Acyl-CoA thioesterase 13 (ACOT13)

Acyl-CoA thioesterase 13 is a mitochondrial enzyme that hydrolyzes long-chain fatty acyl-CoA esters to free fatty acids and CoA, thus modulating mitochondrial fatty acid β-oxidation and regulating cellular energy metabolism[1][2]. In mammals, ACOT13 is essential for sustained cell proliferation, adaptive thermogenesis, and hepatic gluconeogenesis[1][2]. It is also implicated in neurodevelopment, as genetic variants associate with brain structural traits[1]. ACOT13 belongs to the thioesterase superfamily, specifically functioning as a single-hotdog-fold thioesterase domain forming an enzymatically active homotetramer[2]. Loss of ACOT13 enhances insulin sensitivity, protects against diet-induced steatosis, and alters adaptive thermogenesis, highlighting its key role in lipid and glucose metabolism[1][2]. If more detail or more clinical context is needed (such as ligand/drug discovery relevance), current data indicate ACOT13 is mechanistically relevant but not yet a major pharmaceutical target.

Other names

Thioesterase superfamily member 2 (Them2)ACOT13Them2OsACOT (plant homolog)thioesterase superfamily member 2/acyl-CoA thioesterase 13

Hydrolysis of long-chain fatty acyl-CoA to free fatty acids and CoA, regulating the balance between substrate entry into β-oxidation versus other metabolic pathways[1][2]. Drugs targeting this enzyme (theoretically) would modulate mitochondrial energy homeostasis, hepatic glucose output, and lipid oxidation (no clinical examples to date)[1][2].