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

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Lipid Digesting Enzymes

in Smal Intestine
?Digestion of Lipids is

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cleavage of Ester

bonds present in their

structures.

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? Dietary forms of Lipids are

digested:

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?By action of specific Lipid

digesting enzymes of

?Pancreatic and intestinal juice

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Digestion Of Triacylglycerol

(TAG)

By Enzyme Pancreatic Lipase

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? Dietary Fat/Oil which is chemically

TAG is predominant ingested Lipid

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form.

? TAG is significantly digested in

smal intestine

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? After process of Emulsification.
Action of Pancreatic Lipase

? Pancreatic Lipase specifical y

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Digests Triacylglycerol by cleaving

ester bonds present in its structure.

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Colipase Facilitates

Pancreatic Lipase Activity

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Role Of Pancreatic Colipase

? Procolipase secreted from

Pancreas as

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? Activated to Colipase by

Trypsin

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? Colipase anchors Lipase to

an Emulsion.

? One Colipase to one Lipase

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(i.e., 1:1 ratio)

? Pancreatic Colipase

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?Colipase interacts with Pancreatic

Lipase to:

?Displace Bile to al ow recycling

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?Improve activity of Pancreatic Lipase
?Interact PL with Triacylglycerol


? Pancreatic Lipase attack TAG at 1 and 3 positions of

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Ester bonds.

G Fatty Acid1

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G

l

l

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y

Lipase

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y

Fatty Acid1

c

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c Fatty Acid

2 H

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+

e Fatty Acid

2

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2

20

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e

r

r

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Fatty Acid3

ol

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ol

Fatty Acid3

Triacylglycerol

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2-Monoacylglycerol

2 Free Fatty Acids
Triacylglycerol

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Colipase Pancreatic Lipase

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Optimum PH 8 Cleaves 1st and 3 rd ester



bond of TAG

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Free Fatty acids + 2-Monoacylglycerol

(Fatty acid esterified at C2 of Glycerol)

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?Pancreatic Lipase digest

TAG

?By specifical y cleaving first

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and third ester bonds of

TAG structure.
Bile Salts

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Dietary Fat

Lipase 2-Monoacylglycerol

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(large TG droplet)

+ 2 FFA

Lipid emulsion

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? The products of TAG digestion
? By Pancreatic Lipase activity

are:

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?Free Fatty acids
?Monoacylglycerol (2-MAG)
Action of

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Non Specific Lipid Esterases

Of Intestinal Juice

2-Monoacylglycerol

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Non Specific Esterase

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Cleaves Ester bond at C2



Free Fatty acid + Glycerol

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? Non specific Lipid Esterases act

on 2-MAG /Retinol Ester.

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? It cleaves ester bonds and

releases Free Fatty acid and

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Glycerol/Retinol respectively.


Digestion Of Phospholipids

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by Pancreatic Enzymes

Action of Phospholipase A2

and

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Lysophospholipase
Phospholipid

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Phospholipase A2

Cleaves Ester bond at C2 of PL

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Lysophospholipid+ Free Fatty acid

Lysophospholipid

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Lysophospholipase

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Cleaves Ester bond at C1



Glycerophosphorylcholine+ Free Fatty

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acid
? Pancreatic juice enzymes

Phospholipase A2 and

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Lysophospholipase digests

dietary Phospholipids.

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? Phospholipase A2 cleaves second

position ester bond of Phospholipid to

form Lysophospholipid and Free Fatty

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acid.

? Lysophospholipid is then acted by

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Lysophospholipase which cleaves ester

bond at C1 to generate:

Glycerophosphorylcholine and Free

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Fatty acids.
Digestion Of Cholesterol Ester

By

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Cholesterol Esterase

Cholesterol Ester

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Cholesterol Esterase

Cleaves Ester bond at C3

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Free Cholesterol+ Free Fatty acid

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End Products Of Lipid Digestion

? 5 Simple Forms as End products of Lipid Digestion

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1. Free Fatty acids
2. Glycerol
3. 2-Monoacylglycerol (2-MAG)
4. Glycerophosphoryl-Choline
5. Free Cholesterol

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Absorption

of

Dietary End Products

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Of Lipid Digestion

Absorption of Dietary Lipids

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? End products of Lipid digestion

simple and absorbable forms

? Get absorbed In smal

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intestine
? Rate of absorption of different

types of Lipids differ.

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?Pork fat is almost absorbed

completely.

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?Castor oil is not at al absorbed.

Theories Of Lipid Absorption

? Absorption of Lipids is a complex

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mechanism and various theories are

proposed to explain its mechanism.

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?Lipolytic Theory
?Partition Theory
?Bergstorm Theory
(Most Recent and accepted one)
Important Role Of Bile Salts

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In Both

Lipid Digestion and Absorption

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? Bile Salts in intestine helps in

Emulsification of dietary Lipids to

form Emulsions and Facilitates Lipid

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Digestion.

? Later Bile Salts form Mixed Micel es

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and facilitates the absorption of

digestive end products Lipids.

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Role Of Bile Salts In Lipid Absorption



Mechanism Of Lipid Absorption

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? Bile Salts play an important role

in absorption of digestive end

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products of dietary Lipids.

? Bile salts help in formation of

Mixed micel es.

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?Mixed Micelle is aggregation

of

?digestive end products of

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dietary Lipids with a

peripheral layer of Bile Salts.

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?An efficiency of Lipid

absorption depends upon:

?Quantity of Bile salts

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?Which solubilizes and

form Mixed Micelles.

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Mixed Micel e Formation

? Mixed Micel e is a complex of Lipid

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materials and Bile salts soluble in water

?It contains Bile salts, end products of

Phospholipids & Cholesterol at periphery

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of a Mixed Micel es.

?2-Monoacylglycerol, Free fatty acids and

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fat-soluble Vitamins in center of Mixed

Micel es.
Mixed Micel e Formation

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? In Mixed Micel e non polar

long chain fatty acids are at

the center

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? At periphery are Amphipathic

Lipid moieties and Bile salts.
? Bile salts and Amphipathic

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Lipids of Mixed Micelle

? Exert a solubilizing effect on

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non polar Lipid moieties and

help in their absorption.

? Mixed Micel es then get attached

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to an Enterocytes cel membrane.

? This help Lipid end products to

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slowly cross the mucosal

membrane and get internalized.
? Bile salts of Mixed Micel es do

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not cross intestinal mucosal cel

membrane.

? They get retained in intestinal

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lumen and later get recycled.

?Bile salts are reabsorbed

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further down the

Gastrointestinal tract

( In ileum)

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? Bile salts are transported

back to the Liver through

enterohepatic circulation

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? Final y recycled and secreted

back into the digestive tract

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Re-Esterification of Simple Lipids

OR

Resynthesis Of Complex

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Forms Of Lipids

In Intestinal Mucosal Cells
? Once simpler forms of Lipids

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enter the intestinal mucosal

cel s/Enterocytes

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? They are resynthesized into

complex forms of Lipids inside

intestinal mucosal cel s.

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Resynthesis Of Complex Lipids

In Enterocytes

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? Free Fatty acid (FFA) + Glycerol Monoacylglycerol

? MAG +FFA Diacylglycerol

? Diacylglycerol + FFA

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Triacylglycerol

? Glycerophosphorylcholine + FFAs

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Phospholipid

? Cholesterol +FFA Cholesterol Ester
? Note resynthesized

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complex Lipids in intestinal

mucosal cel s

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? Are usual y different from

those ingested through diet.

?Dietary absorbed Lipids in

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intestinal mucosal

cells/Enterocytes are then

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mobilized out as

Lipoproteins.
Formation Of Lipoprotein

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Chylomicrons

In Intestinal Mucosal Cells

For

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Transportation Of

Dietary Lipids

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?Lipids of dietary origin

present in intestinal

mucosal cells are mostly

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non polar (TAG) and

hydrophobic in nature.
? Transport of these dietary Lipids

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through aqueous phase of lymph

and blood is

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? Facilitated through formation of

a Lipoprotein -Chylomicron in

intestinal mucosal cells.

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? Lipoprotein Chylomicron is

synthesized in intestinal

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mucosal cells/Enterocytes by

? Aggregation of dietary

ingested, digested and

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absorbed Lipids and

Apoprotein (ApoB48).

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? Chylomicron structure has the

non polar Lipids aggregated at

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center, the Amphipathic Lipids

and Apoproteins at periphery.
?Chylomicron has 98% of

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TAG (dietary origin)

?1% other Lipids and
?1% Proteins.

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? Chylomicrons from intestinal

mucosal cells are first released in

Lacteals (Lymph vessels) of

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Lymphatic system

? Which then enters the systemic

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blood circulation via Thoracic

duct (Lymphatic duct).

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? Thus Chylomicron serve as a

vehicle for transporting the

exogenous forms of dietary Lipids

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? From Smal intestine to Liver via

aqueous phase of Lymph and

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Blood.


Lipid Digestion Absorption and

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Transport


Mechanism Of

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Lipid Absorption

Simple diffusion

Exocytosis

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Short and

medium

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chain fatty

acids

Overview

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of Lipid

Digestion

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and

Absorption

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Transportation Of

Chylomicrons

Through Blood Circulation

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Action OF Enzyme Lipoprotein Lipase

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On Lipoproteins

(Chylomicrons and VLDL)

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Unlike

Plasma Lipid Clearance

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OR

Role Of Clearing Factor

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? Most of absorbed Lipids from

GIT mucosal cel s do not

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directly enter the blood

stream.

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? Instead, they are packaged

into Chylomicrons and first

released into the lymph.

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? Lymph dumps into Aortic arch (via Thoracic

duct connection with left Sub Clavian vein

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enter systemic blood circulation) .
LPL Clears Chylomicrons from Blood

? Chylomicrons transported through

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blood stream are cleared by LPL

activity and taken up by:

?Adipocytes (Store House Of TAG)

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?Muscle
?Liver

Lipids are Not Carried through

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Enterohepatic Circulation

?Since Liver is not the

store house of Lipids.

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Liver is not a Storage house for TAG

? Unlike Carbohydrates (Glucose) and Protein

(Amino acids) who use enterohepatic circulation

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to reach first to Liver.

? Most Lipids carried through lymphatic and

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systemic circulatory system to reach Liver lastly.


? This allows Lipids to be cleared by the whole

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body and avoids overwhelming of Lipids to Liver .

? Clearance of Lipoproteins

from circulation

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? Is mediated by an enzyme

Lipoprotein Lipase (LPL)

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acting upon TAG of

Lipoproteins.
? Nascent (New) Chylomicrons released

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from intestinal mucosal cells are

circulated first through lymph and

then in systemic blood circulation.

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? Nascent Chylomicrons in

blood circulation get matured

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? After the receipt of Apo C I

and ApoE from HDL.
? Apo C I of Mature Chylomicron then

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stimulates an enzyme Lipoprotein Lipase

(LPL)

? LPL associated in endothelial lining of

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Blood vessels, of Adipose, Heart, Skeletal

Muscles as well as in Lactating Mammary

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glands.

? Stimulated Lipoprotein Lipase then

acts upon the TAG of Lipoproteins

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(Chylomicron and VLDL).

? Lipoprotein Lipase hydrolyze the TAG

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of Lipoproteins to Free Fatty acids and

Glycerol.

? Released Glycerol and Free Fatty acids

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enter the adjacent Adiposecytes.
? Glycerol and FFAs entered

in Adipocytes are

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transformed into TAG.

?TAG is storage form of Fatty

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acids

?TAG serve as a reserve

source of energy.

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Liver Internalizes

Only

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Chylomicron Remnants
?LPL by its activity on

Chylomicrons reduces

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its content of TAG.


? Chylomicrons with

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Maximal y reduced TAG

content and now termed as

Chylomicron Remnant.

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? Chylomicron remnant in

comparison to Nascent

Chylomicron is

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? Smal er in size, and has very

less percentage of dietary

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TAG, associated to it.

? Chylomicron remnants get fixed

to their specific receptors

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present on Hepatocytes and get

internalized.

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? The internalized Chylomicron

remnants inside the Liver gets

further metabolized.

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? Thus Lipoprotein Lipase is

also termed as Clearing

Factor

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? Since Lipoprotein Lipase clears

Lipaemic sera(Chylomicrons)

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in post absorptive phase.

LPL Activity On Chylomicrons

? In Post absorptive phase most of the

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blood Chylomicrons are transformed to

Chylomicron remnants

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? By the Lipoprotein Lipase activity,

? The released moieties from Chylomicrons

are internalized by Adiposecytes and

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Hepatocytes

? This clears the circulating Chylomicrons

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from blood.


v Defect In Lipoprotein Lipase

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Do not clear blood

Lipoproteins

Accumulates Chylomicrons

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and VLDL in blood circulation


Heparin Is a Coenzyme For

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Lipoprotein Lipase

? MI patients are administered

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with Heparin injections

? Which may stimulate

Lipoprotein Lipase activity

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? And clear blood with elevated

Chylomicrons and VLDL.

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Transport of Short Chain Fatty Acids

And

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Medium Chain Fatty Acids

Is Different From

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Long Chain Fatty Acids
? Transport of Short and Medium chain

Fatty acids

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?These enter portal blood directly

from enterocytes

?Transported after bound to Albumin

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in blood

?Albumin?FFA complex

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?FFA are then internalized in Liver

?Oxidized to liberate ATPs

OR

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?Elongated and used for TAG

formation
? Long-chain Fatty acids

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?Transported in form of Chylomicrons

?Drain into Lymphatics via Lacteals

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?Enter blood stream at Thoracic duct

Defective Lipid

Digestion and Absorption

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Leads To

Steatorrhoea
Steatorrhoea

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? Steatorrhoea is a Lipid Malabsorption

condition

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? Where there is no digestion and no

absorption of dietary Lipids from GIT

? Dietary ingested Lipids are excreted out

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through feces as it is.

? Steatorrhoea leads to Fatty stools
? Characteristic whitish/greyish,greasy Stool

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Causes Of Steatorrhoea

? The basic cause to suffer from

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Steatorrhoea is:

?Absence of emulsifying

agents- Bile salts in smal

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intestine.

?Absence of specific Enzymes

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for Lipid digestion.
Any Condition Affecting,

Synthesis, Secretion and

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Transport of Bile to Intestine

Biliary Insufficiency

leads to Steatorrhoea

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? Extensive Liver damage

affects Bile Synthesis.

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? Celiac Diseases:

?Sprue (Intestinal Disorder)
?Crohn's Disease (Inflammatory

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Bowl Disease)

? Surgical removal of intestine
? Obstructive Jaundice

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?Obstruction due to narrowing

of bile duct after surgeries

?Obstruction of CBD due to Gal

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Stones

? Chronic Pancreatic Diseases

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Biochemical Alterations in

Steatorrhea

Excretes Lipids > 6gm/day

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? No/Less Bile and Bile Salts in

small intestine

? No/Less Emulsification of

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dietary Lipids

? No/Less Emulsions formed
? No/Less Contact of Lipids with

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Lipases

? No/Less digestion of dietary Lipids
? No/Less formation of Mixed

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Micel es

? No/Less absorption of dietary

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Lipids

? More excretion of dietary Lipids

through feces.

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? Whitish and greasy stools.
Consequences Of Steatorrhea

? In Steatorrhoea person suffers from

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deficiency of essential Fatty acids

and Fat Soluble Vitamins.

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? Body lacks exogenous TAG as

secondary source of Energy.

? Body lacks from Exogenous source of

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Phospholipids and Cholesterol.
Diagnosis OF Steatorrhoea

? Determination Of Fecal Fat

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? Microscopical y (Fat Globules present)
? Quantitatively (Gravimetric Method)

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Chyluria

? Chylomicrons in Urine is termed as

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Chyluria.

? Abnormal condition where

lymphatic drainage system opens

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in urinary tract.

? Urine appears milky

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? Chyluria occurs in Filariasis.

Chylothorax

? Chylomicrons in Pleural fluid

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is termed as Chylothorax.

? Abnormal y Thoracic duct

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opens in pleural cavity.
Overview Of Lipid Metabolism

vLipid metabolism involves:

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vLipolysis
vLipogenesis
vLiver and Adipose tissue play a

central role in Lipid metabolism.

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vAdipose tissue is main store house

of Triacylglycerol in the body.

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Major Tissues In Lipid Metabolism

? Adipocytes----- Lipolysis
? Liver------------------ Lipogenesis

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vFatty acids are highly reduced

compounds oxidized/catabolized

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to Acetyl CoA

vFatty acids are biosynthesized

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using Acetyl CoA as a precursor.


Lipid Metabolism

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What Is Lipolysis?

OR

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Role Of Hormone Sensitive Lipase

(HSL)

Fat Storage in White Adipose Tissue

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?In a well fed condition

TAG is stored as reserve

source of energy in

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Adiposecytes.

? Lipolysis occurs in an

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emergency conditions

?Fasting Phase
?Between Meals
?When Blood Glucose Lowers

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?Low Insulin High Glucagon
Lipolysis

? Lipolysis is break down of

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Depot Fat-Triacylglycerol(TAG)

? Into Free Fatty acids and

Glycerol

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? By enzyme activity of

Hormone sensitive Lipase

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Triacylglycerol



In Adipocytes Hormone Sensitive Lipase

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Triacylglycerol Lipase

Cleaves Ester bonds

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Glycerol+ Free Fatty acid


Diagrammatic View Of Lipolysis
Significance Of Lipolysis

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?During Lipolysis secondary

source of energy TAG

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?Stored as depot Fat gets

catabolized and utilized.

Conditions Of Lipolysis

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? Lipolysis significantly and efficiently occurs :

?In emergency fasting condition
?In between long hours after meals

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?When primary source of energy Glucose

go below normal range in blood

?Low Insulin and high Glucagon or

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Epinephrine

?By activity of Hormone Sensitive Lipase
? Enzyme Hormone Sensitive Lipase

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of Adipocytes is stimulated By

Hormones:

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? Glucagon and Epinephrine

mediated via cAMP cascade

activity of enzymes.

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?On Lipolysis the Free Fatty

acids and Glycerol are

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mobilized out of

adipocytes in blood

circulation.

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End Products Of Lipolysis

?Free Fatty Acids
?Glycerol

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Fate Of Glycerol After Lipolysis
? Glycerol (polar moiety)released in

emergency condition during

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Lipolysis

? Is carried through blood and

enters in Liver and Muscles.

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Fate Of Glycerol In Muscles
(In Muscles)

Glycerol Enter into

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Glycolytic Pathway

Glycerol

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Glycerol Kinase

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Glycerol-3-Phosphate

Glyceraldehyde-3-PO4

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?Glycerol of Lipolysis is

metabolized via Glycolysis

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in Muscles
? Glycerol in muscles is

Phosphorylated to Glycerol-3-PO4

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? Glycerol-3-PO4 is further oxidized

to Glyceraldehyde-3-PO4

? Thus Glyceraldehyde-3-PO4 in

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Muscles make its entry in

Glycolysis

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? Further gets metabolized to

generate energy (ATP) for

muscle activity.

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Fate Of Glycerol In Liver

(In Liver)

Glycerol Of Lipolysis

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Is a Precursor For Gluconeogenesis

Glycerol Is Used For Glucose

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Biosynthesis In Liver
? Glycerol of Lipolysis is metabolized

via Gluconeogenesis in Liver

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? Glycerol in Liver is Phosphorylated

to Glycerol-3-PO4 by Glycerol

Kinase

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? Glycerol-3-PO4 is further oxidized to

? Glyceraldehyde-3-PO4 and isomerized

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to DHAP

? This then is converted to Glucose.
? Thus Glyceraldehyde-3-PO4

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in Liver make its entry in

Gluconeogenesis and

? Further gets metabolized to

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produce Glucose.

?Glucose formed in Liver is

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mobilized out into blood

and Correct Hypoglycemia.

?Glucose supplied to Brain

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and Hepatocytes in fasting

condition.
Fate Of Free Fatty Acids

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After Lipolysis

? Non polar Long Chain Free Fatty

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acids released in blood

circulation after Lipolysis are not

transported on its own.

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? Needs the help of a polar moiety.
Polar Moiety Albumin

Transports

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Long Chain Free Fatty Acids

In Blood

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Released After Lipolysis

? Long chain Free Fatty acids are

uncharged/nonpolar/hydrophobic

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? They are linked with polar Protein

moiety Albumin

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? FFA-Albumin complex get transported

through blood circulation.
? Albumin remain in the blood

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circulation

? Free Fatty acids make its

entry in Muscle cel s.

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Fatty Acids In Muscles

Oxidized To Liberate Energy

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(ATP)
? Free Fatty acids are highly reduced

compounds.

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? Free Fatty acids entered in Muscles

during emergency condition

? After Lipolysis, are oxidized to

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liberate chemical form of energy

ATP.

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?Thus after Glucose Free

Fatty acid serve as

secondary source of

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energy to body tissues.

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170
Oxidation Of Fatty Acids

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OR

Catabolism/Degradation

Of Fatty Acids

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How Fatty Acid Oxidation

Serve As

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Energy Source?
? Fatty acids are an important

secondary source of energy to

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body.

?As Fatty acids are reduced compounds

?Possess CH2-CH2 hydrocarbon bonds

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with bond energy within it .

? Oxidation of Fatty acid /Catabolism or

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breakdown of Fatty acid is by:

?Removal of Hydrogen from hydrocarbon

chain (CH2-CH2).

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?Which are temporarily accepted by

oxidized form of Coenzymes

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?With formation of reduced Coenzymes
?Reoxidation of these reduced Coenzymes

by entry in ETC /Oxidative Phosphorylation

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generates ATP.
?Oxidation of the Hydrocarbon

bonds of fatty acid chain makes

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them weaker

?Easy Cleavage of hydrocarbon

bonds of Fatty acid

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?Which helps in shortening of

the long Fatty acid chain.

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Types Of

Fatty Acid Oxidation
1. Oxidation Based On Type Of Carbon Atom

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? Alpha() Oxidation(Phytanic acid ?Branched Chain FA)

? Beta () Oxidation (Most Predominant)

? Omega() Oxidation (When defect in Oxidation)

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2.Oxidation Based On Number Of Carbon

Atom

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? Beta Oxidation of Even Carbon Chain

Fatty acid oxidation

? Beta Oxidation of Odd Chain Fatty

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Acid Oxidation

? Very Log Chain Fatty Acid (VLCFA)

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Oxidation
3.Oxidation Based On Nature Of

Bonds

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? Oxidation of Saturated

Fatty acids

? Oxidation of Unsaturated

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Fatty acids

4.Oxidation Based On Cel ular Site

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? Mitochondrial Fatty acid Oxidation

? Endoplasmic Reticulum Fatty acid

Oxidation

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? Peroxisomal Fatty acid Oxidation
How Palmitic Acid is

Completely Oxidized In Human Body?

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Calculate Its Energetics

General Pattern To Study

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Metabolic Pathways
? Synonyms/Different Names of Pathway.
? What is Pathway ? (In brief)
? What type Of Pathway?

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(Catabolic/Anabolic)

? Where thus pathway occurs/Location?
(Organ/Cellular site)
? When pathway occurs/Condition?

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(well fed/emergency/aerobic/anaerobic)

? Requirements for Pathway
(If Anabolic Pathway)
? How pathway Occurs/Stages/Steps?

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(Type of Rxn , Enzymes ,Coenzymes)
? Why Pathway occurred?
(Significance of Pathway)
? Precursor, intermediates, byproducts and

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end products of metabolic Pathway.

? Energetics of pathway/Net ATP Use and

Net Generation of ATPs

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? Interrelation ships with other Pathways
? Regulation of Pathway :Modes of regulation.
? Regulatory Hormone/ Regulatory

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Enzyme/Modulators.

? Inborn Error of the Metabolic Pathway

Beta Oxidation

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Of

Even Carbon

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Saturated Fatty Acid

At Mitochondrial Matrix

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Historical Aspects Of

Beta Oxidation of Fatty Acids

? Albert Lehninger showed that

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? Oxidation of Fatty acids

occurred in the Mitochondria.
? Knoop showed that Fatty

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acid is oxidized and

degraded by removal of 2-C

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units

? F. Lynen and E. Reichart

showed that 2-C unit

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released is Acetyl-CoA, but

not free Acetate.
Beta Oxidation Of Palmitate (C16)

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What Is Beta Oxidation

Of Fatty Acid ?
Definition Of Oxidation

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of Fatty acid

? Oxidation of a Fatty acid at

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Beta Carbon atom/C3 (-CH2)
? Beta Oxidation of Fatty Acid is

most predominant type of

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Fatty acid oxidation.

? Most of Fatty acids in cel s get

oxidized and catabolized via

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Beta Oxidation of Fatty Acid

b-Oxidation OF Fatty Acid

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? b-oxidation of Fatty acids is

catabolic/ degradative , energy

generating metabolic pathway of

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Fatty acids

? It is referred as b-oxidation

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pathway, because oxidation occurs

at b-carbon (C3) of a Fatty acid.

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? During Beta oxidation of

Fatty acid (-CH2) of Beta

position is oxidized and

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? Transformed to Carbonyl

atom (-C=O)

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? Oxidized and transformed Beta

positioned -C-H2 to -C=O during

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steps of Beta Oxidation Proper.

? Makes bond between Alpha

and Beta Carbon atom weaker

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and cleavable to release

2Carbon unit Acetyl-CoA.

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The Weak bond between Alpha and Beta

Carbon Atom is Cleaved to release

2Carbon Unit Acetyl-CoA

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? With a removal of 2-C units

there is shortening of Fatty

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acid chain.

? The 2-C units released after

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steps of Beta Oxidation is

Acetyl-CoA (active Acetate)

which enters TCA for its

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complete oxidation.
b-Oxidation OF Fatty Acid

Is a Catabolic

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Energy Producing Pathway

Organs Involved with

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Beta Oxidation Of Fatty Acid

?Skeletal Muscles
?Heart
?Hepatocytes

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?Kidney
Cel ular Site For

Beta Oxidation Of Fatty Acid

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?Cytosol

(Activation of Fatty acid)

?Mitochondrial Matrix

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(Beta Oxidation Proper)

b-Oxidation pathway:

Fatty acids are degraded in the Mitochondrial Matrix via

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the b-Oxidation Pathway.
Organs Which Do Not Operate

Beta Oxidation Of Fatty Acid

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Remember In

Brain and Erythrocytes

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Fatty Acids

Do Not Serve

As A Source Of Energy

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?Free Fatty acids cannot

cross the blood brain

barrier

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?Hence Fatty acids do

not enter Brain to get

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oxidized.

? Beta Oxidation proper of Fatty

acid takes place in

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Mitochondrial matrix

? Since mature RBC's has no

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Mitochondria

? Hence no oxidation of Fatty

acids occurs in Erythrocytes.

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? In emergency conditions

?Since Brain and Erythrocytes

cannot oxidize Fatty acids and

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use as energy source.

?These organs has to depend

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only on Glucose for getting

energy for their vitality.

Type Of Metabolic Pathway

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? Beta Oxidation Of a Fatty acid is a:

?Catabolic Pathway
?Degradative Pathway

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?Energy generating metabolic

pathway in emergency phase
Condition Of Its Occurrence

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? Usually Beta Oxidation of Fatty acids

efficiently occurs after Lipolysis.

? When there is low use of Glucose by body

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cells

?In Fasting condition
?In between Meals

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?During Severe Exercises and Marathon Races
?In Patients of Diabetes mellitus

Stages And Reaction Steps

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Of Beta Oxidation Of Fatty Acids
Three Stages Of Beta Oxidation

For

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Fatty acid Palmitate

Stage I

Activation of Fatty acid (Acyl Chain) to

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Acyl-CoA In Cytosol

? Palmitate to Palmitoyl-CoA

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In Cytosol
Stage II

Translocation of Activated Fatty acid

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From Cytosol into Mitochondrial

Matrix

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Through The Role of Carnitine

(Carnitine Shuttle)

Stage I I

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Steps of Beta Oxidation Proper

In Mitochondrial Matrix

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?Oxidation Reaction

?Hydration Reaction

?Oxidation Reaction

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?Cleavage Reaction