Acyl-coenzyme A binding protein (ACBP)

Acyl-coenzyme A binding protein (ACBP), also known as diazepam binding inhibitor (DBI) or endozepine, is a highly conserved, small (~10 kDa) cytoplasmic protein that binds medium- and long-chain acyl-CoA esters with high affinity and acts as an intracellular carrier of these key metabolic intermediates[1][3]. Extracellularly, ACBP/DBI functions as a neuropeptide that can modulate the activity of the GABA type A receptor by competing with benzodiazepines at their binding site, thus influencing inhibitory neurotransmission[1][2][3][5]. ACBP/DBI is implicated in the regulation of appetite and body composition, immune responses, and multiple anabolic and catabolic processes including lipid synthesis and mitochondrial fatty acid β-oxidation[2][3][5]. Elevated circulating levels of ACBP/DBI are associated with obesity, aging, increased cancer risk, metabolic syndrome, and inflammation, while targeted neutralization of ACBP/DBI shows therapeutic promise in preclinical models of cancer, osteoarthritis, and metabolic disorders by enhancing autophagy and modulating immune responses[2][3][5]. **References:** [1] Wikipedia: Acyl-CoA-binding protein [2] PMC11378439 [3] Nature Cell Death Discovery [5] Nature Cell Death and Differentiation

Other names

diazepam binding inhibitorDBIendozepineEPendozepine-like peptideoctadecaneuropeptide (ODN)

competitive inhibition/displacement of benzodiazepines at GABA type A receptor; modulation of immune responses by inhibiting autophagy and altering T cell profiles; regulation of lipid metabolic pathways via acyl-CoA transport/binding