Johnson 2015 Aging Cell

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Johnson ML, Lalia AZ, Dasari S, Pallauf M, Fitch M, Hellerstein MK, Lanza IR (2015) Eicosapentaenoic acid but not docosahexaenoic acid restores skeletal muscle mitochondrial oxidative capacity in old mice. Aging Cell 14:734-43.

» PMID: 26010060

Johnson ML, Lalia AZ, Dasari S, Pallauf M, Fitch M, Hellerstein MK, Lanza IR (2015) Aging Cell

Abstract: 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.

Keywords: Aging, Docosahexaenoic acid, Eicosapentaenoic acid, Mitochondria, Omega 3, Proteomics, Sarcopenia

O2k-Network Lab: US MN Rochester Nair KS


Labels: MiParea: Respiration, Exercise physiology;nutrition;life style  Pathology: Aging;senescence 

Organism: Mouse  Tissue;cell: Skeletal muscle  Preparation: Isolated mitochondria 


Coupling state: LEAK, OXPHOS  Pathway: F, N, S, NS, ROX  HRR: Oxygraph-2k