Induction of a Catabolic State in Rats by Dexamethasone: Dose or Time Dependency?

Minet-Quinard, Régine; Moinard, Christophe; Walrand, Stéphane; Villie, F; Normand, Bernadette; Vasson, Marie‐Paule; Chopineau, J.; Cynober, Luc

doi:10.1177/014860710002400130

Cited by 31 publications

(38 citation statements)

References 27 publications

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“…In our work, endotoxaemia led to myofibrillar protein catabolism, since the urinary 3-MH:creatinine ratio increased. As expected, the LPS treatment induced a decrease in nitrogen balance, reflecting net proteolysis in the muscles [35,36]. In addition, endotoxaemia induced a higher NOx excretion; indeed it is well-known that LPS is a potent stimulus for NO production, which is the main mediator of microbiocidal actions of macrophages [37].…”

Section: Effect Of Food Restrictionsupporting

confidence: 54%

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The equivocal metabolic response to endotoxaemia in type 2 diabetic and obese ZDF rats

et al. 2006

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Aims/hypothesis: The metabolic and endocrine disturbances associated with obesity and type 2 diabetes may impair the normal metabolic response to injury. Our objective was to investigate amino acid metabolism in endotoxaemic type 2 diabetic obese rats. Materials and methods: A metabolic study was performed over 4 days using male Zucker diabetic fatty (ZDF) rats (fa/fa) and lean littermates (fa/+) divided into three groups: ad libitum-fed groups which underwent no treatment, lipopolysaccharide (LPS)-treated groups receiving E. coli LPS by i.p. injection, and pair-fed groups to the respective LPS groups. We evaluated the effect of endotoxaemia on body weight, food intake and tissue weights. Nitrogen loss and muscular proteolysis were measured daily by determination of urinary 3-methylhistidine (3-MH) excretion. Plasma, intestine and muscle amino acid levels were measured. Results: The data showed that ad libitum-fed ZDF rats had lower plasma arginine and glutamine levels than ad libitum-fed control rats. Compared with control rats, the LPS-treated ZDF rats presented lower thymic involution, a lower 3-MH:creatinine ratio and higher cumulative nitrogen balance. Conclusions/interpretation: Against our working hypothesis, ZDF rats did not show an impaired metabolic response, and even appeared to be less sensitive to the stress.

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Section: Effect Of Food Restrictionsupporting

confidence: 54%

“…Indeed, it is known that injury is associated with changes in free amino acid concentrations in both plasma and skeletal muscles [36,38]. In particular, a significant decrease in glutamine pools is characteristic of the response to injury [38,39].…”

Section: Effect Of Food Restrictionmentioning

confidence: 99%

The equivocal metabolic response to endotoxaemia in type 2 diabetic and obese ZDF rats

et al. 2006

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“…The type-II GR receptor agonist Dxm reportedly increases the catabolic activity of brain tissue, and Dxm treatment may thereby lead to the fall in body mass in rodents [17,18]. As the decrease in loss of body mass of Dxm-treated animals appeared to parallel the consider- Mice were given physiological saline (I), or 2×0.5 mg/kg (II), 2×12.5 mg/kg (III) and 4×6.25 mg/kg (IV-V) dexamethasone as described in detail in Fig.…”

Section: Discussionmentioning

confidence: 99%

A novel brain trauma model in the mouse: effects of dexamethasone treatment

Hortobágyi

Ortobagyi

Görlach

et al. 2000

Pfl�gers Archiv European Journal of Physiology

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We describe a novel methodological approach for inducing cold lesion in the mouse as a model of human cortical contusion trauma. To validate its reproducibility and reliability, dexamethasone (Dxm) was repeatedly applied to demonstrate possible antioedematous drug effects. Following the induction of anaesthesia with halothane, the dura was exposed via trephination. Using a micromanipulator a pre-cooled (-78 degrees C) copper cylinder, 3 mm in diameter, was pressed down to a depth of 1 mm onto the dura for 30 s under microscopic control. The body temperature was held constant at 37 degrees C throughout the procedure. Blood pressure (BP), measured by a modified photosensor-monitored tail-cuff method, and acid-base status were not significantly different when analysed before and after cold lesion and prior to sacrifice. However, there was a marginal mixed respiratory and metabolic acidosis. The antioedematous action of Dxm was studied in four standard pre-and post-treatment paradigms: 2x0.5 mg/kg (II), 2x12.5 mg/kg (III) and 4x6.25 mg/kg (IV: 3x pre-, 1x post-treatment: V: 1x pre-, 3x post-treatment). Physiological saline injections served as controls. High doses of Dxm (III-V) significantly attenuated the cold-lesion-induced loss of body mass. Dxm treatment also resulted in a reduction of brain water content (III; P<0.05), and brain swelling (IV; P<0.05) in the lesioned hemisphere, relative to controls. In conclusion, we have characterized a novel cold lesion model in the mouse to mimic traumatic brain injury and the beneficial effect of Dxm treatment on the extent of brain oedema.

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“…Experiments were conducted over a 6-day period. The dose and duration of the dexamethasone treatment was chosen with reference to the literature from what is known to induce a reproducible maximum hypercatabolic state [16]. NMR measurements were performed for the first time on the fifth day, when animals were fed.…”

Section: Animalsmentioning

confidence: 99%

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

Dumas

Biélicki²,

Renou³

et al. 2005

Diabetologia

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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 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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Induction of a Catabolic State in Rats by Dexamethasone: Dose or Time Dependency?

Abstract: Five days of treatment by DEX and a dose of 0.75 mg/kg/d induced a marked catabolic state.

Cited by 31 publications

References 27 publications

The equivocal metabolic response to endotoxaemia in type 2 diabetic and obese ZDF rats

The equivocal metabolic response to endotoxaemia in type 2 diabetic and obese ZDF rats

A novel brain trauma model in the mouse: effects of dexamethasone treatment

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

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