From benzodiazepines to fatty acids and beyond: revisiting the role of ACBP/DBI

Thierry Alquier, Catherine A. Christian-Hinman, Julieta Alfonso, Nils J. Færgeman

Research output: Contribution to journalReview articlepeer-review


Four decades ago Costa and colleagues identified a small, secreted polypeptide in the brain that can displace the benzodiazepine diazepam from the GABAA 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.

Original languageEnglish (US)
Pages (from-to)890-903
Number of pages14
JournalTrends in Endocrinology and Metabolism
Issue number11
StatePublished - Nov 2021


  • GABA receptor
  • GPCR
  • acyl-CoA
  • acyl-CoA binding protein (ACBP)
  • diazepam binding inhibitor (DBI)
  • fatty acid metabolism

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology


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