Download MBBS Biochemistry PPT 74 Atherosclerosis Lipid Disorders Lecture Notes

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7 Alpha-Hydroxylase /Cholesterol 7-Alpha

-Monooxygenase
? Cytochrome P450 7A1 is enzyme in ER of Hepatocytes

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? Encoded by CYP7A1 gene

? Important role in cholesterol catabolism

? Catalyzes first rate limiting step in bile acid biosynthesis

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? Oxidizes Cholesterol at position 7 using molecular Oxygen

? Converts Cholesterol to 7-Alpha Hydroxy Cholesterol

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? Regulates Cholesterol level

? Bile acids provide feedback inhibition for CYP7A1

? Inhibition of cholesterol 7-alpha-hydroxylase (CYP7A1)

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represses bile acid biosynthesis

? When blood cholesterol levels are high CYP7A1 is

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upregulated by nuclear receptor LXR

? To increase production of bile acids and reduce level of

cholesterol in hepatocytes.

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? When blood cholesterol levels are low it is downregulated

by Sterol Regulatory Element Binding Proteins (SREBP)

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Salient Biochemical Features

Defect in CYP7A1 Gene

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? Inherited through family

? Signs of premature cholesterol gal stone disease

? Defective Cholesterol Catabolism

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? LDL Cholesterol levels elevated in blood

? Substantially elevated TAG

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? Nonresponsive Statin therapy

? Increases risk of Atherosclerosis

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Study Of Atherosclerosis

? Features of Normal and Atherosclerosed artery
? Risk of development
? Process of development

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? Consequences
? Diagnosis
? Management
? Prevention and Reduction

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Features Of Normal Arterial Wal

? Lumen of healthy arterial wal is lined by:

?Confluent layer of Endothelial cel s

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Normal Endothelium Controls

Important function Of Arterial wal

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vNormal healthy arterial endothelium:
vArteries are soft and Elastic
vRepels cells and inhibits blood clotting

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vRegulates tissue and organ blood flow by

vAbility of blood vessels to dilate-

vasodilatation

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vAbility of blood vessels to constrict-

vasoconstriction
Arteriosclerosis

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What Is Arteriosclerosis?

? Arteriosclerosis is non-specific term used

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to describe

? Hardening and thickening of wal of

medium or large arteries.

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Atherosclerosis

is a form of

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Arteriosclerosis

What Is Atherosclerosis?

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? Term Atherosclerosis, comes from

Greek words

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?Atheros- meaning "gruel" or "paste"

?Sclerosis- meaning "hardness".
Terms related to Atherosclerosis

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? Many terms are associated to Atherosclerosis:

vAtheroma
vAtherosclerotic Plaques

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vFibro Fatty Lesions
vFibrous Plaques

? Atherosclerotic Plaque Results

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From Accumulation of :

?Lipids

?Connective tissue

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?Inflammatory cel s

?Smooth Muscle cel s

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?Foam Cel s

?Minerals

? In an intima of blood vessels.

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Atherosclerosis is

Hardening of Blood Vessels

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due to formation of

Fibro Inflammatory Fatty Lesions/Plaques

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? Atherosclerosis are abnormal

Diseased/defective arteries.

? Becomes hard and non elastic

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? Less or non Functional

? Decreased diameter of lumen

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? Obstruct normal blood flow to

cel s/tissues/organs.
Causes Of Atherosclerosis

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Risk Factors For Atherosclerosis

? Risk factors which accelerate

progression of Atherosclerosis

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and endothelial dysfunction are:

?Oxidative Stress due to free radicals

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?Dyslipidemias/Dyslipoproteinemias

?Hypercholesterolemia

?Other Cardiovascular risk factors

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Improper Dietary Habits

? Eating an imbalanced diet
? Excess of Refined Sugars
? Excess of Saturated fatty acids

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? Use of Trans Fatty acids

v Smoking
vAge and Sex
vPhysical inactivity

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vStressful life style
?Hormonal Imbalances

vDiabetes mel itus
vMetabolic Syndrome

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Unchangeable Risk factors of Atherosclerosis

? Age

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? Genetic Alterations

? Male gender

? Men are at grater risk than are premenopausal

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women, because of the protective effects of natural

Estrogens.

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? Family history of premature coronary heart disease

? Several genetically determined alterations in

lipoprotein and cholesterol metabolism have been

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identified.
Changeable Risk Factors Of

Atherosclerosis

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vHyperlipidemias:

vPresence of Hyperlipidemia is

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strongest risk factor for

Atherosclerosis in persons younger

than 45 years of age.

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vBoth primary and secondary

hyperlipidemia increases risk.

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Dyslipidemias

directly associated with increased risk

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of Atherosclerosis

? Elevated TAG (above reference range)
? Increased LDL (above reference range)
? Decreased HDL (Below reference range)

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? Increased HDL (above reference range)
vHypertension

vHigh blood pressure produces

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mechanical stress on vessel

endothelium.

vMajor risk factor for atherosclerosis in

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al age groups

vMay be as important or more important

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than hypercholesterolemia after age of

45 years.

vBlood Pressure >160 mmHg

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increases risk for MI

?Regulation of Hypertension

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may reduce risk of

Atherosclerosis.
vSubstances toxic to

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endothelial cel s:

vHomocysteine
vC-Reactive Protein

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Less Well Established Risk Factors

? High Serum Homocysteine Levels

? Homocysteine is derived from metabolism of dietary

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Methionine

? Homocysteine inhibits elements of anticoagulant cascade

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and is associated with endothelial damage.

? Infectious agents

? Presence of some organisms (Chlamydia pneumoniae,

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herpesvirus hominis, cytomegalovirus) in atheromatous

lesions has been demonstrated by immunocytochemistry

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? Organisms may play a role in atherosclerotic development

by initiating and enhancing inflammatory response.

? Elevated serum C-Reactive Protein

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? It may increase likelihood of thrombus formation

? Inflammation marker
How An Atherosclerotic Plaque

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Developed?

Common Arteries Atherosclerozied

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?Aorta and its branches

?Coronary arteries

?Large vessels that supply

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Brain

?Peripheral arteries
Pathogenesis Of Atherosclerosis

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?Pathogenesis of

Atherosclerosis includes:

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? Genetic Factors
? Environmental Factors

3 Stages of Atherosclerosis:

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1.Initiation and Formation
2.Adaptation
3.Clinical
Development of Atherosclerosis

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? Key event is damage to endothelium

? Damaged endothelium becomes

more permeable to Lipoproteins.

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? Lipoproteins move below endothelial

layer (get lodged into intima).

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? Damaged Endothelium looses its cel -

repel ent quality.

?Inflammatory cel s move into

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vascular wal .

?Further Endothelial injury occurs by

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attachment of leukocyte

(lymphocyte and monocyte) and

Platelet adherence

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?Smooth muscle cel emigration and

proliferation
?Activated

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macrophages

releases free radicals

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that oxidizes LDL.

vLipid Engulfment by Macrophages

vOxidized LDL engulfed by

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Macrophages transform to form

Foam cel s

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vSubsequent development of an

atherosclerotic plaque with lipid

core

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Effects Of Oxidized LDL
? Oxidized LDL is Toxic to Endothelium:

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? Causes Endothelial loss

? Exposure of subendothelial tissue to blood

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components

? Chemotactic effect

? Lymphocytes and Monocytes

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? Smooth muscle cells from arterial media

? Stimulates production of Cytokines, adhesion

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molecules in endothelium;

? Inhibits endothelium derived releasing factor

(EDRF), favoring vasospasm

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? Stimulates specific immune system (production of

antibodies against oxidized LDL).

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? Activated Macrophages also ingest

oxidized LDL to become foam cel s,

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? Which are present in all stages of

atherosclerotic plaque formation.

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? Lipids released from necrotic foam

cel s accumulate to form lipid core

of unstable plaques/Fatty streaks.

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?Endothelial disruption

leads :

?Platelet adhesion and

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aggregation


?Fibrin deposition

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? Platelets and activated

macrophages release various

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factors that are thought to

promote growth factors

? This modulate proliferation of

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smooth muscle cells and

deposition of extracel ular

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matrix in lesions: Elastin,

Col agen, Proteoglycans.

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? Thus Connective tissue synthesis

and Calcium fixation

determinates stiffness of blood

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vessels.

? Which causes further ulceration

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of Atheromatous plaque.
Summary Of Pathogenesis Of

Atherosclerosis

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? Accumulation of Lipids in vessel wal
? Plasma Lipoproteins
? Low-density lipoproteins LDL
? LDL transported inside macrophages to vessel

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wal s

? Damage to Endothelium
? Adhesion of Macrophages
? Inflammation at the site

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?Fatty Streaks
?Foam cells
?Smal Thrombi
?Calcification

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? Plaque formation
?Ulceration
?Stiffening and Hardening

of blood vessels

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Building Up of Atherosclerotic Plaque

Lesions Associated with

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Atherosclerosis
? Lesions associated with Atherosclerosis are

of three types:

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?Fatty streak
?Fibrous Atheromatous plaque
?Complicated Lesion

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? Latter two are responsible for

clinical y significant manifestations

of disease.

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? More advanced complicated

lesions are characterized by:

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?Hemorrhage
?Ulceration
?Scar tissue deposits
? As a result of all pathogenic

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mechanism

? Atherosclerosis can be defined

as vicious inflammatory process.

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Modern Theory of Atherosclerosis
? Multifactor Theory:

?Structural and functional injury of vascular

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endothelium

?Role of lipoproteins in initiation and

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progression of lesions

?Response to injury of immune cel s and

smooth muscle cel s

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?Role of growth factors and cytokines in

inflammation

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?Role of repeated thrombosis in lesions

progression.

? Endothelial monolayer overlying an intima

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contacts blood.

? Hypercholesterolemia promotes accumulation of LDL

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particles (light spheres) in intima.

? Lipoprotein particles often associate with

constituents of the extracel ular matrix, notably

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proteoglycans.

? Sequestration within intima separates lipoproteins

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from some plasma antioxidants and favors oxidative

modification.

? Modified lipoprotein particles (darker spheres)

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may trigger a local inflammatory response responsible

for subsequent steps in lesion formation.

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? Increased expression of various adhesion

molecules for leukocytes recruits monocytes to the site

of a nascent arterial lesion.

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? Once adherent, some white blood cel s wil migrate

into intima.
? Migration of leukocytes probably

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depends on chemoattractant factors including modified

lipoprotein particles themselves and chemoattractant

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cytokines depicted by the smal er spheres, produced by

vascular wal cel s in response to modified lipoproteins.

? Leukocytes in evolving fatty streak can divide and

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exhibit increased expression of receptors for modified

lipoproteins (scavenger receptors).

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? These mononuclear phagocytes ingest lipids and

become foam cel s, represented by a cytoplasm fil ed

with lipid droplets.

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? As fatty streak evolves into a more complicated

atherosclerotic lesion, smooth-muscle cel s migrate

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from media (bottom of lower panel), through

internal elastic membrane (solid wavy line), and

accumulate within expanding intima where they lay

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down extracel ular matrix that forms the bulk of the

advanced lesion.

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Consequences Of Atherosclerosis

OR

Effects/Complications

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Of Atherosclerosis
? Atherosclerosis is a chronic

process

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? Atherosclerosis affects almost

al people with variable

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severity.

? Atherosclerosis develop over

several decades.

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? If Congenital in origin It may

starts as early as infancy and

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childhood,

? Progress very slowly during

life.

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? Atherosclerosis contributes

to more mortality and

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? More serious morbidity than

any other disorder in the

western world.

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? Atherosclerosis affects the

intimal lining of endothelium

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of

? Large and Medium-sized

elastic and muscular arteries

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of body.
?Atherosclerotic plaque

formation

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?Narrows diameter of

blood vessel lumen.

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? Atherosclerosis leads to the

narrowing or complete blockage of

arteries /Occlusion by:

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?Endothelial Dysfunction

?Lipid deposition

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?Inflammatory reaction in vascular

wal

?Ulcerative Lesions

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Atherosclerosis Brings Alterations Of Arteries :

? Aneurysm-Excessive localized swelling of

blood vessel

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? Stenosis-Abnormal narrowing of vessel

? Occlusion-Closing of blood vessel

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? Thrombosis-Local clotting of blood

? Embolism -blockage of vessel by lodging

of blood clot/fat globule

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? Fissure-Small tear with bleeding

? Ulceration-Removal of top layer

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? Calcification- Accumulation of Calcium

Salts

? Atherosclerosis , can and does, occur

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in almost any artery in the body.

? Atherosclerosis of coronary arteries is

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very crucial

? This blocks,blood circulation to Heart

? Which fails cardiac muscle to sustain.

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? Atherosclerosis leads to disease

of cardiovascular system

affecting blood vessel wal .

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? Causing Ischemic Heart Disease

which is leading cause of death

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in developed countries.

Complications of

Atherosclerosis

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? 1. Acute Occlusion:

Thrombosis

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Occlusion

Ischemia, Infarction

? 2. Chronic Stenosis:

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Chronic ischemia

Atrophy

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Eg. Renal atrophy in renal artery stenosis, ischemic

atrophy of skin in DM
? 3. Aneurysm Formation:

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Extension to media
Aneurysm
Aneurysmal rupture eg. Abdominal

aortic aneurysm

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? 4. Embolism:

Of atherosclerotic plaque or of

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thrombi

? Thrombosis is most important

complication of Atherosclerosis.

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? It is caused by slowing and

turbulence of blood flow in region

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of plaque and ulceration of plaque.
PHYSIOPATHOLOGICAL

CONSEQUENCES OF THE PLAQUE

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v Coronary Artery Disease (CAD) : Angina, MI

v Cerebro Vascular Disease (CVD)

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v Peripheral Artery Disease (PAD)

v Ischemic Stroke (Brain infarct)

v Secondary Erectile Disorder (ED)

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v Chronic Renal Ischemia ( Renal failure)

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? Atherosclerosis commonly

leads to:

?Myocardial infarction

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?Stroke

?Gangrene of extremities
Biochemical Alterations

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In Atherosclerosis

Biochemical Basis Of Atherosclerosis

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? Low Blood supply to Cells/Tissues
? Low Nutrient and Oxygen Supply to cells
? Low Metabolism in cells
? Low Oxidative Phosphorylation
? Low ATP production in cells

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? Low Cellular Activity
? Cellular/Tissue/Organ Dysfunction
? Irreversible Damage of cells/tissues/organ/system
Diagnosis Of Atherosclerosis

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? Checking Lipid Profile/Lipoproteins
? B.P
? ECG
? Angiography
? EEG

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? Color Doppler
? MRI
Management Of Atherosclerosis

? Reducing the risk factors

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? Correcting the underlying causes
? Angioplasty
? Other Surgeries

Reduction Of Atherosclerosis Risk

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Risk of atherosclerotic event can be

decreased by:

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?Normal Balanced diet

?Physically active life

?Regular Exercise

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?Smoking cessation

?Control of high blood pressure

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?Intake of Antioxidants

?Drugs Statins, Ezetimibe

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Development of Atherosclerosis

Process of Atherogenesis

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Progression of CHD

Damage to

endothelium and

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invasion of

macrophages

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Smooth muscle

migration

Cholesterol

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accumulates

around

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macrophage and

muscle cel s

Collagen and

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elastic fibers

form a matrix

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around the

cholesterol,

macrophages

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and muscle cel s

Pathogenesis of Coronary Heart Disease (CHD)
Monocyte Recruitment

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LDL

lumen

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intima

Plaque Rupture and Thrombosis

Tissue Factor

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Platelet Aggregation

Lipid Core
NO Inactivation Due to Oxidative Stress

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Sch?chinger V., Zeiher A.M.: Nephrol Dial Transplant (2002): 2055

Sch?chinger V., Zeiher A.M.: Nephrol Dial Transplant (2002): 2055

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Process of Atherogenesis ? an overview


Formation of Atherosclerotic Plaques

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lumen

neointima

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Lipid Core

Plaque Build up in Artery

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Overview of Artery

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Cardio Vascular Disorders (CVD)

Coronary Artery Disease (CAD)

OR

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Coronary Heart Disease(CHD)

OR

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Ischemic Heart Disease(IHD)
Coronary Heart Disease

? Term Coronary Heart Disease

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(CHD) describes Heart disease

caused by impaired coronary

blood flow.

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? In most cases, it is caused by

Atherosclerosis of coronary

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arteries which supply

Myocardium.

Clinical Manifestations

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?Clinical manifestations of

Atherosclerosis depend on:

?Vessels involved

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?Extent of vessel obstruction

? Atherosclerotic Lesions produce their

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effects through:

?Narrowing of the blood vessel and

production of Ischemia;

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?Sudden vessel obstruction caused by

Plaque hemorrhage or rupture;

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?Thrombosis and formation of emboli

resulting from damage to the vessel

endothelium;

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Coronary Artery Diseases Can cause:

?Angina/Chest Pain

?Myocardial Infarction /Heart attack

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?Cardiac dysrhythmias

?Conduction defects

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?Heart failure

?Sudden death

Myocardial Infarction

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Myocardial Infarction

? MI is an irreversible damage

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to Myocardium(Heart tissue)

? Acute myocardial infarction

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(AMI), also known as a heart

attack
?AMI is caused due to

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associated

Atherosclerotic disease

of the coronary arteries.

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Risk Factors OF MI

Uncontrollable

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Control able

?Sex

?High blood pressure

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?High blood cholesterol

?Hereditary

?Smoking

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?Race

?Physical activity
?Obesity

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?Age

?Diabetes
?Stress and Anger

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Screening and Diagnosis

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re

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fic

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Stress

Coronary

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a
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ect

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cardiogram

Test

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Angiography

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f

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to hear

ulses

ply

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Narrowing in

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Diagnosis Of MI

1. Pain

? Severe and Crushing,

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? Constricting, Suffocating.

? Usual y is Sub Sternal, radiating to the left

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arm, neck, or jaw

? Gastrointestinal Complaints

?Sensation of Epigastric distress

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?Nausea and Vomiting
ECG

? Elevation of the ST segment

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usually indicates acute myocardial

injury.

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? When the ST segment is elevated

without associated Q waves, it is

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called a Non?Q-wave Infarction.

Diagnostic Biochemical Markers Of MI

Enzymes and Proteins

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? Lipid Profile

? CK ?MB

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? AST

? LDH 1 and LDH2

? Trop T and Trop I

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? Myoglobin

? Homocysteine

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? hs CRP

? LP-PLA2
? Creatine kinase (CK), formerly called creatinine

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phosphokinase, is an intracellular enzyme found

in muscle cells. Muscles, including cardiac

muscle, use ATP as their energy source.

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? Creatine Phosphate, which serves as a storage

form of energy in muscle, uses CK to convert

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ADP to ATP.

? CK exceeds normal range within 4 to 8 hours of

myocardial injury and declines to normal within

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2 to 3 days.

? There are three isoenzymes of CK, with the MB

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isoenzyme (CK-MB) being highly specific for

injury to myocardial tissue.

? Myoglobin is an Oxygen-Storing Protein, that is

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normally present in cardiac and skeletal muscle.

? It is a small molecule that is released quickly from

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infarcted myocardial tissue and becomes

elevated within 1 hour after myocardial cell

death, with peak levels reached within 4 to 8

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hours.

? It rapidly eliminates through urine (low

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molecular weight).

? Because myoglobin is present in both cardiac and

skeletal muscle, it is not cardiac specific.

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? Troponin complex consists of three subunits

? Troponin C

? Troponin I

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? Troponin T

? These subunits are released during myocardial

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infarction.

? Cardiac muscle forms of both Troponin T and

Troponin I are used in diagnosis of myocardial

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infarction.

? High sensitive Cardiac Troponin I is current

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Biomarker validation in research of early

diagnosis of AMI

? Troponin I (and Troponin T) rises more

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slowly than myoglobin

? This may be useful for diagnosis of

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infarction, even up to 3 to 4 days after the

event.

? It is thought that cardiac Troponin assays

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are more capable of detecting episodes of

myocardial infarction in which cel damage

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is below that detected by CK-MB level.
Effects of Acute Myocardial

Infarction (AMI)

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? The principal biochemical

consequence of AMI is

? The conversion from aerobic to

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anaerobic metabolism

? With inadequate production of

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energy(ATP) to sustain normal

Myocardial function.

? Ischemic area ceases to

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function within a matter of

minutes, and

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? Irreversible Myocardial cell

damage occurs after 20 to 40

minutes of severe ischemia.

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Treatment

? Reperfusion

? (Re-establishment of blood flow)

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? Thrombolytic therapy

?Streptokinase/ Urokinase

? Revascularization procedures

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?Early Reperfusion (within 15 to

20 minutes) after onset of

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ischemia can prevent necrosis.

?Reperfusion after a longer

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interval can salvage some of the

myocardial cells that would have

died because of longer periods of

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ischemia.

Treatment 1) Stenting

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? A Stent (narrow expandable tube) is introduced into a blood vessel on

a bal oon catheter and advanced into the blocked area of the artery
? The bal oon is then inflated and causes the stent to expand until it fits

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the inner wal of the vessel, conforming to contours as needed
? The bal oon is then deflated and drawn back
?The stent stays in place permanently, holding the vessel open and

improving the flow of blood.

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Treatment 2) Angioplasty

?Bal oon catheter is passed through the guiding catheter to the area

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near the narrowing. A guide wire inside the balloon catheter is then

advanced through the artery until the tip is beyond the narrowing.
? The angioplasty catheter is moved over the guide wire until the

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balloon is within the narrowed segment.
? Balloon is inflated, compressing the plaque against the artery wall
? Once plaque has been compressed and the artery has been

sufficiently opened, the balloon catheter will be deflated and removed.

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Treatment

3) Bypass surgery

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? healthy blood vessel is removed from leg, arm or chest
? blood vessel is used to create new blood flow path in your heart
? the "bypass graft" enables blood to reach your heart by flowing

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around (bypassing)

the blocked portion of

the diseased artery.

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The increased blood

flow reduces angina

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and the risk of heart

attack.

Peripheral Arterial Disease (PAD)

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Peripheral Arterial Disease (PAD)

? PAD refers to the obstruction of

large arteries in lower extremities

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of leg

? It possess, inflammatory

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processes leading to stenosis, an

embolism, or thrombus formation.

Risk of PAD

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? Risk of PAD also increases in

individuals who are:

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?Over the age of 50
?Male Obese
?With a family history of vascular

disease, heart attack, or stroke.

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Symptoms OF PAD

? About 20% of patients with mild PAD may be

asymptomatic;

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? Symptoms of PAD include:

? Pain, weakness, numbness, or cramping in muscles

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due to decreased blood flow

? Sores, wounds, or ulcers that heal slowly or not at all

? Noticeable change in color (blueness or paleness) or

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temperature (coolness) when compared to the other

limb

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? Diminished hair and nail growth on affected limb and

digits.
Prevention Of Dyslipidemias

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And Its

Consequences And Complications

Live Sensible Implement

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?Get regular medical checkups
?Eat a Heart-Balanced healthy diet
?Control your blood pressure
?Check your Blood Cholesterol

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?Don't smoke and drink Alcohol
?Exercise regularly
?Maintain a healthy weight
?Manage stress

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THE HEALTHY PLATE

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FOODS THAT LOWER LDL

CHOLESTEROL

1. Oats

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2. Barley and Whole grains

3. Beans

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4. Eggplant and okra

5. Nuts

6. Vegetable oils (canola, sunflower, safflower)

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7. Apples, grapes, strawberries, citrus fruits

8. Soy

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9. Fatty Fish

10. Fiber supplements
qEat meat sparingly

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qAdd Fish to your diet

qGo for Nuts

qEat Fruits and Vegetables

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qIncrease Complex Carbohydrates and fiber

qOpt for low-Fat dairy products

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qCut down on Saturated fat in cooking

qAvoid Palm and Coconut oils ( Rich in SFAs)

qAvoid Trans Fats

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qReduce Dietary Cholesterol

qReduce Salt intake

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qWatch the Snacks

Blood Cholesterol levels increase

by eating these products

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? Refined Sugars
? Beef
? Poultry
? Fish

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? Milk
? Eggs
? Cheese
? Yogurt
EXERCISE

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qAerobic exercise (jogging, swimming, brisk walking,

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bicycling, etc)

STRESS REDUCTION STEPS

? Be Spiritual

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? Balance All Actions

? Make and Fol ow Right protocols

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? Be Planned and Organized

? Manage works based on priority

? Involve In work which you are chosen for

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? Be Obedient and Have Patience

? Be Happy with what get

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? Not expect too much in life

? Repent, Accept But Do Not Repeat

? Ventilate And Communicate

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Summary To Prevent

? Eat right

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? Watch your weight -even a modest drop in

weight can make a difference

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? Be Active - start a program of light exercise

for at least 30-45 minutes every day

? Lower your stress levels. Practice stress

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reduction techniques

? Stop smoking and drinking alcohol

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? Be Spiritual

Avoid

Promote

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Unhealthy eating

Healthy eating

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Visit your doctor

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Relaxation

regularly

Check your weight

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Balance intake with output

Exercise regularly

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Inborn Errors Of Lipid Metabolism
Inborn Error Of Enzyme

Abnormal

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Lipid

Deficient/

Accumulation

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Metabolism

Defect

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Of

Sudden Infant

Acyl CoA

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Acyl CoAs

Death Syndrome

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Dehydrogenase

(SIDS)

Refsums Disease

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-Phytanic Acid Phytanic Acid

Oxidase

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Zellwegers

Peroxisomal

VLCFAs in

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Syndrome

Oxidation

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Peroxisomes

Inborn Error

Enzyme Defect

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Abnormal

Lipid Storage

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Accumulation Of

Disorders

Niemann Picks

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Sphingomyelinase Sphingomyelin in

Disease

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Liver and Spleen

Tay Sachs Disease Hexoseaminidase Gangliosides in

Defect

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Tissues

Gaucher's Disease eta Glucosidase Glucosides in Tissues
Inborn Enzyme

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Abnormal

Error

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Defect

Accumulation Of

Krabbe's Beta

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Disease Galactosidase Galactocerebroside

Farbers Ceramidase

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Ceramides

Disease

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Role Of Insulin In Lipid Metabolism

? Insulin

? Stimulates LPL

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? increased uptake of FA

from Chylomicrons and

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VLDL

? Stimulates Glycolysis

? increased glycerol

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phosphate synthesis

? increases esterification

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? Induces HSL-phosphatase

? inactivates HSL

? Inhibits Lipolysis

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? Net effect: TG storage

? Lack of Insulin

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?Free Fatty acids build up in

blood

?Can lead to excess Acetoacetic

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acid production and buildup of

acetone (acidosis, which can

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lead to blindness and coma)
Insulin

Most Cel s

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amino

Control

Protein synthesis

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acids

Muscle

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Glucose uptake

Glycogen synthesis

Gastrointestinal

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hormones

triglycerides

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Adipose

Glucose uptake

Glycerol production

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Triglyceride breakdown

Amino

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Pancreas Insulin

Triglyceride synthesis

acids

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Beta cells

Liver

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Blood

Glucose uptake

glucose

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glucose

Glycogen synthesis

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Fatty acid synthesis

Glucose synthesis

Brain

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No effect

Feedback

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Glucagon

Control

Adipose

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Triglyceride breakdown

Fatty acids

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? Triglyceride storage

Exercise

Amino acids

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Pancreas

Alpha cells

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Liver

Glycogen breakdown

Glucose synthesis

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Blood glucose

Epinephrine

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Glucose release

(stress)

Brain

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No effect


Types Of Lipases

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S.

Type Of Lipase

Location

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No

Action Upon

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1

Lingual Lipase

Mouth

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Dietary TAG

(Insignificant Action)

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2

Gastric Lipase

Stomach

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Dietary TAG

(Insignificant Action)

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3

Pancreatic Lipase

Smal Intestine

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Dietary TAG

(Significant Action)

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S. Type Of Lipase

Location

No

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Action

4

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Lipoprotein Lipase

Endothelial Lining

Of Blood Vessels

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Lipoprotein TAG

5

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Hormone Sensitive

Adiposecytes

Lipase

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Hydrolyzes

Stored TAG

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6

Hepatic Lipase

Liver

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TAG

7

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Phopshpholipase A2 Small Intestine

Phospholipids
Questions

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Q.1. Describe in details the digestion

& absorption of dietary form of lipids

& add a note on Steatorrhoea

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OR

Q.1.What are different forms of

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dietary lipids? How the dietary lipids

are digested & absorbed in G.I.T ?
Q.2. What are the different modes of oxidation of

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fatty acids in the body? Give -oxidation of even

chain fatty acid.

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OR

Q.2. Define -oxidation of fatty acid. Explain the

oxidation of Palmitate and calculate its

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energetics./Fate of fatty acids in human body?

OR

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Q.2. Explain -oxidation of odd chain fatty acids.

Q.3. What is Lipogenesis? Describe in

details the De-novo synthesis of fatty

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acid.

OR

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Q.3. Explain the Extra mitochondrial

synthesis of Palmitate.
Q.4. What is ketoacidosis? Give fate &

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formation ketone bodies.
? Short Notes

? Transport & storage of lipids / Role

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lipoproteins.

? Emulsification & its significance / Role of

Bile salts in digestion & absorption of lipid.

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? Lipolysis / Role of Hormone Sensitive

Lipase/Adipose tissue metabolism.

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? Clearing factor / Lipoprotein

lipase.

? Multi-enzyme complex of Fatty

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acid biosynthesis / Fatty acid

synthesis complex.

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? Microsomal synthesis of fatty acid.
? Fatty liver /Lipotropic factors.
? Cholesterol-outline of Biosynthesis.

? Hypercholesterolemia ? causes &

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consequences

? Atherosclerosis

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? Myocardial Infarction

? Enumerate the Inborn errors related to

lipid metabolism.

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? Transport & Excretion of Cholesterol/

Reverse transport of cholesterol.

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? Fate & formation of Acetyl?CoA
? Fate of Propionyl-CoA
? Role of Carnitine in Lipid metabolism
? Role of Liver in Lipid metabolism.
? TAG metabolism.

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? Ketonemia & Ketonuria
? Represent the schematic structure of

lipoprotein.

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? Role of Citrate in lipid metabolism.
? Role of Carnitine in lipid metabolism.
? Hormonal Influence in Lipid

Metabolism

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? Catabolism of Cholesterol.
? CETP activity
? HDL2 and HDL 3
? Zellweger & Refsum's disease.

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? Mixed Micelle
? Four types of Lipoproteins & their role
? Hyperlipoproteinemias
? Hypolipoproteinemia's
? Different types of Lipases & their action.

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Biochemistry Department