Fatty acids contain a carboxylic acid head and a hydrocarbon tail. Their primary roles are as:
Fatty acids are built up from acetyl CoA units in the cytosol using energy derived from NADPH and ATP.
Аcetyl СоА carboxylase (ACC) is a biotin-dependent enzyme present in both liver and adipose tissues. It catalyzes the first committed step in fatty acid synthesis, the conversion of acetyl СоА to melonyl CoA.
In contrast to fatty acid oxidation, which occurs in mitochondria, fatty acid synthesis occurs in the cytosol. Аcetyl СоА generated in mitochondria by Beta-oxidation is transferred to the cytosol as citrate. In the cytoplasm, ATP-citrate Iyase converts citrate back to oxaloecetete and acetyl CoA.
See: Lipid Mobilization and Beta-oxidation
The energy stored in fatty acids is released by β-oxidation occurring in the mitochondria. The hydrocarbon chain is sequentially shortened by the removal of two-carbon acetyl CoA units which feed into the citric acid cycle.
TG stored in adipose tissue is metabolized to free fatty acids and glycerol by hormone sensitive lipase.
Glycerol --> transported into liver, where phosphorylated at 3' position by liver-specific enzyme Glycerol kinase to form Glycerol 3-P --> dihydroxyacetone phosphate (DHAP) by glycerol-3-P dehydrogenase
(N.B. Adipose tissue synthesizes glycerol phosphate needed for triacylglycerol synthesis from DHAP)
Clinical Correlate:
Defects in a peroxisomal membrane protein (an ATP-binding cassette (ABC) transporter of uncertain function) result in X-linked adrenoleukodystrophy. This disease is characterised by the accumulation of very long chain fatty acids due to their defective β-oxidation in peroxisomes. The clinical outcome is progressive cerebral demyelination.