β-oxidation
Mitochondrial pathway that catabolises fatty acids into acetyl-CoA for ATP generation through the citric-acid cycle.
For laboratory and research use only — not for human consumption.
β-oxidation is the principal mitochondrial pathway by which fatty acids are catabolised into acetyl-CoA, NADH, and FADH₂ for ATP generation. Long-chain fatty acids are activated to acyl-CoA in the cytoplasm and transported across the mitochondrial inner membrane by the carnitine shuttle (CPT1 outer membrane, carnitine-acylcarnitine translocase, CPT2 inner membrane), the rate-limiting step under physiological conditions. Inside the mitochondrial matrix, each cycle of β-oxidation comprises four sequential enzymatic reactions — dehydrogenation by acyl-CoA dehydrogenase, hydration by enoyl-CoA hydratase, dehydrogenation by 3-hydroxyacyl-CoA dehydrogenase, and thiolytic cleavage by β-ketothiolase — producing one acetyl-CoA, one NADH, one FADH₂, and a shortened acyl-CoA. Acetyl-CoA enters the citric-acid cycle for further oxidation; NADH and FADH₂ donate electrons to the electron-transport chain. Sustained β-oxidation requires coordinated upregulation of CPT1, mitochondrial biogenesis, and PGC-1α signalling. In peptide and metabolic research, β-oxidation flux is the principal downstream readout for compounds that drive adipose fat-mass reduction: AOD-9604 increases lipolysis (releasing free fatty acids) and increases skeletal-muscle β-oxidation capacity; mitochondrial peptides (MOTS-c, Humanin, SS-31) modulate β-oxidation efficiency through effects on mitochondrial integrity and the NAD⁺/sirtuin axis.