Fiber-type discrimination in disuse and glucocorticoid-induced atrophy

Almon, Richard R.; DuBois, Debra C.

doi:10.1249/00005768-199006000-00006

Cited by 34 publications

(11 citation statements)

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“…EDL muscles are primarily composed of fast twitch muscle fibers [25]. This result may be linked with the modification of the genomic expression that can lead to impaired glucose transport [10,24].…”

Section: Discussionmentioning

confidence: 99%

Dose and Latency Effects of Leucine Supplementation in Modulating Glucose Homeostasis: Opposite Effects in Healthy and Glucocorticoid-Induced Insulin-Resistance States

et al. 2012

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Dexamethasone (DEXA) is a potent immunosupressant and anti-inflammatory agent whose main side effects are muscle atrophy and insulin resistance in skeletal muscles. In this context, leucine supplementation may represent a way to limit the DEXA side effects. In this study, we have investigated the effects of a low and a high dose of leucine supplementation (via a bolus) on glucose homeostasis, muscle mass and muscle strength in energy-restricted and DEXA-treated rats. Since the leucine response may also be linked to the administration of this amino acid, we performed a second set of experiments with leucine given in bolus (via gavage) versus leucine given via drinking water. Leucine supplementation was found to produce positive effects (e.g., reduced insulin levels) only when administrated in low dosage, both via the bolus or via drinking water. However, under DEXA treatment, leucine administration was found to significantly influence this response, since leucine supplementation via drinking water clearly induced a diabetic state, whereas the same effect was not observed when supplied via the gavage.

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Section: Discussionmentioning

confidence: 99%

Dose and Latency Effects of Leucine Supplementation in Modulating Glucose Homeostasis: Opposite Effects in Healthy and Glucocorticoid-Induced Insulin-Resistance States

et al. 2012

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“…Type 2B (fast-twitch) fiber atrophy is prominent in corticosteroid myopathy; however, the precise pathogenetic mechanism is not clear. Previous studies indicated abnormal protein catabolism/anabolism [1][2][3]. Decreased oxidative capacity is observed in mitochondria [6,7] but this mechanism is yet controversial [17,18].…”

Section: Discussionmentioning

confidence: 99%

“…A number of mechanisms have been proposed to explain how chronic corticosteroid treatment produces muscle wasting and weakness. These mechanisms include enhanced protein catabolism [1], decreased protein anabolism [2] and increased export of amino acid from the muscle [3], but the precise mechanism has not been elucidated. On the other hand, experimentally administered corticosteroids are known to impair mitochondrial morphology and function in skeletal muscle.…”

Section: Introductionmentioning

confidence: 99%

Chronic corticosteroid administration causes mitochondrial dysfunction in skeletal muscle

Mitsui¹,

Azuma²,

Nagasawa

et al. 2002

Journal of Neurology

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Corticosteroid myopathy is a major clinical problem in patients undergoing chronic corticosteroid treatment and shows insidious and progressive muscle atrophy in proximal limbs. Although several mechanisms underlying the pathophysiology of muscle injury have been postulated, precise pathogenesis is still not clear. We evaluated the mitochondrial functions in patients receiving corticosteroids compared with those in healthy controls or patients not receiving corticosteroids. The serum levels and total production of lactate were investigated by an aerobic exercise test using a bicycle ergometer. Mitochondrial respiratory activities and oxidative damage in biopsied skeletal muscles were also studied. The results of aerobic exercise tests revealed a significant overproduction of lactate in patients treated with corticosteroids ( p < 0.005), which was positively correlated with total corticosteroid doses administered ( p < 0.0001). In these patients, mitochondrial enzyme activity in complex I was significantly decreased ( p < 0.05) and oxidative damage of biopsied skeletal muscle was remarkable both in mitochondrial and nuclear DNAs ( p < 0.001). The results suggest that chronic corticosteroid administration induces mitochondrial dysfunction and oxidative damage in skeletal muscles, which may be the pathogenesis, at least in part, of corticosteroid-induced myopathy.

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“…However, after resistance exercise, the stimulation of rates of sarcoplasmic protein synthesis was »20% less than that of myoWbrillar protein synthesis (Cuthbertson et al 2006). Likewise, during atrophic state mediated by denervation, negative remodeling occurs predominantly due to contractile protein losses (Almon and Dubois 1990). This indicates that the correct understanding of the translational process of speciWc mRNA (e.g.…”

Section: Mtor/p70s6k and The Protein Synthesismentioning

confidence: 99%

Mechanical stimuli of skeletal muscle: implications on mTOR/p70s6k and protein synthesis

Zanchi

Lancha

2007

Eur J Appl Physiol

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The skeletal muscle is a tissue with adaptive properties which are essential to the survival of many species. When mechanically stimulated it is liable to undergo remodeling, namely, changes in its mass/volume resulting mainly from myofibrillar protein accumulation. The mTOR pathway (mammalian target of rapamycin) via its effector p70s6k (ribosomal protein kinase S6) has been reported to be of importance to the control of skeletal muscle mass, particularly under mechanical stimulation. However, not all mechanical stimuli are capable of activating this pathway, and among those who are, there are differences in the activation magnitude. Likewise, not all skeletal muscle fibers respond to the same extent to mechanical stimulation. Such evidences suggest specific mechanical stimuli through appropriate cellular signaling to be responsible for the final physiological response, namely, the accumulation of myofibrillar protein. Lately, after the mTOR signaling pathway has been acknowledged as of importance for remodeling, the interest for the mechanical/chemical mediators capable of activating it has increased. Apart from the already known MGF (mechano growth factor), some other mediators such as phosphatidic acid (PA) have been identified. This review article comprises and discusses relevant information on the mechano-chemical transduction of the pathway mTOR, with special emphasis on the muscle protein synthesis.

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Fiber-type discrimination in disuse and glucocorticoid-induced atrophy

Cited by 34 publications

References 0 publications

Dose and Latency Effects of Leucine Supplementation in Modulating Glucose Homeostasis: Opposite Effects in Healthy and Glucocorticoid-Induced Insulin-Resistance States

Dose and Latency Effects of Leucine Supplementation in Modulating Glucose Homeostasis: Opposite Effects in Healthy and Glucocorticoid-Induced Insulin-Resistance States

Chronic corticosteroid administration causes mitochondrial dysfunction in skeletal muscle

Mechanical stimuli of skeletal muscle: implications on mTOR/p70s6k and protein synthesis

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