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通过磷-31核磁共振(³¹P NMR)研究发现,地塞米松会损害大鼠的肌肉能量代谢。

Dexamethasone impairs muscle energetics, studied by (31)P NMR, in rats.

作者信息

Dumas J-F, Bielicki G, Renou J-P, Roussel D, Ducluzeau P-H, Malthièry Y, Simard G, Ritz P

机构信息

Inserm EMI-U 00.18, Laboratoire de Biochimie et de Biologie Moléculaire, CHU, 4 rue Larrey, 49033 Angers Cedex, France.

出版信息

Diabetologia. 2005 Feb;48(2):328-35. doi: 10.1007/s00125-004-1631-0. Epub 2005 Jan 8.

DOI:10.1007/s00125-004-1631-0
PMID:15645207
Abstract

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 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.

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.

摘要

目的/假设:糖皮质激素治疗与全身氧消耗增加有关。我们推测肌肉能量代谢受损可能参与了这种能量消耗的增加。

方法

为了研究这种可能性,我们通过(31)P核磁共振波谱法对接受地塞米松治疗的大鼠(1.5毫克/千克/天,持续6天)的肌肉能量学进行了体内研究。将结果与对照组和配对喂养(PF)大鼠在禁食过夜前后进行比较。

结果

地塞米松治疗导致腓肠肌中磷酸肌酸(PCr)浓度和PCr:ATP比值降低,ADP浓度升高,PCr至γ-ATP通量增加,但β-ATP至β-ADP通量无变化。4天的食物限制(PF大鼠)和24小时禁食均未影响高能磷酸代谢。在地塞米松治疗的大鼠中,血浆胰岛素和非酯化脂肪酸浓度增加。

结论/解读:我们得出结论,地塞米松治疗改变了静息状态下的体内骨骼肌能量代谢,通过降低氧化磷酸化,以消耗PCr为代价产生ATP。

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