Unlike a high-fat diet model, mitochondrial ROS production does not appear to contribute to bed rest-induced insulin resistance
- PMID: 32249436
- DOI: 10.1113/JP279575
Unlike a high-fat diet model, mitochondrial ROS production does not appear to contribute to bed rest-induced insulin resistance
Keywords: bed rest; insulin resistance; reactive oxygen species.
Comment on
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Short-term bed rest-induced insulin resistance cannot be explained by increased mitochondrial H2 O2 emission.J Physiol. 2020 Jan;598(1):123-137. doi: 10.1113/JP278920. Epub 2019 Dec 26. J Physiol. 2020. PMID: 31721213
References
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- Dirks ML, Miotto PM, Goossens GH, Senden JM, Petrick HL, van Kranenburg J, van Loon, LJC & Holloway GP (2020). Short-term bed rest-induced insulin resistance cannot be explained by increased mitochondrial H2O2 emission. J Physiol 598, 123-137.
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- Dirks ML, Wall BT, van de Valk B, Holloway TM, Holloway GP, Chabowski A, Goossens GH & van Loon LJ (2016). One week of bed rest leads to substantial muscle atrophy and induces whole-body insulin resistance in the absence of skeletal muscle lipid accumulation. Diabetes 65, 2862-2875.
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