Download MBBS Biochemistry PPT 67 Lipid Absorption And Transport Uptake Lecture Notes

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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