Four decades ago Costa and colleagues identified a small, secreted polypeptide in the brain that can displace the benzodiazepine diazepam from the GABA_A receptor, and was thus termed diazepam binding inhibitor (DBI). Shortly after, an identical polypeptide was identified in liver by its ability to induce termination of fatty acid synthesis, and was named acyl-CoA binding protein (ACBP). Since then, ACBP/DBI has been studied in parallel without a clear and integrated understanding of its dual roles. The first genetic loss-of-function models have revived the field, allowing targeted approaches to better understand the physiological roles of ACBP/DBI in vivo. We discuss the roles of ACBP/DBI in central and tissue-specific functions in mammals, with an emphasis on metabolism and mechanisms of action.

四十年前，Costa 及其同事在大脑中发现了一种小的分泌性多肽，它可以从 GABA _A受体中取代苯二氮卓类地西泮，因此被称为地西泮结合抑制剂 (DBI)。不久之后，通过诱导脂肪酸合成终止的能力在肝脏中鉴定出相同的多肽，并将其命名为酰基辅酶 A 结合蛋白 (ACBP)。从那时起，ACBP/DBI 一直在并行研究，但对其双重角色没有清晰和综合的理解。第一个遗传功能丧失模型使该领域复兴，允许有针对性的方法更好地了解 ACBP/DBI在体内的生理作用. 我们讨论了 ACBP/DBI 在哺乳动物中枢和组织特异性功能中的作用，重点是新陈代谢和作用机制。