The Effect of 4-weeks’ Alcohol Supplementation on the Muscle Atrophy in Rat
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This study was conducted to investigate the effect of chronic alcohol supplementation on muscle atrophy in growing rats. Eighteen male Sprague Dawley rats were randomly divided into two groups: CG group (control group, n=9) and AG group (alcohol supplemented group, n=9). Alcohol group (3 g/kg BW) was orally supplemented every day. After the experimental period, serum components and muscle Akt, p-Akt, FoxO, p-FoxO, MuRF1, and P38 protein expressions were analyzed. In the results, the values of EDL and soleus muscle weights of AG group did not have significant differences compared to the value of the CG group. In the serum components, the value of the serum TG concentration of AG group was significantly increased compared to the value of the CG group. The value of the p-Akt/Akt and p-FoxO/FoxO of the AG group was significantly decreased compared to the value of the CG group (p<0.01). The MuRF1 protein expression of AG group was significantly increased compared to the value of the CG group (p<0.01). However, the values of p-P38/P38 between two groups did not have any significant difference. From these results, it was suggested that 4 weeks of chronic alcohol supplementation induced muscle atrophy via activated protein degradation pathway involving the inhibition of Akt phosphorylation and increased FoxO and MuRF1 protein expression of muscle in growing rats.Keywords:
Muscle Atrophy
It is well known that muscles can waste away (atrophy) due to a lack of physical activity. Muscle wasting commonly presents with reduced muscle strength and an impaired ability to perform daily tasks. Several studies have attempted to categorize muscle atrophy into three main subgroups: physiologic, pathologic, and neurogenic atrophy. Physiologic atrophy is caused by the general underuse of skeletal muscle (e.g., bedridden). Pathologic atrophy is characterized as the loss of stimulus to a specific region (e.g., aging). Neurogenic atrophy results from damage to the nerve innervating a muscle (e.g., SMA, GBS). Mechanisms have been elucidated for many of these pathways (e.g., ubiquitin-proteasome system, NF-κB, etc.). However, many causes of muscle atrophy (e.g., burns, arthritis, etc.) operate through unelucidated signaling cascades. Therefore, this review highlights the underlying mechanisms of each subtype of muscle atrophy while emphasizing the need for additional research in properly classifying and identifying muscle atrophy.
Muscle Atrophy
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Abstract The investigation into the effects of cold acclimation on fish skeletal muscle function and its potential implications for muscle atrophy is of great interest to us. This study examines how rearing zebrafish at low temperatures affects their locomotor activity and the expression of genes associated with muscle atrophy. Zebrafish were exposed to temperatures ranging from 10 °C to 25 °C, and their swimming distance was measured. The expression levels of important muscle atrophy genes, Atrogin-1 and MuRF1, were also evaluated. Our findings show that swimming activity significantly decreases when the water temperature ranges from 10 °C to 15 °C, indicating a decrease in voluntary movement. Additionally, gene expression analysis shows a significant increase in the expression of Atrogin-1 and MuRF1 at 10 °C. This up-regulation could lead to muscle atrophy caused by decreased activity in cold temperatures. To investigate the effects of exercise on reducing muscle atrophy, we subjected zebrafish to forced swimming at a temperature of 8 °C for ten days. This treatment significantly reduced the expression of Atrogin-1 and MuRF1, emphasizing the importance of muscle stimulation in preventing muscle atrophy in zebrafish. These findings suggest that zebrafish can serve as a valuable model organism for studying muscle atrophy and can be utilized in drug screening for muscle atrophy-related disorders. Cold-reared zebrafish provide a practical and ethical approach to inducing disuse muscle atrophy, providing valuable insights into potential therapeutic strategies for addressing skeletal muscle atrophy.
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Context: Distinct from the muscle atrophy that develops from inactivity or disuse, atrophy that occurs after traumatic joint injury continues despite the patient being actively engaged in exercise. Recognizing the multitude of factors and cascade of events that are present and negatively influence the regulation of muscle mass after traumatic joint injury will likely enable clinicians to design more effective treatment strategies. To provide sports medicine practitioners with the best strategies to optimize muscle mass, the purpose of this clinical review is to discuss the predominant mechanisms that control muscle atrophy for disuse and posttraumatic scenarios, and to highlight how they differ. Evidence Acquisition: Articles that reported on disuse atrophy and muscle atrophy after traumatic joint injury were collected from peer-reviewed sources available on PubMed (2000 through December 2019). Search terms included the following: disuse muscle atrophy OR disuse muscle mass OR anterior cruciate ligament OR ACL AND mechanism OR muscle loss OR atrophy OR neurological disruption OR rehabilitation OR exercise. Study Design: Clinical review. Level of Evidence: Level 5. Results: We highlight that (1) muscle atrophy after traumatic joint injury is due to a broad range of atrophy-inducing factors that are resistant to standard resistance exercises and need to be effectively targeted with treatments and (2) neurological disruptions after traumatic joint injury uncouple the nervous system from muscle tissue, contributing to a more complex manifestation of muscle loss as well as degraded tissue quality. Conclusion: Atrophy occurring after traumatic joint injury is distinctly different from the muscle atrophy that develops from disuse and is likely due to the broad range of atrophy-inducing factors that are present after injury. Clinicians must challenge the standard prescriptive approach to combating muscle atrophy from simply prescribing physical activity to targeting the neurophysiological origins of muscle atrophy after traumatic joint injury.
Muscle Atrophy
ACL injury
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Muscle Atrophy
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Muscle atrophy is one of the most common and destructive events in chronic diseases. It is characterized by a decrease in the cross-sectional area of muscle fiber, myonuclear number, protein content, and muscle strength and an increase in fatigability. Muscle atrophy not only causes a decline in the quality of life of patients, but also poses a burden on society [1]. The occurrence of muscle atrophy is related to many factors. From a macro point of view, there are age and disuse. At the micro level, the rate of protein degradation exceeds the rate of protein synthesis [2,3]. To date, a plethora of therapeutic strategies in the treatment of muscle atrophy has been successfully developed, such as nutritional interventions, physical exercise, and electroacupuncture therapy, all of which can prevent and rescue muscle atrophy [4]. However, there is no effective drug to treat...
Muscle Atrophy
Muscle protein
Protein Degradation
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Skeletal muscle atrophy caused by disuse is characterized by both reduction of protein synthesis and protein degradation. In our previous study, we found that ubiquitin ligase plays an important role in muscle atrophy under microgravity conditions. Therefore, it is possible that inhibition of ubiquitin ligase activity might prevent muscle atrophy. In this review, we focused on the role of proteolysis during muscle atrophy and a nutritional approach to prevent muscle atrophy. Understanding the molecular mechanisms of muscle atrophy and its related pathways is critical for the development of new therapeutic approaches.
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Protein Degradation
Proteolysis
Muscle protein
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Muscle atrophy is defined as a decrease in muscle mass, cross-sectional area, and myofibrillar protein content. Causes inducing muscle atrophy may be inactivity, denervation, undernutrition and steroid. Inactivity may decrease protein synthesis and increase protein breakdown of skeletal muscle. The muscle atrophy due to inactivity was induced by bed rest, hindlimb suspension, cast, total hip replacement arthroplasty, anterior cruciate ligament reconstruction. Denervated atrophy may be induced by the loss of innervation from lower motor neuron. The atrophy was apparent in the lower limb of hemiplegic patients following ischemic stroke and in the hindlimb of ischemic stroke rats. Protein breakdown of skeletal muscle in the undernourished state results in muscle atrophy. The atrophy due to undernutrition was evident in cancer and leukemia patients and in the undernourished rats. Steroids have been used to treat allergies, inflammatory diseases, autoimmune diseases and to inhibit immune function following transplantation. Steroids may induce muscle atrophy by protein breakdown of skeletal muscle. Muscle Physiology Laboratoryat College of Nursing, Seoul National University proved that dexamethasone may induce hindlimb muscle atrophy in rats and exercise and DHEA may attenuate hindlimb muscle atrophy induced by the steroid in rats. Nurses working with patients undergoing steroid treatment need to be cognizant of steroid induced muscle atrophy. They need to assess whether muscle atrophy is being occurred during and after the steroid treatment. Moreover, they need to apply exercise and DHEA to the patients undergoing steroid treatment in order to attenuate the steroid induced muscle atrophy.
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Amyotrophy
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Background and purpose Muscle atrophy is generally mild in patients with chronic inflammatory demyelinating polyneuropathy ( CIDP ) compared with the severity and duration of the muscle weakness. Muscle atrophy was evaluated using computed tomography ( CT ) in patients with CIDP . Methods Thirty‐one patients with typical CIDP who satisfied the diagnostic criteria for the definite CIDP classification proposed by the European Federation of Neurological Societies and the Peripheral Nerve Society were assessed. The clinicopathological findings in patients with muscle atrophy were also compared with those in patients without atrophy. Results Computed tomography evidence was found of marked muscle atrophy with findings suggestive of fatty degeneration in 11 of the 31 patients with CIDP . CT ‐assessed muscle atrophy was in the lower extremities, particularly in the ankle plantarflexor muscles. Muscle weakness, which reflects the presence of muscle atrophy, tended to be more pronounced in the lower extremities than in the upper extremities in patients with muscle atrophy, whereas the upper and lower limbs tended to be equally affected in patients without muscle atrophy. Nerve conduction examinations revealed significantly greater reductions in compound muscle action potential amplitudes in the tibial nerves of patients with muscle atrophy. Sural nerve biopsy findings were similar in both groups. The functional prognoses after immunomodulatory therapies were significantly poorer amongst patients with muscle atrophy. Conclusions Muscle atrophy was present in a subgroup of patients with CIDP , including patients with a typical form of the disease. These patients tended to demonstrate predominant motor impairments of the lower extremities and poorer functional prognoses.
Muscle Atrophy
Muscle weakness
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Muscle wasting is an unmet medical need which leads to a reduction of myofiber diameter and a negative impact on the functional performance of daily activities. We previously found that a new neuroprotective drug called NeuroHeal reduced muscle atrophy produced by transient denervation. Aiming to decipher whether NeuroHeal has a direct role in muscle biology, we used herein different models of muscle atrophy: one caused by chronic denervation, another caused by hindlimb immobilization, and lastly, an in vitro model of myotube atrophy with Tumor Necrosis Factor-α (TNFα). In all these models, we observed that NeuroHeal reduced muscle atrophy and that SIRT1 activation seems to be required for that. The treatment downregulated some critical markers of protein degradation: Muscle Ring Finger 1 (MuRF1), K48 poly-Ub chains, and p62/SQSTM1. Moreover, it seems to restore the autophagy flux associated with denervation. Hence, we envisage a prospective use of NeuroHeal at clinics for different myopathies.
Muscle Atrophy
Protein Degradation
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Muscle Atrophy
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