TY - JOUR
T1 - From benzodiazepines to fatty acids and beyond
T2 - revisiting the role of ACBP/DBI
AU - Alquier, Thierry
AU - Christian-Hinman, Catherine A.
AU - Alfonso, Julieta
AU - Færgeman, Nils J.
N1 - Funding Information:
We apologize for not citing other relevant publications owing to space limitations. This work was supported by grants from the Novo Nordisk Foundation ( NNF20OC0064744 to N.J.F), the National Institutes of Health (NIH; R01 NS105825 to C.A.C-H.), and a Brain and Behavior Research Foundation NARSAD (formerly National Alliance for Research on Schizophrenia and Depression) young investigator award ( 24086 to C.A.C-H.), the Chica and Heinz Schaller Foundation (to J.A.), and the Canadian Institutes of Health Research (CIHR; PJT153035 to T.A.). T.A. was supported by a salary award from the Fonds de Recherche Québec-Santé (FRQS). We thank Ditte Neess for valuable graphical help. Figures were created with BioRender.com .
Funding Information:
We apologize for not citing other relevant publications owing to space limitations. This work was supported by grants from the Novo Nordisk Foundation (NNF20OC0064744 to N.J.F), the National Institutes of Health (NIH; R01 NS105825 to C.A.C-H.), and a Brain and Behavior Research Foundation NARSAD (formerly National Alliance for Research on Schizophrenia and Depression) young investigator award (24086 to C.A.C-H.), the Chica and Heinz Schaller Foundation (to J.A.), and the Canadian Institutes of Health Research (CIHR; PJT153035 to T.A.). T.A. was supported by a salary award from the Fonds de Recherche Québec-Santé (FRQS). We thank Ditte Neess for valuable graphical help. Figures were created with BioRender.com. The authors have no interests to declare.
Publisher Copyright:
© 2021 Elsevier Ltd
PY - 2021/11
Y1 - 2021/11
N2 - 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.
AB - 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.
KW - GABA receptor
KW - GPCR
KW - acyl-CoA
KW - acyl-CoA binding protein (ACBP)
KW - diazepam binding inhibitor (DBI)
KW - fatty acid metabolism
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U2 - 10.1016/j.tem.2021.08.009
DO - 10.1016/j.tem.2021.08.009
M3 - Review article
C2 - 34565656
AN - SCOPUS:85115742483
VL - 32
SP - 890
EP - 903
JO - Trends in Endocrinology and Metabolism
JF - Trends in Endocrinology and Metabolism
SN - 1043-2760
IS - 11
ER -