scholarly journals PO-109 Resistance Training prevents Skeletal Muscle Atrophy Induced by hypoxia through regulating Akt-FoxO1 pathway

2018 ◽  
Vol 1 (4) ◽  
Author(s):  
Jiabei Yu ◽  
Hang Yu ◽  
Yanchun Li ◽  
Tianyu Han ◽  
Xuecheng Bai ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Muscle Atrophy ◽  
Biceps Brachii ◽  
Training Group ◽  
Skeletal Muscle Atrophy ◽  
Control Group ◽  
Immunofluorescence Technique ◽  
Hypoxia Group ◽  
Wet Weight

Objective Skeletal muscle atrophy induced by hypoxia on the plateau will lead to the decrease of muscle strength and the degeneration of athletic ability. Resistance training is an efficient method to stimulate the growth of muscle and improve protein synthesis. Akt-FoxO1 (Fork head box protein 1) pathway plays a significant role in the regulation of skeletal muscle protein degradation. However, it is not clear whether resistance training could prevent skeletal muscle atrophy induced by hypoxia and what is the regulation role of Akt-FoxO1 pathway. This study built a rat model that resistance training inhibited the skeletal muscle atrophy induced by hypoxia and explore the variation of Akt, FoxO1, Murf and Atrogin-1. Methods 40 male 8-week-old Sprague-Dawley (SD) rats were divided into 4 groups randomly: control group (C), resistance training group (R), hypoxia group (H) and hypoxia resistance training group (HR). H and HR group were placed into simulated 4000m altitude (12.4%, O2%) and R and HR group received ladder resistance training. Their incremental load is calculated by using average body weight. After 4 weeks intervention of hypoxia and resistance training, body composition, wet weight of skeletal muscle (soleus, musculus gastrocnemius,extensor digitorum longus and muscelus biceps brachii) and skeletal muscle cross-sectional area (CSA) were measured. The expression of Akt, FoxO1, Murf and Atrogin-1 were detected by Western blot and RT-PCR.Moreover,immunofluorescence technique was used to locate the phosphorylation of FoxO1.  Results The lean body mass of HR group was significantly higher than H group (P<0.05). The wet weight and CSA of muscelus biceps brachii in HR group were also higher than H group obviously (P<0.05). The results of real-time fluorescence quantitative PCR and western blot showed that the expression of FoxO1 and MuRF of hypoxia group (H group) were significantly higher than control group. However after the intervention of resistance training, the expression of Akt was significantly up-regulate and FoxO1, MuRF were significantly down-regulate. Immunofluorescence technique was used to observe the location of FoxO1 phosphorylation and the expression out of nucleus. Conclusions Resistance training contribute to prevent the occurrence of skeletal muscle atrophy induced by hypoxia and the form of climbing ladder training can stimulate the hypertrophy of biceps in rats. The results revealed that FoxO1 phosphorylation out of nucleus became higher after resistance training. All above revealed that resistance training could inhibit skeletal muscle atrophy induced by hypoxia. Akt promoted FoxO1 phosphorylation may become the molecular mechanisms that resistance training can inhibit the atrophy of skeletal muscle induced by hypoxia.

scholarly journals PO-306 The effect of four weeks hypoxic resistance training on myostatin and follistatin expression in skeletal muscle of rats

2018 ◽  
Vol 1 (5) ◽  
Author(s):  
Xuecheng Bai Bai ◽  
Yang Hu ◽  
Yanchun Li
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Resistance Exercise ◽  
Mrna Expression ◽  
Muscle Atrophy ◽  
Biceps Brachii ◽  
Skeletal Muscle Atrophy ◽  
Significant Difference ◽  
Wet Weight ◽  
Hypoxic Resistance

Objective Loss of skeletal muscle weight is a common phenomenon in hypoxic environment. It has been recognized that resistance training can reduce hypoxia-induced skeletal muscle atrophy, but its molecular mechanism is still unclear. Myostatin is a major factor that inhibits muscle growth and differentiation, and Follistatin can inhibit Myostatin. Therefore, this study is to clarify the effect of 4-week hypoxic resistance exercise on Myostatin and Follistatin gene expression in skeletal muscle of rats. Methods Twenty four 8-week-old male SD rats were randomly divided into normoxic control group (group C: 6 rats), normoxic exercise group (group R: 6 rats), hypoxic control group (group H: 6 rats) and hypoxic exercise group (group HR: 6 rats). Rats in each hypoxic group were fed in a hypoxic chamber (atmospheric hypoxia) with oxygen concentration of 12.7% (simulated 4000m altitude). Rats in each exercise group were trained according to the rat's resistance training program developed in our laboratory. After all the intervention, DEXA was used to analyze the body composition. The soleus, extensor digitorum longus and biceps brachii muscles of rats were taken and the wet weight of individual muscles was measured. The data were processed by SPSS17.0 statistical software. The expression level of skeletal muscle mRNA was expressed as "median (25-75%)" and the data of body composition and muscle wet weight were expressed as"mean±standard deviation". The differences between the groups were evaluated using a one-way analysis of variance (ANOVA) test. The significance level for the study was less than 0.05. Results Body composition analysis after 4 weeks of hypoxic intervention showed that the body weight of rats in group H decreased significantly (p=0.012), and the muscle mass decreased more significantly (p<0.001). But resistance exercises obviously reduced the muscle atrophy (p<0.01) caused by hypoxia. After analyzing the changes of the wet weight of individual muscles, it was found that the wet weight of biceps brachii in HR group was significantly higher than that in H group (p=0.048). After 4 weeks of hypoxic intervention and hypoxic resistance exercise, the expression of Myostatin mRNA in individual muscles of each group changed differently. The expression of Myostatin mRNA in soleus muscle of H group was significantly higher than that of C group (371.2%) after 4 weeks of hypoxia intervention. Myostatin mRNA expression in soleus and biceps brachii of HR group was significantly lower than that of H group (591.1% and 478.4% respectively). However, there was no significant difference in the expression level of Myostatin mRNA in the extensor digitorum longus between each group (p=0.259). The change of Follistatin mRNA expression in different groups also showed a different trend. The expression of Follistatin mRNA in soleus muscle and biceps brachii muscle was significantly different among groups (p=0.003, p=0.004, respectively). However, there was no significant difference in the expression level of Follistatin mRNA in the extensor digitorum longus between each group (p=0.734). Myostatin mRNA/Follistatin mRNA ratio (M/F) showed a more significant difference. The M/F ratio of soleus muscle in group H was significantly lower than that in group C (p<0.001), but the M/F ratio in group HR was significantly higher than that in group H (p<0.001). The M/F ratio of biceps brachii in group H was significantly lower than that in group C (p<0.001), but the M/F ratio in group HR showed a higher trend than that in group H (p=0.051). Conclusions Hypoxic exposure results in an increase in Myostatin mRNA expression in skeletal muscle, but hypoxic resistance exercise reduces such an increase. On the contrary, the level of Follistatin mRNA expression in skeletal muscle decreased after hypoxic exposure, and hypoxic resistance exercise could slow down the decline. As a result, rat resistance exercise significantly slowed down hypoxia-induced muscle atrophy. In conclusion, the mutual restriction between Myostatin and Follistatin is one of the main links of resistance exercise to reduce hypoxia-induced skeletal muscle atrophy. However, the process of resistance training to reduce the hypoxia-induced skeletal muscle atrophy is very complex. There are many molecular signaling pathways involved, which need further study.

scholarly journals Resistance Training Alleviates Skeletal Muscle Atrophy in Rats Exposed to Hypoxia by inhibiting Autophagy Mediated by Acetyl-FoxO1

2020 ◽  
Author(s):  
Pengyu FU ◽  
KONG Zhaowei ◽  
GONG Lijing ◽  
Hans-Christer Holmberg ◽  
LI Yanchun ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Muscle Atrophy ◽  
Muscular Atrophy ◽  
Training Group ◽  
Skeletal Muscle Atrophy ◽  
Control Group ◽  
Autophagic Flux ◽  
Sequestosome 1 ◽  
Control Group Group

Abstract Background: Skeletal muscle atrophy induced by hypoxia could affect the physical fitness and training effect of the athletes in the rapid altitude, and also affect the production and life of the general public. Resistance training in a hypoxic environment could effectively alleviate the occurrence of muscular atrophy. Whether autophagy lysosomal pathway, as an important proteolysis pathway, is involved in this process, and whether FoxO1, the key gene of atrophy, plays a role by regulating autophagy is unclear. Methods: Male Sprague-Dawley (SD) rats were randomly divided into normoxic control group (group C), normoxic resistance-training group (group R), hypoxic control group (group H), and hypoxic resistance-training group (group HR). The H and HR groups were exposed to 12.4% oxygen for four weeks. The R and HR groups underwent incremental loaded training by climbing a ladder every other day for four weeks. Results: Compared to parameters in group H, resistance training increased lean body mass (LBM) and wet weight and decreased the expression of atrogin1 of the extensor digitorum longus (EDL) after four weeks ( P <0.05). Resistance training decreased the levels of FoxO1 and Ac-FoxO1 and the extent of their localization in the nucleus and cytoplasm, respectively ( P <0.05), as well as the LC3II/LC3I ratio, the integrated optical density (IOD) of LC3 and the levels of autophagy-related gene 7 (Atg7), and elevated the levels of sequestosome 1 (SQSTM1/p62) ( P <0.05). Most differentially expressed autophagy-related genes (ATGs) interacted with FoxO1, and the functions of these ATGs were mainly enriched in the early autophagy phase. Conclusions: Our findings demonstrate that resistance training lowers the levels of both nuclear FoxO1 and cytoplasmic Ac-FoxO1, as well as reduced autophagic flux in the EDL of rats exposed to hypoxia.

scholarly journals Tail suspension is useful as a sarcopenia model in rats

2021 ◽  
Vol 37 (1) ◽  
Author(s):  
Akira Nemoto ◽  
Toru Goyagi
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Experimental Model ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Whole Body ◽  
Skeletal Muscle Atrophy ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Simple Method

Abstract Background Sarcopenia promotes skeletal muscle atrophy and exhibits a high mortality rate. Its elucidation is of the highest clinical importance, but an animal experimental model remains controversial. In this study, we investigated a simple method for studying sarcopenia in rats. Results Muscle atrophy was investigated in 24-week-old, male, tail-suspended (TS), Sprague Dawley and spontaneously hypertensive rats (SHR). Age-matched SD rats were used as a control group. The skeletal muscle mass weight, muscle contraction, whole body tension (WBT), cross-sectional area (CSA), and Muscle RING finger-1 (MuRF-1) were assessed. Enzyme-linked immunosorbent assay was used to evaluate the MuRF-1 levels. Two muscles, the extensor digitorum longus and soleus muscles, were selected for representing fast and slow muscles, respectively. All data, except CSA, were analyzed by a one-way analysis of variance, whereas CSA was analyzed using the Kruskal-Wallis test. Muscle mass weight, muscle contraction, WBT, and CSA were significantly lower in the SHR (n = 7) and TS (n = 7) groups than in the control group, whereas MuRF-1 expression was dominant. Conclusions TS and SHR presented sarcopenic phenotypes in terms of muscle mass, muscle contraction and CSA. TS is a useful technique for providing muscle mass atrophy and weakness in an experimental model of sarcopenia in rats.

scholarly journals Effect of Resistance Training Along with Curcumin Supplementation on Expression of Some Regulator Genes Associated with Cardiac Muscle Structure in Obese Rats

Thrita ◽  
2020 ◽  
Vol 9 (2) ◽  
Author(s):  
Atefeh Rauofi ◽  
Sirous Farsi ◽  
Seyed Ali Hosseini
Keyword(s):  
Physical Activity ◽  
Resistance Training ◽  
Cardiac Muscle ◽  
Muscle Atrophy ◽  
Synergistic Effects ◽  
Training Group ◽  
Control Group ◽  
Gene Expressions ◽  
Obese Rats ◽  
Reduced Physical Activity

Background: Reduced physical activity can cause obesity and metabolic syndrome, leading to fibrosis in cardiac muscles and premature cardiac aging. Physical activity, along with herbal supplements, can have a synergistic effect on preventing cardiac muscle proteolysis. Objectives: In this study, the effects of curcumin and resistance training were assessed on cardiac muscle atrophy in obese rats. Methods: Twenty-four male Sprague rats were categorized into four groups, including the placebo, resistance training, curcumin, and resistance training + curcumin. Resistance training was performed three times a week with three sets in each session, repeated five times for eight weeks. During this time, 150 mg/kg curcumin was administered through gavage. Twenty-four hours after finishing resistance training, surgery was performed on the cardiac muscle, and gene expressions of PGC1-α, FOXO1, Murf-1, Atrogin, Collagen1, and Collagen 3 were assessed with real-time PCR. Results: The expression of PGC1-α and FOXO1 genes in both resistance training and resistance training+curcumin groups significantly increased and decreased, respectively, compared to the control group (P = 0.001). The MuRF1 expression in the curcumin+resistance training group decreased significantly (P = 0.013) compared to the placebo and curcumin groups. The expression of collagen type 1 and type 2 in all the three treatment groups had significant decreases compared to the placebo group (P < 0.05). Conclusions: Considering the results of this study, resistance training and curcumin supplement each alone can prevent cardiac muscle atrophy. However, the simultaneous use of curcumin supplement and resistance training can lead to synergistic effects.

scholarly journals Effects of Resistance Training of Peripheral Muscles Versus Respiratory Muscles in Older Adults With Sarcopenia Who are Institutionalized: A Randomized Controlled Trial

2018 ◽  
Vol 26 (4) ◽  
pp. 637-646 ◽  
Author(s):  
Maria À. Cebrià i Iranzo ◽  
Mercè Balasch-Bernat ◽  
María Á. Tortosa-Chuliá ◽  
Sebastià Balasch-Parisi
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Muscle Mass ◽  
Gait Speed ◽  
Training Group ◽  
Knee Extension ◽  
Respiratory Muscle Training ◽  
Control Group ◽  
Muscle Training ◽  
Peripheral Muscle

This study compares the effects of two resistance training programs in peripheral and respiratory musculature on muscle mass and strength and physical performance and identifies the appropriate muscle mass parameter for assessing the intervention effects. Thirty-seven institutionalized older Spanish adults with sarcopenia were analyzed: control group (n = 17), respiratory muscle training group (n = 9), and peripheral muscle training group (n = 11). Measured outcomes were appendicular skeletal muscle mass (ASM/height2, ASM/weight, and ASM/BMI), isometric knee extension, arm flexion and handgrip strength, maximal inspiratory and expiratory pressures, and gait speed pre- and postintervention. Trained groups participated in a 12-week program and improved in maximum static inspiratory pressure, maximum static expiratory pressure, knee extension, and arm flexion (p < .05), whereas nonsignificant changes were found in gait speed and ASM indexes pre- and postintervention in the three groups. In conclusion, resistance training improved skeletal muscle strength in the studied population, and any ASM index was found to be appropriate for detecting changes after physical interventions.

scholarly journals PO-094 p38 MAPK controls of E3-ligases expression and soleus atrophy attenuation in rat upon hindlimb unloading

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Tatiana Nemirovskaya ◽  
Svetlana Belova ◽  
Boris Shenkman ◽  
Ekaterina Mochalova
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
P38 Mapk ◽  
Muscle Atrophy ◽  
Mapk Signaling ◽  
Hindlimb Unloading ◽  
Hindlimb Suspension ◽  
Skeletal Muscle Atrophy ◽  
Control Group ◽  
E3 Ligases

Objective Unloading causes rapid skeletal muscle atrophy mainly due to the increased protein degradation. Muscle proteolysis results from the activation of ubiquitin-proteasome systems. The ubiquitination proteins are carried out by muscle-specific E3 ubiquitin ligases – MuRF-1 and MAFbx. It is known that MuRF-1 and MAFbx expression significantly increases on the third day of muscle unloading. We tested the hypothesis that p38 MAPK participates in the regulation of E3 ligases expression and the development of skeletal muscle atrophy during unloading. To check this idea we inhibited p38 MAPK by VX-745. Methods 21 male Wistar rats were divided into 3 groups (7 rats in each group): intact control (C), rats suspended for 3 days (HS) and rats suspended and injected i.p. with VX-745 (10 mg/kg/day) (VX). The hindlimb suspension was carried out according to Morey-Holton technique. The animals were anaesthetised with an i.p. injection of tribromoethanol (240 mg/kg). Under anesthesia, the m.soleus were excised, frozen in liquid nitrogen, and stored at -80°C until further analysis. All procedures with the animals were approved by the Biomedicine Ethics Committee of the Institute of Biomedical Problems of the Russian Academy of Sciences/Physiology section of the Russian Bioethics Committee. The statistical analysis was performed using the REST 2009 v.2.0.12 and Origin Pro programs at the significance level set at 0,05. The results are given as median in percent and interquartile range (0.25-0.75). Results The muscle weight in HS group was significantly reduced (72,3±2,5 mg) compared to C (83,0±3 mg), p<0.05, while the soleus weight of VX group didn’t differ from the control (84.2±5 mg). The MuRF1 mRNA expression was elevated dramatically in HS group (165 (138-210) %) when compared with the control (100 (64.6-112.5) %), p<0.05.  In the VX group the level of MuRF1 mRNA expression (127 (105-138) %) didn’t differ from the control group. The MAFbx mRNA expression was observed to increase equally in both suspended groups (294 (265-342) % and (271 (239-309) %).) vs C (100 (91-106) %) so, VX-745 administration did not have any significant effect on its expression. We also found that the level of ubiquitin mRNA expression in the soleus of HS rats was higher (423 (325-485) %) in comparison with the C group (100 (78-166) %, p<0.05) while VX-745 injection prevented increasing the  mRNA ubiquitin expression (200 (190-237) %). We discovered that the elevation of calpain-1 mRNA expression upon HS was prevented by VX-745 administration and its level didn’t differ from the control group (C - 100 (97-105) %, HS – 120 (116-133) %, VX - 107 (100-115) %, p<0.05). Conclusions Thus, the results indicate that the p38 MAPK signaling pathway takes part in the regulation of E3-ligase MuRF1 but not MAFbx expression. The p38 MAPK inhibition prevents muscle atrophy and the elevation of ubiquitin and calpain mRNA expression at the early stage of hindlimb unloading. This work was supported by RFBR grant No.17-04-01838.

Resistance training affects GLUT-4 content in skeletal muscle of humans after 19 days of head-down bed rest

1999 ◽  
Vol 86 (3) ◽  
pp. 909-914 ◽  
Author(s):  
Izumi Tabata ◽  
Youji Suzuki ◽  
Tetsuo Fukunaga ◽  
Toshiko Yokozeki ◽  
Hiroshi Akima ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Membrane Protein ◽  
Vastus Lateralis ◽  
Bed Rest ◽  
Training Group ◽  
Control Group ◽  
Glut 4 ◽  
Before And After ◽  
Voluntary Contractions

This study assessed the effects of inactivity on GLUT-4 content of human skeletal muscle and evaluated resistance training as a countermeasure to inactivity-related changes in GLUT-4 content in skeletal muscle. Nine young men participated in the study. For 19 days, four control subjects remained in a −6° head-down tilt at all times throughout bed rest, except for showering every other day. Five training group subjects also remained at bed rest, except during resistance training once in the morning. The resistance training consisted of 30 isometric maximal voluntary contractions for 3 s each; leg-press exercise was used to recruit the extensor muscles of the ankle, knee, and hip. Pauses (3 s) were allowed between bouts of maximal contraction. Muscle biopsy samples were obtained from the lateral aspect of vastus lateralis (VL) muscle before and after the bed rest. GLUT-4 content in VL muscle of the control group was significantly decreased after bed rest (473 ± 48 vs. 398 ± 66 counts ⋅ min−1 ⋅ μg membrane protein−1, before and after bed rest, respectively), whereas GLUT-4 significantly increased in the training group with bed rest (510 ± 158 vs. 663 ± 189 counts ⋅ min−1 ⋅ μg membrane protein−1, before and after bed rest, respectively). The present study demonstrated that GLUT-4 in VL muscle decreased by ∼16% after 19 days of bed rest, and isometric resistance training during bed rest induced a 30% increase above the value of GLUT-4 before bed rest.

scholarly journals Distinct protein degradation profiles are induced by different disuse models of skeletal muscle atrophy

2011 ◽  
Vol 43 (19) ◽  
pp. 1075-1086 ◽  
Author(s):  
Peter Bialek ◽  
Carl Morris ◽  
Jascha Parkington ◽  
Michael St. Andre ◽  
Jane Owens ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Muscle Fiber ◽  
Skeletal Muscle Atrophy ◽  
Rapid Induction ◽  
Genome Wide ◽  
Fiber Size ◽  
Ubiquitin Proteasome ◽  
Wet Weight ◽  
Genome Wide Expression

Skeletal muscle atrophy can be a consequence of many diseases, environmental insults, inactivity, age, and injury. Atrophy is characterized by active degradation, removal of contractile proteins, and a reduction in muscle fiber size. Animal models have been extensively used to identify pathways that lead to atrophic conditions. We used genome-wide expression profiling analyses and quantitative PCR to identify the molecular changes that occur in two clinically relevant mouse models of muscle atrophy: hindlimb casting and Achilles tendon laceration (tenotomy). Gastrocnemius muscle samples were collected 2, 7, and 14 days after casting or injury. The total amount of muscle loss, as measured by wet weight and muscle fiber size, was equivalent between models on day 14, although tenotomy resulted in a more rapid induction of muscle atrophy. Furthermore, tenotomy resulted in the regulation of significantly more mRNA transcripts then did casting. Analysis of the regulated genes and pathways suggest that the mechanisms of atrophy are distinct between these models. The degradation following casting was ubiquitin-proteasome mediated, while degradation following tenotomy was lysosomal and matrix-metalloproteinase mediated, suggesting a possible role for autophagy. These data suggest that there are multiple mechanisms leading to muscle atrophy and that specific therapeutic agents may be necessary to combat atrophy resulting from different conditions.

scholarly journals D-Methionine Ameliorates Cisplatin-Induced Muscle Atrophy via Inhibition of Muscle Degradation Pathway

2019 ◽  
Vol 18 ◽  
pp. 153473541982883 ◽  
Author(s):  
Ching-Te Wu ◽  
Jiuan-Miaw Liao ◽  
Jiunn-Liang Ko ◽  
Yao-Ling Lee ◽  
Hui-Yi Chang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Gastric Emptying ◽  
Muscle Atrophy ◽  
Muscle Tissue ◽  
Skeletal Muscle Atrophy ◽  
Tissue Homogenate ◽  
C2c12 Myotubes ◽  
Control Group ◽  
Related Gene ◽  
Feeding Efficiency

Cisplatin induces anorexia, weight loss, loss of adipose tissue, skeletal muscle atrophy, and serious adverse effects that can cause premature termination of chemotherapy. The aim of this study was to use an animal model to assess cisplatin therapy (3 cycles) with and without d-methionine to investigate its protective effects on cisplatin-induced anorexia and skeletal muscle wasting. Wistar rats were divided into 3 groups and treated as follows: saline as control (group 1), intraperitoneal cisplatin once a week for 3 weeks (group 2), and intraperitoneal cisplatin once a week for 3 weeks plus oral administration of d-methionine (group 3). Tissue somatic index (TSI), gastric emptying index (GEI), and feeding efficiency were measured. Both hepatic lipid metabolism and muscle atrophy-related gene expressions and C2C12 myotubes were determined by polymerase chain reaction. Micro–computed tomography (micro-CT) was used to conduct assessment of bone microarchitecture indices. Pathological changes of the gastric mucosa were assessed by hematoxylin and eosin staining after euthanizing the animals. d-Methionine increased food intake, weight gain, gastric emptying, and feeding efficiency, as well as decrease stomach contents, after cisplatin injections. Cisplatin caused shortening of myofibers. Cisplatin-induced muscle mass wasting was mediated by the elevation of mRNA expressions of MAFbx and MuRF-1 in ubiquitin ligases in muscle tissue homogenate. The mRNA expressions of MyoD and myogenin, markers of muscle differentiation, declined following cisplatin administration. The administration of d-methionine not only led to significant improvements in myofiber diameter and cross-sectional fiber areas but also reversed muscle atrophy-related gene expression. However, there were no significant changes in stomach histology or microarchitecture of trabecular bone among the study groups. The results indicate that d-methionine has an appetite-enhancing effect and ameliorates cisplatin-induced adipose and muscle tissue loss during cisplatin-based chemotherapy.

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