• Title, Summary, Keyword: Skeletal muscle

Search Result 995, Processing Time 0.055 seconds

Exercise and obesity-induced insulin resistance in skeletal muscle

  • Kwak, Hyo-Bum
    • Integrative Medicine Research
    • /
    • v.2 no.4
    • /
    • pp.131-138
    • /
    • 2013
  • The skeletal muscle in our body is a major site for bioenergetics and metabolism during exercise. Carbohydrates and fats are the primary nutrients that provide the necessary energy required to maintain cellular activities during exercise. The metabolic responses to exercise in glucose and lipid regulation depend on the intensity and duration of exercise. Because of the increasing prevalence of obesity, recent studies have focused on the cellular and molecular mechanisms of obesity-induced insulin resistance in skeletal muscle. Accumulation of intramyocellular lipid may lead to insulin resistance in skeletal muscle. In addition, lipid intermediates (e.g., fatty acyl-coenzyme A, diacylglycerol, and ceramide) impair insulin signaling in skeletal muscle. Recently, emerging evidence linking obesity-induced insulin resistance to excessive lipid oxidation, mitochondrial overload, and mitochondrial oxidative stress have been provided with mitochondrial function. This review will provide a brief comprehensive summary on exercise and skeletal muscle metabolism, and discuss the potential mechanisms of obesity-induced insulin resistance in skeletal muscle.

Effect of 'Sexiang Shuhuo Jing' for CPK, LDH Activities and Skeletal Muscle ${\alpha}-actin$ mRNA Expression after Skeletal Muscle in Rats (골격근 손상에 대한 '사향서활정'(麝香舒活精)치료의 혈청 CK, LDH활성도 및 골격근 ${\alpha}-actin$ mRNA 발현 변화의 관찰)

  • Kim, Jin-Hang;Song, Je-Ho
    • Journal of Physiology & Pathology in Korean Medicine
    • /
    • v.20 no.4
    • /
    • pp.992-996
    • /
    • 2006
  • The study examined clinical effect of the 'Sexiang Shuhuo Jing' on serum CK and LDH activities and skeletal muscle ${\alpha}-actin$ mRNA expression concentration 140days after skeletal muscle injury in rats. The clinical research consisted of observing and measuring the serum CK, LDH activities and skeletal muscle ${\alpha}-actin$ mRNA expression, at the time of injury and during recovery. All experimental data were analyzed by repeated measurement with ANOVA on of SPSS(11.5v), accepting level for all significances was above ${\alpha}\;=.05.$ The results were as follows: That skeletal muscle injury in rats there existed a substantial increase serum CK, LDH activities and expression of skeletal muscle ${\alpha}-actin$ mRNA And Sexiang Shuhuo Jing treatment group's serum CK, LDH activities lower and faster recovery than control group. The 1 st day after skeletal muscle injury, Sexiang Shuhuo Jing treatment group's skeletal muscle ${\alpha}-actin$ mRNA expression was much more higher than control group, after 2 day's faster recovery normal level than control group. There existed a substantial increase again serum CK, LDH activities and skeletal muscle ${\alpha}-actin$ mRNA expression 3rd days after injury in control group. But in Sexiang Shuhuo Jing treatment group's can't be found that.

The Korean Traditional Medicine Gyeongshingangjeehwan Reduces Lipid Accumulation in Skeletal Muscle and C2C12 Cells

  • Yoon, Mi-Chung
    • Biomedical Science Letters
    • /
    • v.17 no.4
    • /
    • pp.283-289
    • /
    • 2011
  • Our previous study demonstrated that the Korean traditional medicine Gyeongshingangjeehwan (GGEx) activates AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor ${\alpha}$ ($PPAR{\alpha}$) critical for fatty acid oxidation in skeletal muscle and C2C12 skeletal muscle cells. Thus, we examined whether GGEx can reduce lipid accumulation in these cells and tissues. After obese and type 2 diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats were treated with GGEx, we studied the effects of GGEx on skeletal muscle lipid accumulation. The effects of GGEx and/or the AMPK inhibitor compound C on lipid accumulation and expression of AMPK and $PPAR{\alpha}$ were measured in C2C12 skeletal muscle cells. Compared with lean Long-Evans Tokushima Otsuka rats, obese OLETF rats had increased triglyceride droplets. However, administration of GGEx to OLETF rats for 8 weeks significantly decreased triglyceride droplets in skeletal muscle. Consistent with the $in$ $vivo$ data, GGEx inhibited lipid accumulation, the degree of which was comparable to Wy14,643, the potent activator of $PPAR{\alpha}$. GGEx also increased skeletal muscle mRNA levels of AMPK${\alpha}1$, AMPK${\alpha}2$, and $PPAR{\alpha}$. However, compound C inhibited these effects in C2C12 cells. These results suggest that GGEx suppresses skeletal muscle lipid accumulation and this process may be mediated by AMPK and $PPAR{\alpha}$ activation.

The Effects of Skeletal Muscle Mass and Muscle Fatigue on the Proprioceptive Position Sense of the Knee Joint (뼈대근육량과 근피로가 무릎관절 고유수용성 위치감각에 미치는 영향)

  • Park, Sookyoung;Park, Kanghui
    • Journal of The Korean Society of Integrative Medicine
    • /
    • v.8 no.2
    • /
    • pp.139-147
    • /
    • 2020
  • Purpose : Proprioceptive position sense plays a key role in providing joint stability, and multiple factors are related to proprioceptive position sense. Thus, this study aimed to determine the effects of body composition, particularly skeletal muscle mass on proprioceptive position sense following muscle fatigue. Methods : Healthy female subjects agreed to have their body composition analyzed. Only subjects who had 18.5-22.9 kg/㎡ of BMI (body mass index) were included in this study, and the participants were divided into two groups by skeletal muscle mass level. The experimental group had a level of skeletal muscle lower than the standard level (n=9), while the control group showed a standard or high level of skeletal muscle mass (n=11). To determine the change in proprioceptive position sense of the knee joint, the absolute angle error (AAE) was evaluated following muscle fatigue on low extremity. The muscle fatigue was induced by isokinetic resistance exercise program of Biodex system. AAE was measured by the Biodex system and compared the result before and after muscle fatigue. Results : The experimental group showed a significant AAE difference between before (3.16±2.48 °) and after (5.40±2.61 °) muscle fatigue. In addition, there was a AAE difference between the experimental (5.40±2.61 °) and control groups (3.53±1.67 °) after fatigue; however, there was no significance. Those results indicated that low level of skeletal muscle mass might influence the proprioceptive position sense of the knee joint after muscle fatigue. Conclusion : Thus, maintaining the proper level of skeletal muscle mass is pivotal to reduce the risk of injury following muscle fatigue in ADL or sport activities.

Sexually Dimorphic Control of Obesity and Skeletal Muscle Lipid Metabolism by Fenofibrate

  • Lim, Hyesook;Lee, Hyunghee;Yoon, Michung
    • Biomedical Science Letters
    • /
    • v.19 no.1
    • /
    • pp.17-24
    • /
    • 2013
  • Animals show a sexual dimorphism in metabolic responses. We investigated to verify whether the peroxisome proliferator-activated receptor ${\alpha}$ ($PPAR{\alpha}$) agonist fenofibrate regulates obesity and skeletal muscle lipid metabolism with sexual dimorphism and to determine the changes in skeletal muscle expression of $PPAR{\alpha}$ target genes. After both sexes of C57BL/6J mice received a high fat diet with or without fenofibrate for 7 weeks, we examined the effects of fenofibrate on not only body weight, adipose tissue mass, and skeletal muscle lipid accumulation, but also the mRNA expression of $PPAR{\alpha}$-related genes in skeletal muscle. Male mice given a fenofibrate-supplemented high fat diet showed decreased body weight gain and adipose tissue mass compared with mice fed a high fat diet alone, whereas fenofibrate did not reduce them in high fat diet-fed female mice. Lipid accumulation in skeletal muscle was inhibited by fenofibrate in male mice, but not in female mice. Gene expression analysis revealed that fenofibrate increased the mRNA levels of $PPAR{\alpha}$ target enzymes only in male mice. Therefore, our results suggest that sex-dependence differences in obesity and intramuscular lipid levels under fenofibrate treatment could be due in part to the differences in skeletal muscle $PPAR{\alpha}$ activation between male and female mice.

The Effects of Daekumeumja on Alcohol-induced Muscle Atrophy in Rats (대금음자(對金飮子)가 흰쥐의 만성 알콜성 근위축에 미치는 영향)

  • Kim, Bum Hoi
    • Herbal Formula Science
    • /
    • v.24 no.3
    • /
    • pp.153-161
    • /
    • 2016
  • Chronic alcoholic myopathy is one of the most common skeletal muscle disorders. It is characterized by a reduction in the entire skeletal musculature, skeletal muscle weakness, and difficulties in gait. Patients with alcoholic hepatitis and cirrhosis have severe muscle loss that contributes to worsening outcome. Although the myopathy selectively affects Type II (fast twitch, glycolytic, anaerobic) skeletal muscle fibers, total skeletal musculature is reduced. The severity of the muscle atrophy is proportional to the duration and amount of alcohol consumed and leads to decreased muscle strength. The mechanisms for the myopathy are generally unknown but it is not due to overt nutritional deficiency, nor due to either neuropathy or severe liver disease. Skeletal muscle mass and protein content are maintained by a balance between protein synthesis and breakdown and in vivo animal models studies have shown that ethanol inhibits skeletal muscle protein synthesis. Daekumeumja is a traditional Korean medicine that is widely employed to treat various alcohol-induced diseases. Muscle diseases are often related to liver diseases and conditions. The main objective of this study was to assess that Daekumeumja extract could have protective effect against alcoholic myopathy in a Sprague-Dawley rat model. Rats were orally given 25% ethanol (5ml/kg, body weight) for 8 weeks. After 30 minutes, rats were administrated with Daekumeumja extract. Controls were similarly administrated with the vehicle alone. The weights of gastrocnemius, soleus and plantaris muscles were assessed and the morphologic changes of gastrocnemius and plantaris muscles were also assessed by hematoxylin and eosin staining. In results, The muscles from ethanol treated rats displayed a significant reduction in muscle weight and average cross section area compared to Normal group. Daekumeumja extract treated group showed increased muscle weight and muscle fiber compared to the ethanol treated group. It was concluded that Daekumeumja extract showed ameliorating effects on chronic alcohol myopathy in skeletal muscle.

Effects of exercise on obesity-induced mitochondrial dysfunction in skeletal muscle

  • Heo, Jun-Won;No, Mi-Hyun;Park, Dong-Ho;Kang, Ju-Hee;Seo, Dae Yun;Han, Jin;Neufer, P. Darrell;Kwak, Hyo-Bum
    • The Korean Journal of Physiology and Pharmacology
    • /
    • v.21 no.6
    • /
    • pp.567-577
    • /
    • 2017
  • Obesity is known to induce inhibition of glucose uptake, reduction of lipid metabolism, and progressive loss of skeletal muscle function, which are all associated with mitochondrial dysfunction in skeletal muscle. Mitochondria are dynamic organelles that regulate cellular metabolism and bioenergetics, including ATP production via oxidative phosphorylation. Due to these critical roles of mitochondria, mitochondrial dysfunction results in various diseases such as obesity and type 2 diabetes. Obesity is associated with impairment of mitochondrial function (e.g., decrease in $O_2$ respiration and increase in oxidative stress) in skeletal muscle. The balance between mitochondrial fusion and fission is critical to maintain mitochondrial homeostasis in skeletal muscle. Obesity impairs mitochondrial dynamics, leading to an unbalance between fusion and fission by favorably shifting fission or reducing fusion proteins. Mitophagy is the catabolic process of damaged or unnecessary mitochondria. Obesity reduces mitochondrial biogenesis in skeletal muscle and increases accumulation of dysfunctional cellular organelles, suggesting that mitophagy does not work properly in obesity. Mitochondrial dysfunction and oxidative stress are reported to trigger apoptosis, and mitochondrial apoptosis is induced by obesity in skeletal muscle. It is well known that exercise is the most effective intervention to protect against obesity. Although the cellular and molecular mechanisms by which exercise protects against obesity-induced mitochondrial dysfunction in skeletal muscle are not clearly elucidated, exercise training attenuates mitochondrial dysfunction, allows mitochondria to maintain the balance between mitochondrial dynamics and mitophagy, and reduces apoptotic signaling in obese skeletal muscle.

Insulin Resistance Does Not Influence Gene Expression in Skeletal Muscle

  • Nguyen, Lisa L.;Kriketos, Adamandia D.;Hancock, Dale P.;Caterson, Ian D.;Denyer, Gareth S.
    • BMB Reports
    • /
    • v.39 no.4
    • /
    • pp.457-463
    • /
    • 2006
  • Insulin resistance is commonly observed in patients prior to the development of type 2 diabetes and may predict the onset of the disease. We tested the hypothesis that impairment in insulin stimulated glucose-disposal in insulin resistant patients would be reflected in the gene expression profile of skeletal muscle. We performed gene expression profiling on skeletal muscle of insulin resistant and insulin sensitive subjects using microarrays. Microarray analysis of 19,000 genes in skeletal muscle did not display a significant difference between insulin resistant and insulin sensitive muscle. This was confirmed with real-time PCR. Our results suggest that insulin resistance is not reflected by changes in the gene expression profile in skeletal muscle.

Effects of exercise on myokine gene expression in horse skeletal muscles

  • Lee, Hyo Gun;Choi, Jae-Young;Park, Jung-Woong;Park, Tae Sub;Song, Ki-Duk;Shin, Donghyun;Cho, Byung-Wook
    • Asian-Australasian Journal of Animal Sciences
    • /
    • v.32 no.3
    • /
    • pp.350-356
    • /
    • 2019
  • Objective: To examine the regulatory effects of exercise on myokine expression in horse skeletal muscle cells, we compared the expression of several myokine genes (interleukin 6 [IL-6], IL-8, chemokine [C-X-C motif] ligand 2 [CXCL2], and chemokine [C-C motif] ligand 4 [CCL4]) after a single bout of exercise in horses. Furthermore, to establish in vitro systems for the validation of exercise effects, we cultured horse skeletal muscle cells and confirmed the expression of these genes after treatment with hydrogen peroxide. Methods: The mRNA expression of IL-6, IL-8, CXCL2, and CCL4 after exercise in skeletal muscle tissue was confirmed using quantitative-reverse transcriptase polymerase chain reactions (qRT-PCR). We then extracted horse muscle cells from the skeletal muscle tissue of a neonatal Thoroughbred. Myokine expression after hydrogen peroxide treatments was confirmed using qRT-PCR in horse skeletal muscle cells. Results: IL-6, IL-8, CXCL2, and CCL4 expression in Thoroughbred and Jeju horse skeletal muscles significantly increased after exercise. We stably maintained horse skeletal muscle cells in culture and confirmed the expression of the myogenic marker, myoblast determination protein (MyoD). Moreover, myokine expression was validated using hydrogen peroxide ($H_2O_2$)-treated horse skeletal muscle cells. The patterns of myokine expression in muscle cells were found to be similar to those observed in skeletal muscle tissue. Conclusion: We confirmed that several myokines involved in inflammation were induced by exercise in horse skeletal muscle tissue. In addition, we successfully cultured horse skeletal muscle cells and established an in vitro system to validate associated gene expression and function. This study will provide a valuable system for studying the function of exercise-related genes in the future.

Sarcopenia targeting with autophagy mechanism by exercise

  • Park, Sung Sup;Seo, Young-Kyo;Kwon, Ki-Sun
    • BMB Reports
    • /
    • v.52 no.1
    • /
    • pp.64-69
    • /
    • 2019
  • The loss of skeletal muscle, called sarcopenia, is an inevitable event during the aging process, and significantly impacts quality of life. Autophagy is known to reduce muscle atrophy caused by dysfunctional organelles, even though the molecular mechanism remains unclear. Here, we have discuss the current understanding of exercise-induced autophagy activation in skeletal muscle regeneration and remodeling, leading to sarcopenia intervention. With aging, dysregulation of autophagy flux inhibits lysosomal storage processes involved in muscle biogenesis. AMPK-ULK1 and the $FoxO/PGC-1{\alpha}$ signaling pathways play a critical role in the induction of autophagy machinery in skeletal muscle, thus these pathways could be targets for therapeutics development. Autophagy has been also shown to be a critical regulator of stem cell fate, which determines satellite cell differentiation into muscle fiber, thereby increasing muscle mass. This review aims to provide a comprehensive understanding of the physiological role of autophagy in skeletal muscle aging and sarcopenia.