O'Brien 2017 Abstract IOC122: Difference between revisions
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PPARΞ± independent effects of nitrate supplementation on skeletal muscle mitochondrial function in hypoxia. |
Link: Mitochondr Physiol Network 22.01
O'Brien KA, Horscroft JAH, Lindsay RT, Philp A, Harridge SDR, Murray AJ (2017)
Event: IOC122
Oxygen insufficiency (hypoxia), either in response to environmental exposure or pathological states, induces metabolic stress and remodelling the details of which remain ill-defined. A controversial aspect of acclimation is skeletal muscle metabolic remodelling, a process that may be aided by nitrate supplementation. Mechanisms of nitrate action have been demonstrated previously in skeletal muscle to involve interaction with a master regulator of fat metabolism, peroxisome proliferator-activated receptor alpha (PPARΞ±)[1]. In the present study, the potential for dietary nitrate supplementation to aid hypoxic acclimatisation through protection of skeletal muscle mitochondrial function and the requirement for PPARΞ± in this response were investigated. Hypoxia induced a 26% decrease (pβ€0.001) in mass specific long chain fatty acid LEAK state respiration and a 23% decrease (pβ€0.01) in carbohydrate oxidative phosphorylation capacity in control (chloride treated) mice of both PPARΞ±+/+ and PPARΞ±-/- genotypes. These significant decreases were not apparent in nitrate supplemented mice, indicating a nitrate dependent recovery of mitochondrial function. A nitrate effect was observed in both PPARΞ±+/+ and PPARΞ±-/- mice, suggesting a mechanism acting independently of PPARΞ±. Our results confirm previous reports of hypoxia suppressing skeletal muscle mitochondrial function and show this effect can be partially alleviated through dietary nitrate supplementation. Whilst the signalling mechanisms remain uncertain, this process appears to occur independently of PPARΞ±.
β’ Bioblast editor: Kandolf G
β’ O2k-Network Lab: UK Cambridge Murray AJ
Labels: MiParea: Respiration, Pharmacology;toxicology
Stress:Oxidative stress;RONS Organism: Mouse Tissue;cell: Skeletal muscle
Coupling state: LEAK, OXPHOS Pathway: F HRR: Oxygraph-2k
Affiliations
- OβBrien KA(1,2), Horscroft JAH(2), Lindsay RT(2), Philp A(3), Harridge SDR(1), Murray AJ(2)
- Centre Human & Aerospace Physiol Sciences, Kingβs College London
- Dept Physiol, Development Neuroscience, Univ Cambridge
- MRC Arthritis Research UK Centre Musculoskeletal Ageing Research, School Sport, Exercise Rehabilitation Sciences, Univ Birmingham
- United Kingdom. - [email protected]
References
- Ashmore T, Roberts LD, Morash AJ, Kotwica AO, Finnerty J, West JA, Murfitt SA, Fernandez BO, Branco C, Cowburn AS, Clarke K, Johnson RS, Feelisch M, Griffin JL, Murray AJ Nitrate enhances skeletal muscle fatty acid oxidation via a nitric oxide-cGMP-PPAR-mediated mechanism. BMC Biol 13:1-17.