Role of pufa in atherosclerosis


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Role of pufa in atherosclerosis

  1. 1. Dr. Saurabh kr. Bajpai M.V.Sc. scholar Division- Animal Nutrition I.V.R.I. Bareilly
  2. 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. 3. Atherosclerosis The thickening and hardening of arterial walls as a consequence of atheroma
  4. 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. 5. Minor Risk Factors: 1. Obesity 2. Hormones: Oestrogen deficiency 3. Physical inactivity 4. Stressful life
  6. 6. 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.
  7. 7. Omega-3 Fatty Acids ALA C18:3 EPA C20:5 DHA C22:6
  8. 8. Omega-6 Fatty Acids Linoleic acid C18:2 Arachidonic acid C20 :4
  9. 9. 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
  10. 10. HOW n-3 PUFA reduses inflammation?  Compete with n-6 fatty acids for prostaglandin and leukotriene synthesis  Bind reactive oxygen species
  11. 11. 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)
  12. 12. Bind with reactive oxygen species Decreased production of H2O2 Inhibition of nuclear factor-κB system of transcription factors
  13. 13. n3- PUFA n3- PUFA NF-κB NF-κB Chemokines,Cytokines,ROS Chemokines,Cytokines,ROS Vasoconstriction Vasoconstriction Adhesion molecules Adhesion molecules    Endothelial protection
  14. 14. Cytokines Cytokines ROS ROS NF-κB NF-κB Chemokines&Cytokines Chemokines&Cytokines Vasoconstriction Vasoconstriction Adhesion molecules Adhesion molecules    Endothelial dysfunction
  15. 15. 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
  16. 16. 3.Plaque stabalization
  17. 17. 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
  18. 18. F.A. DGAT VLDL β-oxidation Acetyl CoA HDL
  19. 19. Anti-inflammatory and proresolving lipid mediators generated from PUFAs Lipoxins Resolvins Protectin Maresin
  20. 20. 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
  21. 21. 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.