1. ELONGATION, DESATURATION of FATTY ACIDS
The Department of Biochemistry
of Medical Faculty
Presents now
ELONGATION, DESATURATION of FATTY ACIDS
and FORMATION of ACTIVE MOLECULES
Edited by Attila Sandor

2. Mechanism of fatty acid elongation in animal cells
CH3-(CH2)14-CO-SCoA + OOC-CH2-CO-SCoA
acyl-CoA
malonyl-acyl-CoA
CO2
Elongation system located in the ER
HSCoA
CH3-(CH2)14-CO-CH2-CO-SCoA
2 NADPH2
H2O
Reduced to saturated C18 stearic acid
via three basic ezymes of fatty acid synthesis
Fatty acids are elongated on the head
Elongation system acts on CoA esters rather than on ACP-esters
Elongation system also uses malonyl-CoA as acceptor
Authors`picture

3. Mechanism of fatty acid desaruration in animal cells
O-O 4-
Belongs to the “mixed- function oxidases”, that is,
oxidases two substrate at the same time
Acts on CoA esters in the ER togethe with the Cyt b5 reductase
Intoduces duoble bonds before the 9th carbon atomin cis position
Lehn.,4th ed p. 799

4. Action of plant desaturases
The plant desaturases enzymes act on
fatty acid chains in phosholipids rather
than on CoA esters and introduce
double bounds before and after the 9th
carbon atom.
Lehn.,4th ed p. 800

5. Formation of the most important fatty acids
via combination of elongation and
desaturation
animals can put double bond only
before the 9th C atom
advantage of the w system:
after elongation the numbering does not turn upside down
w 6,9,12
w 6,9,12
w 6,9,12,15
Lehn.,4th ed p. 797

6. a
Strayer 3rd edition,20-19, p.490

7. CONCLUDING REMARKS
The overall equation of the synthesis of a palmitic acid :
7malonylCoA + 1AcCoA + 14 NADPH2  CH3-(CH2)14–COOH + 7 CO2 + 14NADP+ +6H2O + 8CoA
The fatty acids are elongated at the head by C2 untits
thus, the most fatty acids are even numbered.
The cytosolic fatty acid synthase enzyme synthetises
only palmitic acid.
The longer and/or unsaturated fatty acids are formed by
different microsomal enzymes
The odd-numbered fatty acids are synthtised when AT accepts
proponyl-CoA by mistake

8. Spliting sites of phospholipases
Lehn.,4th ed p. 355

9. Source of arachidonic acid
Arachidonic acid (20:4, w 6,9,12,15) is the parenthal compound of many
biologically active fatty acid derivatives. It is located in membrane
phosholipids and released by phosholipase A2.
Steroids
Lehn.,4th ed p. 358

10. Biologically active derivatives of arachidonic acid
Anti-inflamatory drugs
inhibit:
Prostaglandins
Steroids:
Prostaglandins
Tromboxans
Leukotriens
Non-steroids:
Prostaglandins
Tromboxans
Steroids
Aspirin
Tromboxans
Cyclooxygenase
COX I,II
Lipoxygenase
Leukotriens
Unknown author

11. Non-steroids (aspirin) inhibit:
Lehn.,4th ed. p. 888
Steroids
Steroids inhibit:
Prostaglandins
Tromboxans
Leukotriens
Non-steroids (aspirin)
inhibit:
Tromboxans
Prostaglandins
Non-steroids
(aspirin)
lipoxygenase
Cyclooxygenane (COX I,II

12. Mechanism of action of non-steroid
(e.g.aspirin) anti-inflamatory drugs

13. Lehn.,4th ed /b p. 801

14. Structure of Phosphatidic acid
Lehn.,4th ed.10-8 p. 350

15. Lehn.,4th ed.10-8 p. 350

16. Phosphatidylinositol 4,5 bisphosphate,
Two major roles of inositol-phosphates as second messengers
Spliting by phospholipase C
Phosphatidylinositol 4,5 bisphosphate,
PIP2
Phosphatidyl-inositol 3 kinase
P I 3 K (enzyme)
Diacyl-glycerol,
DAG
Inositol 1,4,5, triphosphate
IP3
Phosphatidyl-inositol 3,4,5 trisphosphate,
PIP3
Author`s picture

17. Actions of IP3 and DAG
Lehn.,4th ed , p. 443

18. PIP3 mediating the intracellular actions of insulin
Author`s
picture
IRS=insulin receptor substrate; GSK3=glycogen synthase kinase 3;
PKB/Akt= protein kinase B; GS= Glycogen synthase;

21. THANK YOU FOR YOUR ATTENTION
The honored audience has the opportunity now to
download
the pictures of this lecture
from here or from the intranet ActiveMoleculesfromFatty Acids.ppt
Attila Sandor