Journal article
Do Fish Oil Omega-3 Fatty Acids Enhance Antioxidant Capacity and Mitochondrial Fatty Acid Oxidation in Human Atrial Myocardium via PPARγ Activation?
Antioxidants & redox signaling, Vol.21(8), pp.1156-1163
09/10/2014
DOI: 10.1089/ars.2014.5888
PMCID: PMC4142835
PMID: 24597798
Abstract
Studies in experimental models suggest that n-3 polyunsaturated fatty acids (PUFAs) improve metabolic and anti-inflammatory/antioxidant capacity of the heart, although the mechanisms are unclear and translational evidence is lacking. In this study, patients ingested a moderately high dose of n-3 PUFAs (3.4 g/day eicosapentaenoic (EPA) and doxosahexaenoic acid (DHA) ethyl-esters) for a period of 2–3 weeks before having elective cardiac surgery. Blood was obtained before treatment and at the time of surgery, and myocardial tissue from the right atrium was also dissected during surgery. Blood EPA levels increased and myocardial tissue EPA and DHA levels were significantly higher in n-3 PUFA-treated patients compared with untreated, standard-of-care control patients. Interestingly, n-3 PUFA patients had greater nuclear transactivation of peroxisome proliferator-activated receptor-γ (PPARγ), fatty acid metabolic gene expression, and enhanced mitochondrial respiration supported by palmitoyl-carnitine in the atrial myocardium, despite no difference in mitochondrial content. Myocardial tissue from n-3 PUFA patients also displayed greater expression and activity of key antioxidant/anti-inflammatory enzymes. These findings lead to our hypothesis that PPARγ activation is a mechanism by which fish oil n-3 PUFAs enhance mitochondrial fatty acid oxidation and antioxidant capacity in human atrial myocardium, and that this preoperative therapeutic regimen may be optimal for mitigating oxidative/inflammatory stress associated with cardiac surgery.
Antioxid. Redox Signal.
21, 1156–1163.
Details
- Title: Subtitle
- Do Fish Oil Omega-3 Fatty Acids Enhance Antioxidant Capacity and Mitochondrial Fatty Acid Oxidation in Human Atrial Myocardium via PPARγ Activation?
- Creators
- Ethan J Anderson - 2Department of Cardiovascular Sciences and East Carolina Heart Institute, Brody School of Medicine, East Carolina University, Greenville, North CarolinaKathleen A Thayne - 1Department of Pharmacology & Toxicology, Brody School of Medicine, East Carolina University, Greenville, North CarolinaMitchel Harris - 3Department of Biochemistry and Molecular Biology, Brody School of Medicine, East Carolina University, Greenville, North CarolinaSaame Raza Shaikh - 3Department of Biochemistry and Molecular Biology, Brody School of Medicine, East Carolina University, Greenville, North CarolinaTimothy M Darden - 1Department of Pharmacology & Toxicology, Brody School of Medicine, East Carolina University, Greenville, North CarolinaDaniel S Lark - 4Department of Kinesiology, Brody School of Medicine, East Carolina University, Greenville, North CarolinaJohn Mark Williams - 2Department of Cardiovascular Sciences and East Carolina Heart Institute, Brody School of Medicine, East Carolina University, Greenville, North CarolinaW. Randolph Chitwood - 2Department of Cardiovascular Sciences and East Carolina Heart Institute, Brody School of Medicine, East Carolina University, Greenville, North CarolinaAlan P Kypson - 2Department of Cardiovascular Sciences and East Carolina Heart Institute, Brody School of Medicine, East Carolina University, Greenville, North CarolinaEvelio Rodriguez - 5St. Thomas Heart Cardiovascular Surgery, Nashville, Tennessee
- Resource Type
- Journal article
- Publication Details
- Antioxidants & redox signaling, Vol.21(8), pp.1156-1163
- Publisher
- Mary Ann Liebert, Inc
- DOI
- 10.1089/ars.2014.5888
- PMID
- 24597798
- PMCID
- PMC4142835
- ISSN
- 1523-0864
- eISSN
- 1557-7716
- Language
- English
- Date published
- 09/10/2014
- Academic Unit
- Pharmaceutical Sciences and Experimental Therapeutics; Fraternal Order of Eagles Diabetes Research Center; Health and Human Physiology
- Record Identifier
- 9984065503202771
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