Article Dans Une Revue (Data Paper) Nature Metabolism Année : 2024

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

Yifan Xia
  • Fonction : Auteur
Stephanie Moriceau
Zeyu Luo
  • Fonction : Auteur
Yang Ou
  • Fonction : Auteur
Frederic Castinetti
  • Fonction : Auteur
Thierry Brue
Hongsheng Wang
Yuting Ma

Résumé

Cushing’s syndrome is caused by an elevation of endogenous or pharmacologically administered glucocorticoids. Acyl coenzyme A binding protein (ACBP, encoded by the gene diazepam binding inhibitor, Dbi) stimulates food intake and lipo-anabolic reactions. Here we found that plasma ACBP/DBI concentrations were elevated in patients and mice with Cushing’s syndrome. We used several methods for ACBP/DBI inhibition in mice, namely, (1) induction of ACBP/DBI autoantibodies, (2) injection of a neutralizing monoclonal antibody, (3) body-wide or hepatocyte-specific knockout of the Dbi gene, (4) mutation of the ACBP/DBI receptor Gabrg2 and (5) injections of triiodothyronine or (6) the thyroid hormone receptor-β agonist resmetirom to block Dbi transcription. These six approaches abolished manifestations of Cushing’s syndrome such as increased food intake, weight gain, excessive adiposity, liver d am age, hyp ertr ig lyce- ridaemia and type 2 diabetes. In conclusion, it appears that ACBP/DBI constitutes an actionable target that is causally involved in the development of Cushing’s syndrome.
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hal-04889711 , version 1 (15-01-2025)

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Hui Pan, Ai-Ling Tian, Hui Chen, Yifan Xia, Allan Sauvat, et al.. Pathogenic role of acyl coenzyme A binding protein (ACBP) in Cushing’s syndrome. Nature Metabolism, 2024, 6, pp.2281 - 2299. ⟨10.1038/s42255-024-01170-0⟩. ⟨hal-04889711⟩
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