ArticleAmerican journal of physiology. Cell physiology2025
Ketone body β-hydroxybutyrate-mediated histone β-hydroxybutyrylation upregulates lipolysis and attenuates metabolic syndrome.
Article in American journal of physiology. Cell physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Gut microbiome drives glycodeoxycholic acid-mediated attenuation of hypertension.Gut microbes · 2026Article
- Adaptation to glucose restriction and β-hydroxybutyrate supplementation is associated with metabolic flexibility in lung cancer cells.Scientific reports · 2026Article
- Hepatic mitochondrial signaling as a systemic hub: inter-organ communication networks in aging and aging-related diseases.Frontiers in cell and developmental biology · 2026Review
- From ketogenic metabolism to targeted therapeutics: current advances in β-hydroxybutyrylation.Frontiers in immunology · 2025Review
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Authors and funding
8 authors.
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Abstract
Metabolic syndrome (MetS) is on the rise globally. Features of MetS include obesity, hypertension, and abnormal glucose tolerance. Exercise, keto diets, and intermittent fasting are lifestyle modifications recommended to lower MetS, all of which increase the production of the endogenous ketone body β-hydroxybutyrate. β-hydroxybutyrate has signaling and epigenetic effects, but the epigenetic mechanisms by which β-hydroxybutyrate could regulate MetS are understudied. Our previous work demonstrates that exogenous β-hydroxybutyrate supplementation lowers hypertension. The mechanism was traced to a key modification of histone-3 lysine 9 via β-hydroxybutyrylation, which remodeled the epitranscriptome to increase the accessibility of chromatin to transcriptionally upregulate key lipolytic genes,
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