
bonds of fatty acid chain makes
them weaker
?Easy Cleavage of hydrocarbon
bonds of Fatty acid
?Which helps in shortening of
the long Fatty acid chain.
Types Of
Fatty Acid Oxidation
1. Oxidation Based On Type Of Carbon Atom
? Alpha() Oxidation(Phytanic acid ?Branched Chain FA)
? Beta () Oxidation (Most Predominant)
? Omega() Oxidation (When defect in Oxidation)
2.Oxidation Based On Number Of Carbon
Atom
? Beta Oxidation of Even Carbon Chain
Fatty acid oxidation
? Beta Oxidation of Odd Chain Fatty
Acid Oxidation
? Very Log Chain Fatty Acid (VLCFA)
Oxidation
3.Oxidation Based On Nature Of
Bonds
? Oxidation of Saturated
Fatty acids
? Oxidation of Unsaturated
Fatty acids
4.Oxidation Based On Cel ular Site
? Mitochondrial Fatty acid Oxidation
? Endoplasmic Reticulum Fatty acid
Oxidation
? Peroxisomal Fatty acid Oxidation
How Palmitic Acid is
Completely Oxidized In Human Body?
Calculate Its Energetics
General Pattern To Study
Metabolic Pathways
? Synonyms/Different Names of Pathway.
? What is Pathway ? (In brief)
? What type Of Pathway?
(Catabolic/Anabolic)
? Where thus pathway occurs/Location?
(Organ/Cellular site)
? When pathway occurs/Condition?
(well fed/emergency/aerobic/anaerobic)
? Requirements for Pathway
(If Anabolic Pathway)
? How pathway Occurs/Stages/Steps?
(Type of Rxn , Enzymes ,Coenzymes)
? Why Pathway occurred?
(Significance of Pathway)
? Precursor, intermediates, byproducts and
end products of metabolic Pathway.
? Energetics of pathway/Net ATP Use and
Net Generation of ATPs
? Interrelation ships with other Pathways
? Regulation of Pathway :Modes of regulation.
? Regulatory Hormone/ Regulatory
Enzyme/Modulators.
? Inborn Error of the Metabolic Pathway
Beta Oxidation
Of
Even Carbon
Saturated Fatty Acid
At Mitochondrial Matrix
Historical Aspects Of
Beta Oxidation of Fatty Acids
? Albert Lehninger showed that
? Oxidation of Fatty acids
occurred in the Mitochondria.
? Knoop showed that Fatty
acid is oxidized and
degraded by removal of 2-C
units
? F. Lynen and E. Reichart
showed that 2-C unit
released is Acetyl-CoA, but
not free Acetate.
Beta Oxidation Of Palmitate (C16)
What Is Beta Oxidation
Of Fatty Acid ?
Definition Of Oxidation
of Fatty acid
? Oxidation of a Fatty acid at
Beta Carbon atom/C3 (-CH2)
? Beta Oxidation of Fatty Acid is
most predominant type of
Fatty acid oxidation.
? Most of Fatty acids in cel s get
oxidized and catabolized via
Beta Oxidation of Fatty Acid
b-Oxidation OF Fatty Acid
? b-oxidation of Fatty acids is
catabolic/ degradative , energy
generating metabolic pathway of
Fatty acids
? It is referred as b-oxidation
pathway, because oxidation occurs
at b-carbon (C3) of a Fatty acid.
? During Beta oxidation of
Fatty acid (-CH2) of Beta
position is oxidized and
? Transformed to Carbonyl
atom (-C=O)
? Oxidized and transformed Beta
positioned -C-H2 to -C=O during
steps of Beta Oxidation Proper.
? Makes bond between Alpha
and Beta Carbon atom weaker
and cleavable to release
2Carbon unit Acetyl-CoA.
The Weak bond between Alpha and Beta
Carbon Atom is Cleaved to release
2Carbon Unit Acetyl-CoA
? With a removal of 2-C units
there is shortening of Fatty
acid chain.
? The 2-C units released after
steps of Beta Oxidation is
Acetyl-CoA (active Acetate)
which enters TCA for its
complete oxidation.
b-Oxidation OF Fatty Acid
Is a Catabolic
Energy Producing Pathway
Organs Involved with
Beta Oxidation Of Fatty Acid
?Skeletal Muscles
?Heart
?Hepatocytes
?Kidney
Cel ular Site For
Beta Oxidation Of Fatty Acid
?Cytosol
(Activation of Fatty acid)
?Mitochondrial Matrix
(Beta Oxidation Proper)
b-Oxidation pathway:
Fatty acids are degraded in the Mitochondrial Matrix via
the b-Oxidation Pathway.
Organs Which Do Not Operate
Beta Oxidation Of Fatty Acid
Remember In
Brain and Erythrocytes
Fatty Acids
Do Not Serve
As A Source Of Energy
?Free Fatty acids cannot
cross the blood brain
barrier
?Hence Fatty acids do
not enter Brain to get
oxidized.
? Beta Oxidation proper of Fatty
acid takes place in
Mitochondrial matrix
? Since mature RBC's has no
Mitochondria
? Hence no oxidation of Fatty
acids occurs in Erythrocytes.
? In emergency conditions
?Since Brain and Erythrocytes
cannot oxidize Fatty acids and
use as energy source.
?These organs has to depend
only on Glucose for getting
energy for their vitality.
Type Of Metabolic Pathway
? Beta Oxidation Of a Fatty acid is a:
?Catabolic Pathway
?Degradative Pathway
?Energy generating metabolic
pathway in emergency phase
Condition Of Its Occurrence
? Usually Beta Oxidation of Fatty acids
efficiently occurs after Lipolysis.
? When there is low use of Glucose by body
cells
?In Fasting condition
?In between Meals
?During Severe Exercises and Marathon Races
?In Patients of Diabetes mellitus
Stages And Reaction Steps
Of Beta Oxidation Of Fatty Acids
Three Stages Of Beta Oxidation
For
Fatty acid Palmitate
Stage I
Activation of Fatty acid (Acyl Chain) to
Acyl-CoA In Cytosol
? Palmitate to Palmitoyl-CoA
In Cytosol
Stage II
Translocation of Activated Fatty acid
From Cytosol into Mitochondrial
Matrix
Through The Role of Carnitine
(Carnitine Shuttle)
Stage I I
Steps of Beta Oxidation Proper
In Mitochondrial Matrix
?Oxidation Reaction
?Hydration Reaction
?Oxidation Reaction
?Cleavage Reaction
This post was last modified on 05 April 2022