Journal article
Mitochondrial antioxidative capacity regulates muscle glucose uptake in the conscious mouse: effect of exercise and diet
Journal of applied physiology (1985), Vol.113(8), pp.1173-1183
10/15/2012
DOI: 10.1152/japplphysiol.01344.2011
PMCID: PMC3472490
PMID: 22653994
Abstract
The objective of this study was to test the hypothesis that exercise-stimulated muscle glucose uptake (MGU) is augmented by increasing mitochondrial reactive oxygen species (mtROS) scavenging capacity. This hypothesis was tested in genetically altered mice fed chow or a high-fat (HF) diet that accelerates mtROS formation. Mice overexpressing SOD2 (sod2Tg), mitochondria-targeted catalase (mcatTg), and combined SOD2 and mCAT (mtAO) were used to increase mtROS scavenging. mtROS was assessed by the H2O2 emitting potential (JH2O2) in muscle fibers. sod2Tg did not decrease JH2O2 in chow-fed mice, but decreased JH2O2 in HF-fed mice. mcatTg and mtAO decreased JH2O2 in both chow- and HF-fed mice. In parallel, the ratio of reduced to oxidized glutathione (GSH/GSSG) was unaltered in sod2Tg in chow-fed mice, but was increased in HF-fed sod2Tg and both chow- and HF-fed mcatTg and mtAO. Nitrotyrosine, a marker of NO-dependent, reactive nitrogen species (RNS)-induced nitrative stress, was decreased in both chow- and HF-fed sod2Tg, mcatTg, and mtAO mice. This effect was not changed with exercise. Kg, an index of MGU was assessed using 2-[14C]-deoxyglucose during exercise. In chow-fed mice, sod2Tg, mcatTg, and mtAO increased exercise Kg compared with wild types. Exercise Kg was also augmented in HF-fed sod2Tg and mcatTg mice but unchanged in HF-fed mtAO mice. In conclusion, mtROS scavenging is a key regulator of exercise-mediated MGU and this regulation depends on nutritional state.
Details
- Title: Subtitle
- Mitochondrial antioxidative capacity regulates muscle glucose uptake in the conscious mouse: effect of exercise and diet
- Creators
- Li Kang - Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TennesseeMary E Lustig - Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TennesseeJeffrey S Bonner - Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TennesseeRobert S Lee-Young - Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TennesseeWesley H Mayes - Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TennesseeFreyja D James - Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TennesseeChien-Te Lin - East Carolina Diabetes and Obesity Institute and Departments of Physiology and Kinesiology, East Carolina University, Greenville, North CarolinaChristopher G. R Perry - East Carolina Diabetes and Obesity Institute and Departments of Physiology and Kinesiology, East Carolina University, Greenville, North CarolinaEthan J Anderson - East Carolina Diabetes and Obesity Institute and Departments of Physiology and Kinesiology, East Carolina University, Greenville, North CarolinaP. Darrell Neufer - East Carolina Diabetes and Obesity Institute and Departments of Physiology and Kinesiology, East Carolina University, Greenville, North CarolinaDavid H Wasserman - Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee
- Resource Type
- Journal article
- Publication Details
- Journal of applied physiology (1985), Vol.113(8), pp.1173-1183
- DOI
- 10.1152/japplphysiol.01344.2011
- PMID
- 22653994
- PMCID
- PMC3472490
- NLM abbreviation
- J Appl Physiol (1985)
- ISSN
- 8750-7587
- eISSN
- 1522-1601
- Publisher
- American Physiological Society; Bethesda, MD
- Language
- English
- Date published
- 10/15/2012
- Academic Unit
- Pharmaceutical Sciences and Experimental Therapeutics; Fraternal Order of Eagles Diabetes Research Center; Health, Sport, and Human Physiology
- Record Identifier
- 9984065695002771
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