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Cited by 85Regulation of Appetite and ObesityPharmacology and Obesity TreatmentAdipokines, Inflammation, and Metabolic Diseases

Disulfiram Treatment Normalizes Body Weight in Obese Mice

Open access
Bernier, Michel, Mitchell, Sarah J., Wahl, Devin, Diaz, Antonio, Singh, Abhishek, Seo, Wonhyo, Wang, Mingy, Ali, Ahmed +31 more·2020·Cell Metabolism
DOI 10.1016/j.cmet.2020.04.019PMC PMC7957855
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Abstract

Obesity is a top public health concern, and a molecule that safely treats obesity is urgently needed. Disulfiram (known commercially as Antabuse), an FDA-approved treatment for chronic alcohol addiction, exhibits anti-inflammatory properties and helps protect against certain types of cancer. Here, we show that in mice disulfiram treatment prevented body weight gain and abrogated the adverse impact of an obesogenic diet on insulin responsiveness while mitigating liver steatosis and pancreatic islet hypertrophy. Additionally, disulfiram treatment reversed established diet-induced obesity and metabolic dysfunctions in middle-aged mice. Reductions in feeding efficiency and increases in energy expenditure were associated with body weight regulation in response to long-term disulfiram treatment. Loss of fat tissue and an increase in liver fenestrations were also observed in rats on disulfiram. Given the potent anti-obesogenic effects in rodents, repurposing disulfiram in the clinic could represent a new strategy to treat obesity and its metabolic comorbidities.

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Crossref · 10.1016/j.cmet.2020.04.019

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  • DIS 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 [125]

    The Results and Discussion report improved insulin sensitivity in high-fat-diet-fed mice and benefits involving the liver and pancreas. They also report lower fasting glucose and faster glucose disposal during an insulin tolerance test, but do not establish improved glucose tolerance with a glucose tolerance test. The glucose-tolerance part of the claim is therefore not fully supported. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • 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 [125]

    The Results and Discussion report improved energy metabolism and preservation of liver structure after disulfiram treatment, but do not attribute these findings to integrated liver transcriptomic/proteomic analyses. Searches for transcriptomic, proteomic, and autophagy passages found no report of shared signatures or potent autophagy activation in our copy; the STAR Methods passage describes liver histology instead. Page numbers were not available in the indexed passages. (LLM, conf=0.76)

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Authors
Bernier, M., Mitchell, S. J., Wahl, D., Diaz, A., Singh, A., Seo, W., Wang, M., Ali, A., Kaiser, T., Price, N. L., Aon, M. A., Kim, E.-Y., Petr, M. A., Cai, H., Warren, A., Di Germanio, C., Di Francesco, A., Fishbein, K., Guiterrez, V., Harney, D., Koay, Y. C., Mach, J., Enamorado, I. N., Pulpitel, T., Wang, Y., Zhang, J., Zhang, L., Spencer, R. G., Becker, K. G., Egan, J. M., Lakatta, E. G., O’Sullivan, J., Larance, M., LeCouteur, D. G., Cogger, V. C., Gao, B., Fernandez-Hernando, C., Cuervo, A. M., & de Cabo, R.
Affiliations
  • National Institutes of Health (US)
  • The University of Sydney (AU)
  • Yale University (US)
  • Anzac Research Institute (AU)
Corresponding author
Bernier, Michel
ORCID
Venue
Cell Metabolism
Publisher
Elsevier BV
Published
2020-08
Volume
32
Issue
2
Pages
203-214.e4
ISSN
1550-4131 (ISSN-L)
DOI
10.1016/j.cmet.2020.04.019
PMC
PMC7957855
OpenAlex
W3024061948
Cited by
85
References
50
Citations by year
2026: 9 · 2025: 9 · 2024: 19 · 2023: 16 · 2022: 13 · 2021: 15 · 2020: 4
FWCI
6.16
Type
journal article
Language
en
Open access
Licence
Locations
  • Cell Metabolism (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute on Aging (AG038072, AG031782)
  • National Health and Medical Research Council (APP1120475)
  • National Institutes of Health (R35HL135820)
  • Korea Research Institute of Bioscience and Biotechnology
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Pharmacology › Pharmacology and Obesity Treatment
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
disulfiram, obesity, drug repurposing, body weight regulation, diet-induced obesity, insulin resistance, hepatic steatosis, energy expenditure, fat tissue loss, metabolic comorbidities
MeSH terms
Animals, Body Weight, Diet, Disulfiram, Female, Male, Mice, Inbred C57BL, Obesity, Rats, Sprague-Dawley, Mice, Knockout, Anti-Obesity Agents, Mice, Rats

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