ArticleJCI insight2025
Oral octanoylcarnitine alleviates exercise intolerance in mouse models of long-chain fatty acid oxidation disorders.
Article in JCI insight, 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.
- LipiDecipher: A Structure-Oriented Analytical Framework for Interpretable Clinical Lipidomics.Metabolites · 2026Article
- Immunometabolic Reprogramming by Black Soldier Fly (Animals : an open access journal from MDPI · 2026Review
- Hope for a heart's lonesome hunt: metabolic roadblocks and cardiac electrical instability in long-chain fatty acid oxidation deficiency.American journal of physiology. Heart and circulatory physiology · 2026Article
- Gut microbiota, circulating metabolites, and pancreatic cancer risk: a multi-method causal inference study with cross-population validation.Frontiers in microbiology · 2025Article
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10 authors.
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Abstract
Long-chain fatty acid oxidation disorders (LC-FAODs) cause energy deficits in heart and skeletal muscle that are only partially corrected by current medium-chain lipid therapies such as triheptanoin. We find that heart and muscle lack medium-chain acyl-CoA synthetases, limiting the capacity for β-oxidation of medium-chain fatty acids. Instead, heart and muscle mitochondria robustly respire on medium-chain acylcarnitines. The mitochondrial matrix enzyme carnitine acetyltransferase (CrAT) efficiently converts orally delivered octanoylcarnitine (C8-carnitine) to octanoyl-CoA for energy generation. C8-carnitine exhibits twice the oral bioavailability of triheptanoin and distributes to muscle and heart. A single oral dose significantly enhances grip strength and treadmill endurance while attenuating lactic acidosis in 2 mouse models of LC-FAODs. Thus, medium-chain acylcarnitines overcome a previously unrecognized metabolic bottleneck in LC-FAOD muscle and may represent an alternative to triglyceride-based therapies for bioenergetic disorders.
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