[HTML][HTML] Dexamethasone impairs muscle energetics, studied by 31P NMR, in rats

JF Dumas, G Bielicki, JP Renou, D Roussel… - Diabetologia, 2005 - Springer
JF Dumas, G Bielicki, JP Renou, D Roussel, PH Ducluzeau, Y Malthièry, G Simard, P Ritz
Diabetologia, 2005Springer
Aims/hypothesis Glucocorticoid treatments are associated with increased whole-body
oxygen consumption. We hypothesised that an impairment of muscle energy metabolism
can participate in this increased energy expenditure. Methods To investigate this possibility,
we have studied muscle energetics of dexamethasone-treated rats (1.5 mg kg− 1 day− 1 for
6 days), in vivo by 31 P NMR spectroscopy. Results were compared with control and pair-fed
(PF) rats before and after overnight fasting. Results Dexamethasone treatment resulted in …
Aims/hypothesis
Glucocorticoid treatments are associated with increased whole-body oxygen consumption. We hypothesised that an impairment of muscle energy metabolism can participate in this increased energy expenditure.
Methods
To investigate this possibility, we have studied muscle energetics of dexamethasone-treated rats (1.5 mg kg−1 day−1 for 6 days), in vivo by 31P NMR spectroscopy. Results were compared with control and pair-fed (PF) rats before and after overnight fasting.
Results
Dexamethasone treatment resulted in decreased phosphocreatine (PCr) concentration and PCr:ATP ratio, increased ADP concentration and higher PCr to γ-ATP flux but no change in β-ATP to β-ADP flux in gastrocnemius muscle. Neither 4 days of food restriction (PF rats) nor 24 h fasting affected high-energy phosphate metabolism. In dexamethasone-treated rats, there was an increase in plasma insulin and non-esterified fatty acid concentration.
Conclusions/interpretation
We conclude that dexamethasone treatment altered resting in vivo skeletal muscle energy metabolism, by decreasing oxidative phosphorylation, producing ATP at the expense of PCr.
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