Supplementation with the gut microbial-derived metabolites acetate and butyrate has been shown to lower blood pressure in experimental models of hypertension. However, the translational potential of these metabolites has been unexplored. We provide clinical evidence that acetate and butyrate lower blood pressure in untreated patients with hypertension.
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References
Xu, C. & Marques, F. Z. How dietary fibre, acting via the gut microbiome, lowers blood pressure. Curr. Hypertens. Rep. 24, 509–521 (2022). A review article that presents the latest evidence on dietary fibre and blood pressure.
Kaye, D. M. et al. Deficiency of prebiotic fibre and insufficient signalling through gut metabolite sensing receptors leads to cardiovascular disease. Circulation 141, 1393–1403 (2020). This paper reports on the use of acetate and butyrate to lower blood pressure in an experimental animal model.
Nakai, M. et al. Essential hypertension is associated with changes in gut microbial metabolic pathways: a multisite analysis of ambulatory blood pressure. Hypertension 78, 804–815 (2021). This paper reports lower levels of SCFA producers and GPR43 in human hypertension.
Yang, T. et al. Gut dysbiosis is linked to hypertension. Hypertension 65, 1331–1340 (2015). This paper reports lower levels of SCFA producers in experimental hypertension.
Xie, L. et al. Dietary fibre controls blood pressure and cardiovascular risk by lowering large intestinal pH and activating the proton-sensing receptor GPR65. Preprint at bioRxiv https://doi.org/10.1101/2022.11.17.516695 (2022). This paper reports on a new G-protein-coupled receptor that lowers blood pressure via the fiber–microbiome–SCFA axis.
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This is a summary of: Jama, H. A. et al. Prebiotic intervention with HAMSAB in untreated essential hypertensive patients assessed in a phase II randomized trial. Nat. Cardiovas. https://doi.org/10.1038/s44161-022-00197-4 (2023).
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Gut microbial metabolites lower blood pressure in patients with hypertension. Nat Cardiovasc Res 2, 18–19 (2023). https://doi.org/10.1038/s44161-022-00204-8
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DOI: https://doi.org/10.1038/s44161-022-00204-8
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