Ageing and dexamethasone associated sarcopenia: Peculiarities of regeneration

Kaasik, Priit; Umnova, M. M.; Pehme, Ando; Alev, Karin; Aru, Maire; Selart, Anne; Seene, Teet

doi:10.1016/j.jsbmb.2006.11.024

Cited by 32 publications

(43 citation statements)

References 24 publications

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“…This attenuation may be a direct consequence of the improvement of insulin signal transduction through the phosphatidylinositol-3-kinase/ Akt-1 pathway, IRS-1 and IRS-2 activity and GLUT-4 expression discussed earlier. (Tanner et al 2002;Luciano et al 2002) It has been suggested that DEX treatment decreases body weight in a dose-dependent manner (De Vries et al 2002;Komamura et al 2003;Ahtikoski et al 2004;Rhee et al 2004;Coderre et al 2007;Kaasik et al 2007;Menezes et al 2007;Rafacho et al 2008). In the present study, both DEX-treated groups had signiWcantly reduced body weight.…”

Section: Discussionmentioning

confidence: 99%

“…Body weight loss is usually followed by muscle atrophy and skeletal muscle protein loss, including collagen IV, which may aVect muscle contraction (De Vries et al 2002;Komamura et al 2003;Ahtikoski et al 2004;Lumbers et al 2005;Gilson et al 2007;Kaasik et al 2007;Menezes et al 2007). This present study demonstrated that sedentary animals had a 33.5% reduction on TA muscle weight after DEX treatment.…”

Section: Discussionmentioning

confidence: 99%

“…Muscle atrophy may be explained by several causes: (1) resistance to leucine during protein synthesis, contributing to the develop of sarcopenia (Kaasik et al 2007;Menezes et al 2007); (2) IGF-1 decreases (Schakman et al 2005);…”

Section: Discussionmentioning

confidence: 99%

“…In addition, it has been observed that a dose-dependent reduction of body weight occurs in animals treated with glucocorticoids (De Vries et al 2002;Komamura et al 2003;Ahtikoski et al 2004;Rhee et al 2004;Coderre et al 2007;Kaasik et al 2007;Menezes et al 2007). This weight loss is usually followed by muscle atrophy and a reduction of several muscle proteins, contributing to impaired muscle function (De Vries et al 2002;Komamura et al 2003;Ahtikoski et al 2004;Lumbers et al 2005;Gilson et al 2007;Kaasik et al 2007;Menezes et al 2007).…”

Section: Introductionmentioning

confidence: 99%

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Exercise training prevents hyperinsulinemia, muscular glycogen loss and muscle atrophy induced by dexamethasone treatment

et al. 2009

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This study investigated whether exercise training could prevent the negative side effects of dexamethasone. Rats underwent a training period and were either submitted to a running protocol (60% physical capacity, 5 days/week for 8 weeks) or kept sedentary. After this training period, the animals underwent dexamethasone treatment (1 mg/kg per day, i.p., 10 days). Glycemia, insulinemia, muscular weight and muscular glycogen were measured from blood and skeletal muscle. Vascular endothelial growth factor (VEGF) protein was analyzed in skeletal muscles. Dexamethasone treatment evoked body weight loss (-24%), followed by muscular atrophy in the tibialis anterior (-25%) and the extensor digitorum longus (EDL, -15%). Dexamethasone also increased serum insulin levels by 5.7-fold and glucose levels by 2.5-fold compared to control. The exercise protocol prevented atrophy of the EDL and insulin resistance. Also, dexamethasone-treated rats showed decreased muscular glycogen (-41%), which was further attenuated by the exercise protocol. The VEGF protein expression decreased in the skeletal muscles of dexamethasone-treated rats and was unaltered by the exercise protocol. These data suggest that exercise attenuates hyperglycemia and may also prevent insulin resistance, muscular glycogen loss and muscular atrophy, thus suggesting that exercise may have some benefits during glucocorticoid treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Exercise training prevents hyperinsulinemia, muscular glycogen loss and muscle atrophy induced by dexamethasone treatment

et al. 2009

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“…The model of dexamethasone-induced atrophy has been used in several previous studies in our laboratory [4][5][6][7]. For example, the administration of glucocorticoids decreased the turnover rate of myosin heavy chain (MHC) and reduced the proportion of fast type MHC isoforms [5].…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoid-induced alterations in titin, nebulin, myosin heavy chain isoform content and viscoelastic properties of rat skeletal muscle

Aru¹,

Alev²,

Gapeyeva³

et al. 2013

ABC

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Viscoelastic properties of skeletal muscle are associated with a complex network of cytoskeletal proteins where titin and nebulin play a substantial role. The need for evaluation of muscle viscoelastic properties is widely accepted in clinical use to evaluate the effect of treatment or progression of muscle pathology (atrophy). We tested the hypothesis that the viscoelastic properties (elasticity, tone and stiffness) change in atrophied muscles with concomitant changes in cytoskeletal proteins (titin, nebulin) and contractile protein (myosin heavy chain) proportion. Sixteen 24-week-old male rats of the Wistar strain were randomly allocated to two groups: dexamethasone group treated each day for 10 consecutive days with dexamethasone in order to induce atrophy and control group. Skeletal muscle viscoelastic properties (elasticity, tone and stiffness) were determined using a myotonometer. Titin, nebulin and myosin heavy chain content were quantified using SDS-PAGE electrophoresis. We found that glucocorticoid-induced muscle atrophy is accompanied by reduced elasticity and increased tone and stiffness, with concomitant changes in titin, nebulin and myosin heavy chain content. The elasticity decreased by 10.9% (P < 0.05), tone increased from 26.69 Hz to 37.73 Hz (P < 0.05), and stiffness was significantly lower in dexamethasone group (627.3 N/m vs 758.6 N/m); (P < 0.05). Compared with the control group, the content of titin, nebulin and myosin heavy chain in atrophied muscle was 76.4%, 70.6% and 82.3%, respectively. Our results may lead to a better understanding of the mechanism of muscle atrophy and provide better guidance for rehabilitation practices and help to find rational therapeutic intervention in the future.

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Gryllus bimaculatus‐containing diets protect against dexamethasone‐induced muscle atrophy, but not high‐fat diet‐induced obesity

Kim

et al. 2023

Food Science & Nutrition

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Sarcopenia and obesity are emerging as major social problems. In this study, we examined whether Gryllus bimaculatus (GB), an edible insect, prevents dexamethasone‐induced muscle atrophy (sarcopenia) or high‐fat diet (HFD)‐induced obesity in mice. We generated a standard chow diet (SCD) + GB (85% SCD and 15% GB powder) and HFD + GB (85% HFD and 15% GB powder). SCD + GB feeding increased gains in body weight and white adipose tissue (WAT). Despite no difference in weight change between HFD + GB‐ and HFD‐fed mice, HFD + GB feeding aggravated insulin resistance compared with HFD feeding. SCD + GB or HFD + GB feeding did not change most gene expressions in the liver and WAT but did increase MyHC1 expression in the muscle, meaning that GB increased muscle generation. Therefore, we fed SCD + GB with dexamethasone, which induces muscle degeneration. As a result, muscle fiber size increased, as did grip strength compared with dexamethasone‐injected mice. In addition, SCD + GB reduced the expression of muscle degradation factors, such as atrogin1 and muscle RING‐finger protein 1 (MuRF1). Furthermore, SCD + GB feeding increased Akt, mTOR, and p70S6K phosphorylation and MyHC1 expression, meaning that it may have increased protein synthesis. In conclusion, GB has great potential for inhibiting dexamethasone‐induced muscle mass loss by increasing muscle protein synthesis and inhibiting muscle protein degradation.

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Ageing and dexamethasone associated sarcopenia: Peculiarities of regeneration

Cited by 32 publications

References 24 publications

Exercise training prevents hyperinsulinemia, muscular glycogen loss and muscle atrophy induced by dexamethasone treatment

Exercise training prevents hyperinsulinemia, muscular glycogen loss and muscle atrophy induced by dexamethasone treatment

Glucocorticoid-induced alterations in titin, nebulin, myosin heavy chain isoform content and viscoelastic properties of rat skeletal muscle

Gryllus bimaculatus‐containing diets protect against dexamethasone‐induced muscle atrophy, but not high‐fat diet‐induced obesity

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