Short-Chain Fatty Acids in the Metabolism of Heart Failure - Rethinking the Fat Stigma.

Autor:	Palm CL; Department of Cardiology, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands., Nijholt KT; Department of Cardiology, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands., Bakker BM; Department of Pediatrics, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands., Westenbrink BD; Department of Cardiology, University Medical Centre Groningen, University of Groningen, Groningen, Netherlands.
Jazyk:	angličtina
Zdroj:	Frontiers in cardiovascular medicine [Front Cardiovasc Med] 2022 Jul 11; Vol. 9, pp. 915102. Date of Electronic Publication: 2022 Jul 11 (Print Publication: 2022).
DOI:	10.3389/fcvm.2022.915102
Abstrakt:	Heart failure (HF) remains a disease with immense global health burden. During the development of HF, the myocardium and therefore cardiac metabolism undergoes specific changes, with decreased long-chain fatty acid oxidation and increased anaerobic glycolysis, diminishing the overall energy yield. Based on the dogma that the failing heart is oxygen-deprived and on the fact that carbohydrates are more oxygen-efficient than FA, metabolic HF drugs have so far aimed to stimulate glucose oxidation or inhibit FA oxidation. Unfortunately, these treatments have failed to provide meaningful clinical benefits. We believe it is time to rethink the concept that fat is harmful to the failing heart. In this review we discuss accumulating evidence that short-chain fatty acids (SCFAs) may be an effective fuel for the failing heart. In contrast to long-chain fatty acids, SCFAs are readily taken up and oxidized by the heart and could serve as a nutraceutical treatment strategy. In addition, we discuss how SCFAs activate pathways that increase long chain fatty acid oxidation, which could help increase the overall energy availability. Another potential beneficial effect we discuss lies within the anti-inflammatory effect of SCFAs, which has shown to inhibit cardiac fibrosis - a key pathological process in the development of HF. Competing Interests: The UMCG, which employs KN and BW, has received research grants and/or fees from AstraZeneca, Abbott, Boehringer Ingelheim, Cardior Pharmaceuticals Gmbh, Ionis Pharmaceuticals, Inc., Novo Nordisk, and Roche. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2022 Palm, Nijholt, Bakker and Westenbrink.)
Databáze:	MEDLINE
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