Long Term Adrenal Insufficiency Induces Skeletal Muscle Atrophy and Increases the Serum Levels of Active Form Myostatin in Rat Serum

2005 ◽  
Vol 22 (2) ◽  
pp. 229-236 ◽  
Author(s):  
Tohru Hosoyama ◽  
Chikashi Tachi ◽  
Keitaro Yamanouchi ◽  
Masugi Nishihara
Keyword(s):  
Skeletal Muscle ◽  
Adrenal Insufficiency ◽  
Muscle Atrophy ◽  
Active Form ◽  
Serum Levels ◽  
Skeletal Muscle Atrophy ◽  
Rat Serum

scholarly journals Thyroid Hormone Action in Muscle Atrophy

Metabolites ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 730
Author(s):  
Maria Angela De Stefano ◽  
Raffaele Ambrosio ◽  
Tommaso Porcelli ◽  
Gianfranco Orlandino ◽  
Domenico Salvatore ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Thyroid Hormone ◽  
Muscle Atrophy ◽  
Molecular Mechanisms ◽  
Muscle Protein ◽  
Active Form ◽  
Skeletal Muscle Atrophy ◽  
Target Tissue ◽  
Muscle Mass Loss

Skeletal muscle atrophy is a condition associated with various physiological and pathophysiological conditions, such as denervation, cachexia, and fasting. It is characterized by an altered protein turnover in which the rate of protein degradation exceeds the rate of protein synthesis, leading to substantial muscle mass loss and weakness. Muscle protein breakdown reflects the activation of multiple proteolytic mechanisms, including lysosomal degradation, apoptosis, and ubiquitin–proteasome. Thyroid hormone (TH) plays a key role in these conditions. Indeed, skeletal muscle is among the principal TH target tissue, where TH regulates proliferation, metabolism, differentiation, homeostasis, and growth. In physiological conditions, TH stimulates both protein synthesis and degradation, and an alteration in TH levels is often responsible for a specific myopathy. Intracellular TH concentrations are modulated in skeletal muscle by a family of enzymes named deiodinases; in particular, in muscle, deiodinases type 2 (D2) and type 3 (D3) are both present. D2 activates the prohormone T4 into the active form triiodothyronine (T3), whereas D3 inactivates both T4 and T3 by the removal of an inner ring iodine. Here we will review the present knowledge of TH action in skeletal muscle atrophy, in particular, on the molecular mechanisms presiding over the control of intracellular T3 concentration in wasting muscle conditions. Finally, we will discuss the possibility of exploiting the modulation of deiodinases as a possible therapeutic approach to treat muscle atrophy.

scholarly journals Liver fibrosis-induced muscle atrophy is mediated by elevated levels of circulating TNFα

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Tamaki Kurosawa ◽  
Momo Goto ◽  
Noriyuki Kaji ◽  
Satoshi Aikiyo ◽  
Taiki Mihara ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Liver Cirrhosis ◽  
Liver Fibrosis ◽  
Muscle Atrophy ◽  
Diploid Cell ◽  
Serum Levels ◽  
Skeletal Muscle Atrophy ◽  
Mouse Serum ◽  
Fibrotic Liver ◽  
Duct Ligation

AbstractLiver cirrhosis is a critical health problem associated with several complications, including skeletal muscle atrophy, which adversely affects the clinical outcome of patients independent of their liver functions. However, the precise mechanism underlying liver cirrhosis-induced muscle atrophy has not been elucidated. Here we show that serum factor induced by liver fibrosis leads to skeletal muscle atrophy. Using bile duct ligation (BDL) model of liver injury, we induced liver fibrosis in mice and observed subsequent muscle atrophy and weakness. We developed culture system of human primary myotubes that enables an evaluation of the effects of soluble factors on muscle atrophy and found that serum from BDL mice contains atrophy-inducing factors. This atrophy-inducing effect of BDL mouse serum was mitigated upon inhibition of TNFα signalling but not inhibition of myostatin/activin signalling. The BDL mice exhibited significantly up-regulated serum levels of TNFα when compared with the control mice. Furthermore, the mRNA expression levels of Tnf were markedly up-regulated in the fibrotic liver but not in the skeletal muscles of BDL mice. The gene expression analysis of isolated nuclei revealed that Tnf is exclusively expressed in the non-fibrogenic diploid cell population of the fibrotic liver. These findings reveal the mechanism through which circulating TNFα produced in the damaged liver mediates skeletal muscle atrophy. Additionally, this study demonstrated the importance of inter-organ communication that underlies the pathogenesis of liver cirrhosis.

scholarly journals Salidroside mitigates skeletal muscle atrophy in rats with cigarette smoke-induced COPD by up-regulating myogenin and down-regulating myostatin expression

2019 ◽  
Vol 39 (11) ◽  
Author(s):  
Dan Zhang ◽  
Lihua Cao ◽  
Zhenshan Wang ◽  
Haoshen Feng ◽  
Xu Cai ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Lung Function ◽  
Cigarette Smoking ◽  
Muscle Atrophy ◽  
Skeletal Muscle Atrophy ◽  
High Dose ◽  
Air Exposure ◽  
Tnf Α ◽  
Healthy Control

Abstract Objectives: The present study aimed at investigating the therapeutic effect of Salidroside on skeletal muscle atrophy in a rat model of cigarette smoking-induced chronic obstructive pulmonary disease (COPD) and its potential mechanisms. Methods: Male Wistar rats were randomized, and treated intraperitoneally (IP) with vehicle (injectable water) or a low, medium or high dose of Salidroside, followed by exposure to cigarette smoking daily for 16 weeks. A healthy control received vehicle injection and air exposure. Their lung function, body weights and gastrocnemius (GN) weights, grip strength and cross-section area (CSA) of individual muscular fibers in the GN were measured. The levels of TNF-α, IL-6, malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH) in serum and GN tissues as well as myostatin and myogenin expression in GN tissues were measured. Results: In comparison with that in the healthy control, long-term cigarette smoking induced emphysema, significantly impaired lung function, reduced body and GN weights and CSA values in rats, accompanied by significantly increased levels of TNF-α, IL-6 and MDA, but decreased levels of SOD and GSH in serum and GN tissues. Furthermore, cigarette smoking significantly up-regulated myostatin expression, but down-regulated myogenin expression in GN tissues. Salidroside treatment decreased emphysema, significantly ameliorated lung function, increased antioxidant, but reduced MDA, IL-6 and TNF-α levels in serum and GN tissues of rats, accompanied by decreased myostain, but increased myogenin expression in GN tissues. Conclusion: Salidroside mitigates the long-term cigarette smoking-induced emphysema and skeletal muscle atrophy in rats by inhibiting oxidative stress and inflammatory responses and regulating muscle-specific transcription factor expression.

Beneficial effects of GH/IGF-1 on skeletal muscle atrophy and function in experimental heart failure

2004 ◽  
Vol 286 (1) ◽  
pp. C138-C144 ◽  
Author(s):  
Luciano Dalla Libera ◽  
Barbara Ravara ◽  
Maurizio Volterrani ◽  
Valerio Gobbo ◽  
Mila Della Barbera ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Exercise Capacity ◽  
Muscle Atrophy ◽  
Serum Levels ◽  
Skeletal Muscle Atrophy ◽  
Gh Treatment ◽  
Tnf Α ◽  
Myocyte Apoptosis ◽  
Contraction And Relaxation

Muscle atrophy is a determinant of exercise capacity in heart failure (CHF). Myocyte apoptosis, triggered by tumor necrosis factor-α (TNF-α) or its second messenger sphingosine (SPH), is one of the causes of atrophy. Growth hormone (GH) improves hemodynamic and cardiac trophism in several experimental models of CHF, but its effect on skeletal muscle in CHF is not yet clear. We tested the hypothesis that GH can prevent skeletal muscle apoptosis in rats with CHF. CHF was induced by injecting monocrotaline. After 2 wk, 2 groups of rats were treated with GH (0.2 mg·kg–1·day–1 and 1.0 mg·kg–1·day–1) subcutaneously. A third group of controls had saline. After 2 additional weeks, rats were killed. Tibialis anterior cross-sectional area, myosin heavy chain (MHC) composition, and a study on myocyte apoptosis and serum levels of TNF-α and SPH were carried out. The number of apoptotic nuclei, muscle atrophy, and serum levels of TNF-α and SPH were decreased with GH at high but not at low doses compared with CHF rats. Bcl-2 was increased, whereas activated caspases and bax were decreased. The MHC pattern in GH-treated animals was similar to that of controls. Monocrotaline slowed down both contraction and relaxation but did not affect specific tetanic force, whereas absolute force was decreased. GH treatment restored contraction and relaxation to control values and brought muscle mass and absolute twitch and tetanic tension to normal levels. These findings may provide an insight into the therapeutic strategy of GH given to patients with CHF to improve exercise capacity.

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