The mitochondrial oxidation of long-chain fatty acids is initiated by the sequential action of carnitine palmitoyltransferase I (which is located in the outer membrane and is detergent-labile) and carnitine palmitoyltransferase II (which is located in the inner membrane and is detergent-stable), together with a carnitine-acylcarnitine translocase. CPT I is the key enzyme in the carnitine-dependent transport across the mitochondrial inner membrane and its deficiency results in a decreased rate of fatty acid beta-oxidation. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]
Forensic Context
A study in pigs demonstrated that the CPT1A gene and protein expression was uniquely upregulated in the skeletal muscle of cold-exposed Tibetan pigs, indicating a substrate switch to fatty acid utilization for thermogenesis [Yang et al. DOI:10.3390/ijms24087431]. In a separate forensic study, the CPT1A gene exhibited analogous time-dependent expression patterns in rats and pigs following skeletal muscle contusion, and it was part of a computational framework that successfully predicted gene expression across species for wound age estimation, enabling injury time classification with high accuracy [Wang et al. DOI:10.1007/s00414-026-03727-y].