1. Dr. Saurabh kr. Bajpai
M.V.Sc. scholar
Division- Animal
Nutrition
I.V.R.I. Bareilly

2. 1.Atherosclerosis definition
2.Risk factors in atherosclerosis
3.Atherosclerotic plaque formation
4.PUFAs
5.Role of PUFA in Atherosclerosis
6.New endogenous anti-inflammatory and
proresolving lipid mediators
7.Conclusion

3. Atherosclerosis
The
thickening
and hardening
of arterial
walls as a
consequence
of atheroma

4. Risk Factors in Atherosclerosis
Major risk factors
1) Major Constitutional risk factors:
i. Age
ii. Sex
2) Major Acquired risk factors:
i. Hyperlipidaemia
ii. Hypertension
iii. Diabetes mellitus

5. Minor Risk Factors:
1. Obesity
2. Hormones: Oestrogen deficiency
3. Physical inactivity
4. Stressful life

15. PUFAs
PUFA stands for Poly-Unsaturated Fatty Acid. In
chemical terms, that means that the fatty acid has
more than one (poly) double bond in the carbon
chain
There are two main types of PUFA’s —
 omega-3 polyunsaturated fatty acids
omega 6 polyunsaturated fatty acids.

16. Omega-3 Fatty Acids
ALA C18:3
EPA C20:5
DHA C22:6

17. Omega-6 Fatty Acids
Linoleic acid C18:2
Arachidonic acid C20 :4

18. Protective role of n-3 PUFA in
atherosclerosis
1. Resolation of inflammatory process
2. Change in biological function of cell
membrane
3. Plaque stabalization
4. Change in serum lipid profile
5. Improved flow mediated arterial dilation
6. Antithrombotic

19. HOW n-3 PUFA reduses inflammation?
 Compete with n-6 fatty acids for
prostaglandin
and leukotriene synthesis
 Bind reactive oxygen species

20. Omega-3 F.A.
Omega-3 F.A.
Omega-6 F.A.
Omega-6 F.A.
CYCLOOXYGENASE/LIPOXYGENASE Pathway
CYCLOOXYGENASE/LIPOXYGENASE Pathway
PGE3,LTB5
PGE3,LTB5
(anti-inflammatory)
(anti-inflammatory)
PGE2,LTB4
PGE2,LTB4
(pro-inflammatory)
(pro-inflammatory)

21. Bind with reactive oxygen
species
Decreased production of H2O2
Inhibition of nuclear factor-κB system of
transcription factors

22. n3- PUFA
n3- PUFA
NF-κB
NF-κB
Chemokines,Cytokines,ROS
Chemokines,Cytokines,ROS
Vasoconstriction
Vasoconstriction
Adhesion molecules
Adhesion molecules
Endothelial protection

23. Cytokines
Cytokines
ROS
ROS
NF-κB
NF-κB
Chemokines&Cytokines
Chemokines&Cytokines
Vasoconstriction
Vasoconstriction
Adhesion molecules
Adhesion molecules
Endothelial dysfunction

25. 2.Change in biological function of cell
membrane
Incorporation of EPA and DHA in to CM
Influences it,s organisation,fludity, and
permeability
Modulate K,Na,andCa channel activities
Induction of NO release

26. 3.Plaque stabalization

27. 4.Change in serum lipid profile
Omega-3 fatty acids decrease hepatic VLDLTG production and secretion
Omega-3 fatty acids increase the conversion
of VLDL to LDL particles

28. F.A.
DGAT
VLDL
β-oxidation
Acetyl CoA
HDL

29. Anti-inflammatory and proresolving
lipid mediators generated from PUFAs
Lipoxins
Resolvins
Protectin
Maresin

30. CONCLUSION
Through their positive antithrombotic, lipidlowering, proendothelial functional activities, n-3
PUFAs play an important role on the
mechanisms of atherosclerosis
LC-n3-PUFAs significantly interact with
inflammation-related mechanisms, such as
endothelial activation, modification of eicosanoid
metabolism, and resolution of the inflammatory
process

31. REFERENCES
1.Emken EA. In: Proceedings from the Scientific Conference on Omega-3 Fatty Acids in Nutrition,
Vascular Biology, and Medicine. Dallas, TX: American Heart Association, 1995, pp. 9-18.
2.Horrobin DF and Manku MS. In: Omega-6 Essential Fatty Acids. Horrobin DF, ed. New York, NY:
Alan R. Liss, 1990, pp. 21-53.
3.Ferretti A and Flanagan VP. Prostaglandins Leukot Essent Fatty Acids. 1996;54:451-455.
4. Ratnayake WMN and Chen Z-Y. Lipids. 1996;31(Suppl):S279-S282.
5.Ackman RG and Cunnane SC. In: Advances in Applied Lipid Research. Padley FB, ed. London: JAI
Press Ltd., 1992, pp. 167-215.
6. Houwelingen AC v and Hornstra G. World Rev Nutr Diet. 1994;75:175-178.
7. Salem Jr N, et al. Lipids. 1996;31(Suppl):S153-S156. 16. Brossard N, et al. Am J Clin
Nutr. 1996;64:577-586.