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Volume 27
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10.3390/ijms27125354
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This is an early access version, the complete PDF, HTML, and XML versions will be available soon.
Article

Cardioprotective Effects of 1,3 Butanediol in MASLD via Reversal of Cardiac Lipid Accumulation and Suppression of Cardiac Fibrosis

by
Olufunto O. Badmus
1,
Landon D. Parrow
1,
Karis E. McGowen
1,
LaBrenda Bell
1,
Jennifer R. Greer
1,
Marcela de Carvalho Cruz
1,
Terry D. Hinds, Jr.
2 and
David E. Stec
1,*
1
Department of Physiology & Biophysics, Cardiovascular-Renal Research Center, Cardiorenal and Metabolic Diseases Research Center, University of Mississippi Medical Center, Jackson, MS 39216, USA
2
Drug & Disease Discovery D3 Research Center, Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, USA
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2026, 27(12), 5354; https://doi.org/10.3390/ijms27125354 (registering DOI)
Submission received: 30 April 2026 / Revised: 9 June 2026 / Accepted: 11 June 2026 / Published: 13 June 2026
(This article belongs to the Section Molecular Pharmacology)
Versions Notes

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) is highly associated with the development of cardiovascular disease (CVD); however, the mechanisms responsible are currently unknown. We have developed a model of MASLD due to the loss of hepatocyte peroxisome proliferator-activated receptor α (PPARαHEPKO). We found that plasma beta-hydroxybutyrate (BHOB) levels were significantly reduced in PPARαHEPKO mice and aimed to investigate the therapeutic potential of restoring BHOB levels in the development of CVD in these mice. Thirty-week-old PPARαHEPKO and control PPARαFL/FL mice were randomized to receive 1,3 butanediol (1,3-BDO), a precursor of BHOB, in drinking water for 6 weeks. 1,3-BDO treatment resulted in a significant increase in plasma BHOB levels, a significant decrease in mean arterial blood pressure, improvement in systolic and diastolic function, a decrease in vascular stiffness, and improved exercise performance in PPARαHEPKO mice. 1,3-BDO treatment did not alleviate hepatic steatosis in PPARαHEPKO mice; however, it improved plasma cholesterol levels and decreased cardiac lipid accumulation, fibrosis, and apoptosis. 1,3-BDO treatment also resulted in a significant increase in cardiac AMP-activated protein kinase (AMPK) levels. Increasing plasma BHOB levels reverses CVD in our mouse model of MASLD. A similar approach could be an effective strategy for preventing the development of CVD in patients with human MASLD.
Keywords: peroxisome proliferator-activated receptor α; hypertension; fatty liver peroxisome proliferator-activated receptor α; hypertension; fatty liver

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MDPI and ACS Style

Badmus, O.O.; Parrow, L.D.; McGowen, K.E.; Bell, L.; Greer, J.R.; Cruz, M.d.C.; Hinds, T.D., Jr.; Stec, D.E. Cardioprotective Effects of 1,3 Butanediol in MASLD via Reversal of Cardiac Lipid Accumulation and Suppression of Cardiac Fibrosis. Int. J. Mol. Sci. 2026, 27, 5354. https://doi.org/10.3390/ijms27125354

AMA Style

Badmus OO, Parrow LD, McGowen KE, Bell L, Greer JR, Cruz MdC, Hinds TD Jr., Stec DE. Cardioprotective Effects of 1,3 Butanediol in MASLD via Reversal of Cardiac Lipid Accumulation and Suppression of Cardiac Fibrosis. International Journal of Molecular Sciences. 2026; 27(12):5354. https://doi.org/10.3390/ijms27125354

Chicago/Turabian Style

Badmus, Olufunto O., Landon D. Parrow, Karis E. McGowen, LaBrenda Bell, Jennifer R. Greer, Marcela de Carvalho Cruz, Terry D. Hinds, Jr., and David E. Stec. 2026. "Cardioprotective Effects of 1,3 Butanediol in MASLD via Reversal of Cardiac Lipid Accumulation and Suppression of Cardiac Fibrosis" International Journal of Molecular Sciences 27, no. 12: 5354. https://doi.org/10.3390/ijms27125354

APA Style

Badmus, O. O., Parrow, L. D., McGowen, K. E., Bell, L., Greer, J. R., Cruz, M. d. C., Hinds, T. D., Jr., & Stec, D. E. (2026). Cardioprotective Effects of 1,3 Butanediol in MASLD via Reversal of Cardiac Lipid Accumulation and Suppression of Cardiac Fibrosis. International Journal of Molecular Sciences, 27(12), 5354. https://doi.org/10.3390/ijms27125354

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