Eicosapentaenoic acid but not docosahexaenoic acid restores skeletal muscle mitochondrial oxidative capacity in old mice.

Autor: Johnson ML; Division of Endocrinology and Metabolism, Mayo Clinic College of Medicine, Rochester, MN, USA., Lalia AZ; Division of Endocrinology and Metabolism, Mayo Clinic College of Medicine, Rochester, MN, USA., Dasari S; Division of Biomedical Statistics and Informatics, Mayo Clinic College of Medicine, Rochester, MN, USA., Pallauf M; Division of Endocrinology and Metabolism, Mayo Clinic College of Medicine, Rochester, MN, USA., Fitch M; Department of Nutritional Sciences and Toxicology, University of California Berkeley, Berkeley, CA, USA., Hellerstein MK; Department of Nutritional Sciences and Toxicology, University of California Berkeley, Berkeley, CA, USA., Lanza IR; Division of Endocrinology and Metabolism, Mayo Clinic College of Medicine, Rochester, MN, USA.
Jazyk: angličtina
Zdroj: Aging cell [Aging Cell] 2015 Oct; Vol. 14 (5), pp. 734-43. Date of Electronic Publication: 2015 May 25.
DOI: 10.1111/acel.12352
Abstrakt: Mitochondrial dysfunction is often observed in aging skeletal muscle and is implicated in age-related declines in physical function. Early evidence suggests that dietary omega-3 polyunsaturated fatty acids (n-3 PUFAs) improve mitochondrial function. Here, we show that 10 weeks of dietary eicosapentaenoic acid (EPA) supplementation partially attenuated the age-related decline in mitochondrial function in mice, but this effect was not observed with docosahexaenoic acid (DHA). The improvement in mitochondrial function with EPA occurred in the absence of any changes in mitochondrial abundance or biogenesis, which was evaluated from RNA sequencing, large-scale proteomics, and direct measurements of muscle mitochondrial protein synthesis rates. We find that EPA improves muscle protein quality, specifically by decreasing mitochondrial protein carbamylation, a post-translational modification that is driven by inflammation. These results demonstrate that EPA attenuated the age-related loss of mitochondrial function and improved mitochondrial protein quality through a mechanism that is likely linked with anti-inflammatory properties of n-3 PUFAs. Furthermore, we demonstrate that EPA and DHA exert some common biological effects (anticoagulation, anti-inflammatory, reduced FXR/RXR activation), but also exhibit many distinct biological effects, a finding that underscores the importance of evaluating the therapeutic potential of individual n-3 PUFAs.
(© 2015 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.)
Databáze: MEDLINE
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