Cholesterol is a lipid that is essential for cell membrane structure and hormone production. It is synthesized through a metabolic pathway and regulated at the rate-limiting step by HMG-CoA reductase. High cholesterol levels can lead to atherosclerosis, a hardening of the arteries due to plaque buildup. Plaque forms when cholesterol builds up in artery walls as macrophages take up cholesterol and become foam cells. Over time, plaque can narrow arteries and risk blockages leading to heart attacks and other problems. Risk factors for high cholesterol and atherosclerosis include diet, obesity, smoking, and other lifestyle and genetic factors.

1. CHOLESTEROLAND
ATHEROSCLEROSIS

2. PRESENTED BY:
SMRITI AULAKH
SUKHLEEN KAUR
SUKHMANI
SUPREET KAUR
TARANVIR KAUR
YAISHWAR SRAN

3. Cholesterol
– The word cholesterol is derived from greek word “chole”
=Bile, “steros”= solid, “ol” =alcohol.
– Choleterol is widely distributed in animal tissues but is
absent in plants.
– It is soluble in chloroform and fat soluble vitamins

4. Structure of Cholesterol
– Cholesterol has cyclopentanoperhydrophenanthrene ring
system
– Total 27 carbon, one OH group at third position double
bond between C-5 &C-6.
– An eight carbon β-oriented side chain is attached to 17th
carbon.
– Two methyl groups attached at position 10 & 13.

6. Functions of Cholesterol
– It is a component of cell membrane.
– It is used to insulate nerve fibers.
– Bile acids and bile salts are derived from cholesterol.
– It is a precursor for steroid hormones & Vitamin D3.

7. BIOSYNTHESIS OF
CHOLESTEROL
– It is also known as De-Novo synthesis,which means
synthesis from raw materials.
– Almost all nucleated cells (including arterial walls) can
synthesise cholesterol.
– Equal amounts of cholesterol are obtained from diet and
de-novo synthesis.
– It requires single precursor acetyl-CoA.It also requires
reducing equivalents that are supplied by NADPH which is
formed during HMP shunt.

10. REGULATION
– It mainly regulated at the level of HMG-CoA
reductase,which is a rate limiting enzyme.
– Regulation occurs by two means:Feedback and Hormonal
regulation.
– FEEDBACK REGULATION: The end product of the
pathway,cholesterol,and already stored cholesterol esters
inside the cell, controls the de novo synthesis by feedback
mechanism at the level of transcription of gene HMG CoA
reductase.

11. HORMONAL
REGULATION

12. DEGRADATION OF
CHOLESTEROL
Cholesterol does not degrade to release energy unlike most
of the other biomolecules. It has a different fate
alltogether.
1. Synthesis of bile acids
2. Synthesis of steroid hormone
3. Synthesis of vitamin D

14. ATHEROSCLEROSIS
– ‘Athero’ means artery, ‘sclerosis’ means hardening.
– Atherosclerosis is a result of hypercholesterolemia.
– Coronary artery disease and myocardial infarction due to
atherosclerosis top the list of killer diseases of the world.
– In india,20% deaths are due to CAD. It is estimated that it
will increase to 33% by 2020.

16. CAUSES OF
HYPERCHOLESTROLEMIA
– Obesity
– Diet rich in cholesterol
– Diabetes mellitus
– Hypothyroidism
– Obstructive jaundice

17. FORMATION OF
PLAQUE
– STAGE 1- The increased level of cholesterol causes
overloading of macrophages with cholesterol in arterial
wall, known as foam cells.
– STAGE 2- PROGRESSION OF ATHEROSCLEROSIS: In this,
smooth muscle cells containing lipid droplets are seen in
the lesion.
– STAGE 3- FIBROUS PROLIFERATION: Due to liberation of
various growth factors by macrophages, collagen is
accumulated. Thus, their is definite component of
inflammation in atherosclerosis.

18. – STAGE 4- ADVANCING FIBROUS PLAQUE: This leads to the
narrowing of vessel walls when proliferative changes
occur. The blood floe through the narrow lumen is more
turbulent and their is tendency of clot formation.

19. RISK FACTORS
– Low HDL level
– High LDL level
– Lipoprotein a
– Smoking
– Diabetes mellitus
– Hypertension
– Obesity and sedentary lifestyle

20. MYOCARDIAL
INFARCTION
This is the ultimate risk of atherosclerosis. A clot is formed,
which occludes major vessels. Thrombosis in coronary
artery leads to ischemia of cardiac tissue due to hindrance
in O2 supply. Eventually, infarction(death of tissue) occurs
resulting in inefficient blood supply to the body ,leading to
death of the individual.

21. PREVENTION OF
ATHEROSCLEROSIS
– Reduce dietary cholesterol
– Intake of vegetable oils and PUFA
– Intake of green leafy vegetables
– Avoid sucrose and cigarette
– Regular exercise
– Avoid trans fatty acids
– Hypolipidemic drugs

23. QUESTIONS??
Q. Which ring system is present in
cholesterol structure?
Q. Which is the rate limiting step of
cholesterol synthesis?
Q. At what level of gene expression does
feedback inhibition of HMG reductase
enzyme is regulated?

24. Q. In which form HMG CoA reductase is
active?
Q. Which is the only way of excretion of
cholesterol form?