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Fatty Acid Oxidation

  1. Oxidation of fatty acids generates the high-energy compounds reduced NAD (NADH) and reduced flavin adenine dinucleotide (FADH2) and yields acetyl CoA.
  2. In β-oxidation two carbons are cleaved at a time from acyl-CoA molecules, starting at the carboxyl end. The chain is broken between the α(2)- and β(3)- carbon atoms, hence the name β-oxidation.

Site : Mitochondria

1. Activation of fatty acids


  Thus in effect, 2 high energy phosphates are expended during activation of each fatty.


2. Role of carnitine: Long chain fatty acyl CoAs cannot freely diffuse across the inner mitochondrial membrane. Carnitine in the inner mitochondrial membrane mediates transfer of fatty acyl groups from the cytosol to the mitochondrial matrix where they are oxidized.


3. Pathway of -oxidation. In the mitochondrial matrix, long-chain fatty acyl CoAs are subjected to a repeated four-steps process that successively removes two-carbon units from the chain untill the last two-carbon fragment remains. Each cycle of β oxidation generates one FADH2 and one NADH. 16 carbon Palmitic acid will undergo 7 cycles of β-oxidation. Total 8 Acetyl CoA is formed.

4.  Stoichiometry of
β-oxidation of Palmitic acid


Recent advances


Palmitic acid undergoes β-oxidation 7 cycles

Therefore 7 NADH &  7 FADH2



This gives 7X2.5 +7X1.5 = 17.5 + 10.5 = 28 ATPs

Total 8 Acetyl CoA is formed            



Therefore 8X10=80 ATPs

Therefore ATPs = 28+80=108

Initially 2 ATPs consumed for activation



Therefore Net gain = 108-2 = 106 ATPs


Oxidation of Fatty Acids With an Odd Number of Carbon Atoms

  1. They undergo Β-oxidation as acyl CoA derivatives until a three-carbon fragment, propionyl coa, is formed.
  2. Propionyl CoA is carboxylated to methylmalonyl CoA by biotin-dependent propionyl CoA carboxylase.
  3. Methylmalonyl CoA is converted to succinyl CoA by methylmalonyl CoA mutase.
  4. Succinyl CoA can be metabolized via the citric acid cycle.

α- And ω Oxidation of Fatty Acids

-oxidation, i.e., the removal of one carbon at a time from the carboxyl end of the molecule, has been detected in brain tissue. It does not require CoA intermediates and does not generate high-energy phosphates.


ω -oxidation, is normally a minor pathway and is brought about by hydroxylase enzymes involving cytochrome P450 in the endoplasmic reticulum.


1.  Peroxisomes Oxidize Very Long Chain Fatty Acids

  1. A modified form of β oxidation is found in peroxisomes and leads to the formation of acetyl-CoA and H2O2 (from the flavoprotein-linked dehydrogenase step), which is broken down by catalase. 
  2. this dehydrogenation in peroxisomes is not linked directly to phosphorylation and the generation of ATP.
  3. The system facilitates the oxidation of very long chain fatty acids (eg, C20, C22). These enzymes are induced by high-fat diets and in some species by hypolipidemic drugs such as clofibrate.
  4. The enzymes in peroxisomes do not attack shorter-chain fatty acids; the β-oxidation sequence ends at octanoyl-CoA. Octanoyl and acetyl groups are both further oxidized in mitochondria. Another role of peroxisomal β oxidation is to shorten the side chain of cholesterol in bile acid formation.
  5. Peroxisomes also take part in the synthesis of ether glycerolipids, cholesterol, and dolichol.                                          

2.  Ketone Body Metabolism

Ketone bodies acetoacetate, β-hydroxybutyrate, acetone are the preferred energy substrates of the heart and brain in saturation.

 3.  Biosynthesis of Ketone Bodies
  1. Thiolase catalyzes the formation of two acetyl CoA molecules from acetoacetyl CoA.
  2. HMG CoA synthase catalyzes the addition of another acetyl CoA to acetoacetyl CoA to form HMG CoA.. HMG CoA synthase is regulatory enzyme of Ketogenesis.
  3. HMG CoA lyase catalyzes the cleavage of HMG CoA to acetoacetate and acetyl CoA.
  4. β-Hydroxybutyrate dehydrogenase catalyzes the formation of β-hydroxybutyrate from acetoacetate when the NADH/NAD+ ratio is high, as it is in the liver during fasting.
  5. Acetone is formed spontaneously from a small fraction of the circulating acetoacetate and is exhaled by the lungs.


4.  Oxidation of Ketone Body
  1. A 3-keto acid CoA transferase catalyzes the formation of the CoA thioester of acetoacetate. This enzyme is absent in Liver. Therefore ketone bodies are not used as energy source by the liver.
  2. Thiolase catalyzes the cleavage of acetoacetyl CoA to two acetyl CoA molecules with the use of CoA, providing two-carbon fragments for oxidation by the citric acid cycle.

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