Elucidating the mechanisms by which disulfiram protects against obesity and metabolic syndrome
Open accessAbstract
There is an unmet need and urgency to find safe and effective anti-obesity interventions. Our recent study in mice fed on obesogenic diet found that treatment with the alcohol aversive drug disulfiram reduced feeding efficiency and led to a decrease in body weight and an increase in energy expenditure. The intervention with disulfiram improved glucose tolerance and insulin sensitivity, and mitigated metabolic dysfunctions in various organs through poorly defined mechanisms. Here, integrated analysis of transcriptomic and proteomic data from mouse and rat livers unveiled comparable signatures in response to disulfiram, revealing pathways associated with lipid and energy metabolism, redox, and detoxification. In cell culture, disulfiram was found to be a potent activator of autophagy, the malfunctioning of which has negative consequences on metabolic regulation. Thus, repurposing disulfiram may represent a potent strategy to combat obesity.
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Integrated liver transcriptomic/proteomic analyses reveal shared signatures in lipid/energy metabolism, redox balance, detoxification, and potent autophagy activation.
“Integrated liver transcriptomic/proteomic analyses reveal shared signatures in lipid/energy metabolism, redox balance, detoxification, and potent autophagy activation.124,125”
From Off-label and repurposed use of disulfiram beyond alcohol dependence: A systematic review of clinical and preclinical evidence (2026) · cites this paper as [124]
The Introduction reports that liver transcriptomic and proteomic analyses identified consistent signatures in lipid and energy metabolism, redox processes, and detoxification. The Results and discussion section reports increased autophagic flux after disulfiram treatment, but that finding comes from cultured fibroblast experiments, not from the integrated liver analyses as the sentence implies. (LLM, conf=0.87)
Experimental — accuracy not yet measuredDIS improves glucose tolerance, insulin sensitivity, and multi-organ metabolic function in obesity models.
“DIS improves glucose tolerance, insulin sensitivity, and multi-organ metabolic function in obesity models.”
From Off-label and repurposed use of disulfiram beyond alcohol dependence: A systematic review of clinical and preclinical evidence (2026) · cites this paper as [124]
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- Authors
- Bernier, M., Harney, D., Koay, Y. C., Diaz, A., Singh, A., Wahl, D., Pulpitel, T., Ali, A., Guiterrez, V., Mitchell, S. J., Kim, E.-Y., Mach, J., Price, N. L., Aon, M. A., LeCouteur, D. G., Cogger, V. C., Fernandez-Hernando, C., O’Sullivan, J., Larance, M., Cuervo, A. M., & de Cabo, R.
- Affiliations
- National Institutes of Health (US)
- The University of Sydney (AU)
- Yale University (US)
- ORCID
- Venue
- npj Aging and Mechanisms of Disease
- Published
- 2020-07-21
- Volume
- 6
- Issue
- 1
- Pages
- 8-8
- ISSN
- 2056-3973 (ISSN-L)
- PMC
- PMC7374720
- OpenAlex
- W3044852492
- Cited by
- 26
- References
- 66
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 5 · 2023: 6 · 2022: 1 · 2021: 4 · 2020: 2
- FWCI
- 1.95
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- npj Aging and Mechanisms of Disease (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- U.S. Department of Health & Human Services | NIH | National Institute on Aging
- Topics
- Health Sciences › Medicine › Pharmacology › Pharmacology and Obesity Treatment
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- disulfiram, obesity, metabolic syndrome, obesogenic diet, energy expenditure, glucose tolerance, insulin sensitivity, liver transcriptome, liver proteomics, autophagy, lipid metabolism, redox metabolism, detoxification
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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