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Pathogenic role of acyl coenzyme A binding protein (ACBP) in Cushing’s syndrome

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Pan, Hui | Tian, Ai-Ling | Chen, Hui | Xia, Yifan | Sauvat, Allan | Moriceau, Stephanie | Lambertucci, Flavia | Motiño, Omar | Zhao, Liwei | Liu, Peng | Mao, Misha | Li, Sijing | Zhang, Shuai | Joseph, Adrien | Durand, Sylvère | Aprahamian, Fanny | Luo, Zeyu | Ou, Yang | Shen, Zhe | Xue, Enfu | Pan, Yuhong | Carbonnier, Vincent | Stoll, Gautier | Forveille, Sabrina | Leduc, Marion | Cerrato, Giulia | Cerone, Alexandra | Maiuri, Maria, Chiara | Castinetti, Frederic | Brue, Thierry | Wang, Hongsheng | Ma, Yuting | Martins, Isabelle | Kepp, Oliver | Kroemer, Guido

Edité par CCSD ; Nature Publishing Group -

International audience. Cushing’s syndrome is caused by an elevation of endogenous orpharmacologically administered glucocorticoids. Acyl coenzyme A bindingprotein (ACBP, encoded by the gene diazepam binding inhibitor, Dbi)stimulates food intake and lipo-anabolic reactions. Here we found thatplasma ACBP/DBI concentrations were elevated in patients and mice withCushing’s syndrome. We used several methods for ACBP/DBI inhibition inmice, namely, (1) induction of ACBP/DBI autoantibodies, (2) injection of aneutralizing monoclonal antibody, (3) body-wide or hepatocyte-specificknockout of the Dbi gene, (4) mutation of the ACBP/DBI receptor Gabrg2and (5) injections of triiodothyronine or (6) the thyroid hormone receptor-βagonist resmetirom to block Dbi transcription. These six approachesabolished manifestations of Cushing’s syndrome such as increased foodintake, weight gain, excessive adiposity, liver d am age, hyp ertr ig lyce-ridaemia and type 2 diabetes. In conclusion, it appears that ACBP/DBIconstitutes an actionable target that is causally involved in the developmentof Cushing’s syndrome.

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