ArticleNature metabolism2024
Pathogenic role of acyl coenzyme A binding protein (ACBP) in Cushing's syndrome.
Article in Nature metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Article
- Cell death-induced release of the pro-aging protein acyl CoA binding protein (ACBP) into the circulation.Cell death and differentiation · 2026Article
- Acyl-CoA-binding protein (ACBP): a poor-prognosis biomarker in sepsis and a target for disease mitigation.Signal transduction and targeted therapy · 2026Article
- Neutralization of acyl-CoA-binding protein attenuates glucocorticoid-mediated suppression of cancer immunosurveillance.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Identification of ACBP as a potential target in ciliopathic obesity through multi-omics network analysis.Nature communications · 2026Article
- Article
- ACBP/DBI neutralization for the prevention and treatment of malignant and non-malignant liver diseases.Cell death & disease · 2025Review
- Neutralization of acyl CoA binding protein (ACBP) for the experimental treatment of osteoarthritis.Cell death and differentiation · 2025Article
- Review
- Autophagy-dependent hepatocyte secretion of DBI/ACBP induced by glucocorticoids determines the pathogenesis of Cushing syndrome.Autophagy · 2025Article
Corrections and comments
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Authors and funding
35 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 damage, hypertriglyceridaemia 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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.