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Acyl-CoA-binding protein (ACBP) is a highly conserved, small cytosolic protein (approximately 10 kDa, ~90 amino acids) found across eukaryotes and some prokaryotes. It binds medium- and long-chain acyl-CoA esters with high specificity and affinity, facilitating intracellular fatty acid transport and metabolism, as well as membrane and sphingolipid biosynthesis. ACBP is also known as diazepam binding inhibitor (DBI) or endozepine, reflecting its additional neuroregulatory capacity to displace diazepam from GABA type A receptor binding sites. This dual role links ACBP to energy metabolism, cell signaling, and neuroregulation. Pathologically, its dysregulation is associated with metabolic diseases (obesity, diabetes, steatohepatitis), appetite disorders (including anorexia), and inflammatory processes. Experimental therapeutic approaches targeting ACBP/DBI, such as monoclonal antibodies, have shown promise in animal models for mitigating metabolic disease and fibrosis, though the full risk profile is still under study.
Inhibition of autophagy via interaction with the γ2 subunit of GABA type A receptor when extracellular. Modulation of appetite and energy metabolism (mechanism in central regulation is not fully elucidated).
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