Dexamethasone impairs muscle energetics, studied by 31P nmr, in rats

• Published in: Diabetologia Vol. 48; no. 2; pp. 328 - 335
• Main Authors: DUMAS, J.-F, BIELICKI, G, RENOU, J.-P, ROUSSEL, D, DUCLUZEAU, P.-H, MALTHIERY, Y, SIMARD, G, RITZ, P
• Format: Journal Article
• Language: English
• Published: Berlin Springer 01.02.2005; Springer Nature B.V
• Subjects: Biological and medical sciences; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Medical sciences; Endocrinopathy; Corticosteroid; Dexamethasone; Rat; Steroid hormone; Diabetes mellitus; Rodentia; Phosphocreatine; Glucocorticoid; Food restriction; Vertebrata; Mammalia; Oxidative phosphorylation; Animal; Muscle; ATP
• ISSN: 0012-186X; 1432-0428
• DOI: 10.1007/s00125-004-1631-0

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. 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. Dexamethasone treatment resulted in decreased phosphocreatine (PCr) concentration and PCr:ATP ratio, increased ADP concentration and higher PCr to gamma-ATP flux but no change in beta-ATP to beta-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. We conclude that dexamethasone treatment altered resting in vivo skeletal muscle energy metabolism, by decreasing oxidative phosphorylation, producing ATP at the expense of PCr.