• Journal of Nutrition and Health
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• v.54 no.6
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• pp.594-602
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• 2021

Purpose: The zinc transporter ZIP7 is known to regulate glucose metabolism in skeletal muscles, and skeletal muscles are known to play a critical role in glycemic control. The present study examines the effects of dietary zinc supplementation on the blood glucose concentration and expression of ZIP7 in skeletal muscle obtained from obese mice fed a high-fat diet (HF). Methods: C57BL/6J male mice were divided into three groups and were administered either a HF (60% of total calories from fat), HF supplemented with zinc (HF+Zn, 60% calories from fat + 300 mg zinc/kg diet), or low-fat diet (CON, 10% calories from fat), for 15 weeks. Results: Compared to CON group mice, the final body weights and adipose tissue weights were significantly increased, while the skeletal muscle weights were significantly decreased in mice belonging to the HF and HF+Zn groups. The HF+Zn group had significantly lower levels of fasting blood glucose concentrations than the HF group. Similarly, zinc supplementation significantly decreased the HF-elevated area under the curve values obtained from the oral glucose tolerance test. Skeletal muscle protein levels of ZIP7 in samples obtained from the HF group were significantly decreased as compared to the CON group. Conversely, the skeletal ZIP7 protein levels in the HF+Zn group were significantly increased as compared to the HF group. Moreover, the protein levels of phosphorylated-AKT and glucose transporter 4 in the skeletal muscle were significantly increased subsequent to zinc supplementation. Conclusion: Our data demonstrates that zinc supplementation up-regulates the skeletal muscle ZIP7 expression, which is associated with improved glucose tolerance in the obesity.

• Journal of Life Science
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• v.27 no.8
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• pp.879-887
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• 2017

It is well established that brain-derived neurotrophic factor (BDNF) is expressed not only in the brain but also in skeletal muscle, and is required for normal neuromuscular system function. Histone deacetylases (HDACs) and insulin-like growth factor-I (IGF-I) are potent regulators of skeletal muscle myogenesis and muscle gene expression, but the mechanisms of HDAC and IGF-I in skeletal muscle-derived BDNF expression have not been examined. In this study, we examined the effect of IGF-I and suberoylanilide hydroxamic acid (SAHA), a pan-HDAC inhibitor, on BDNF induction. Proliferating or differentiating C2C12 skeletal muscle cells were treated with increasing concentrations (0-50 ng/ml) of IGF-I in the absence or presence of $5{\mu}M$ SAHA for various time periods (3-24 hr). Treatment of C2C12 cells with IGF-I resulted in a dose- and time-dependent decrease in BDNF mRNA expression. However, inhibition of HDAC led to a significant increase in the expression of BDNF mRNA levels. In addition, immunocytochemistry revealed high BDNF protein levels in undifferentiated C2C12 skeletal muscle cells, whether untreated, IGF-I-treated, or exposed to SAHA. These results represent the first evidence that IGF-I can suppress the mRNA and protein expression of BDNF; conversely, SAHA attenuates the effects of IGF-I. Consequently, SAHA upregulates BDNF expression in C2C12 skeletal muscle cells.

• Journal of Microbiology and Biotechnology
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• v.34 no.2
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• pp.270-279
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• 2024

Macrophages are versatile immune cells that play crucial roles in tissue repair, immune defense, and the regulation of immune responses. In the context of skeletal muscle, they are vital for maintaining muscle homeostasis but macrophage-induced chronic inflammation can lead to muscle dysfunction, resulting in skeletal muscle atrophy characterized by reduced muscle mass and impaired insulin regulation and glucose uptake. Although the involvement of macrophage-secreted factors in inflammation-induced muscle atrophy is well-established, the precise intracellular signaling pathways and secretion factors affecting skeletal muscle homeostasis require further investigation. This study aimed to explore the regulation of macrophage-secreted factors and their impact on muscle atrophy and glucose metabolism. By employing RNA sequencing (RNA-seq) and proteome array, we uncovered that factors secreted by lipopolysaccharide (LPS)-stimulated macrophages upregulated markers of muscle atrophy and pro-inflammatory cytokines, while concurrently reducing glucose uptake in muscle cells. The RNA-seq analysis identified alterations in gene expression patterns associated with immune system pathways and nutrient metabolism. The utilization of gene ontology (GO) analysis and proteome array with macrophage-conditioned media revealed the involvement of macrophage-secreted cytokines and chemokines associated with muscle atrophy. These findings offer valuable insights into the regulatory mechanisms of macrophage-secreted factors and their contributions to muscle-related diseases.

• Asian-Australasian Journal of Animal Sciences
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• v.27 no.5
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• pp.757-766
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• 2014

Postnatal muscle hypertrophy of beef cattle is the result of enhanced myofibrillar protein synthesis and reduced protein turnover. Skeletal muscle hypertrophy has been studied in cattle fed ${\beta}$-adrenergic agonists (${\beta}$-AA), which are receptor-mediated enhancers of protein synthesis and inhibitors of protein degradation. Feeding ${\beta}$-AA to beef cattle increases longissimus muscle cross-sectional area 6% to 40% compared to non-treated cattle. The ${\beta}$-AA have been reported to improve live animal performance, including average daily gain, feed efficiency, hot carcass weight, and dressing percentage. Treatment with ${\beta}$-AA increased mRNA concentration of the ${\beta}_2$ or ${\beta}_1$-adrenergic receptor and myosin heavy chain IIX in bovine skeletal muscle tissue. This review will examine the effects of skeletal muscle and adipose development with ${\beta}$-AA, and will interpret how the use of ${\beta}$-AA affects performance, body composition, and growth in beef cattle.

• Nutrition Research and Practice
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• v.15 no.2
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• pp.203-212
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• 2021

BACKGROUND/OBJECTIVES: The branched-chain amino acids (BCAA), including isoleucine, leucine, and valine, promote muscle protein synthesis. However, obesity may interfere with protein synthesis by dysregulating mitochondrial function in the muscles. This study aimed to examine the association between dietary intake levels of BCAA and skeletal muscle mass index (SMI) in middle-aged participants, and the effect of obesity/abdominal obesity on this association. SUBJECTS/METHODS: The data of 3,966 men and women aged 50-64 years who participated in the 2008-2011 Korea National Health and Nutrition Examination Survey were analyzed. Intake levels of energy-adjusted dietary amino acids were obtained using a 24-hour dietary recall. SMI was calculated by dividing the appendicular skeletal muscle mass by body weight (kg) and multiplying the result by 100%. Multivariable general linear models were used to analyze the association of dietary BCAA intake levels with SMI. RESULTS: The beneficial effects of energy-adjusted dietary BCAA intakes on SMI were greater in the non-obesity/non-abdominal obesity groups; however, no significant associations were observed in the obesity/abdominal obesity groups (P > 0.05). CONCLUSIONS: Healthy weight and sufficient intake of dietary BCAA are recommended to maintain muscle mass.

• Journal of Nutrition and Health
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• v.55 no.6
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• pp.684-698
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• 2022

Purpose: Recent studies have reported a significant association between skeletal muscle, muscle strength and non-alcoholic fatty liver disease (NAFLD). The effect of nutrient intake on the prediction of skeletal muscle mass and strength or its suggested correlation with metabolic diseases has been primarily reported in healthy individuals. The current study explores the association between energy intake and handgrip strength (HGS) in individuals with NAFLD. Methods: Data were obtained from the Korea National Health and Nutrition Examination Surveys 2016-2018. Data from 12,469 participants were extracted and 1,293 men and 1,401 women aged 20 years and older were included in the analyses of patients with NAFLD. The presence of NAFLD was determined using the hepatic steatosis index. To estimate relative skeletal muscle strength, HGS was measured using a digital dynamometer and calculated by adjusting the body mass index of the dominant arm. Study subjects in the NAFLD and non-NAFLD groups were separately categorized according to quartiles of the calculated HGS. Results: We found that individuals with low (EQ1) energy intake had lower odds of HGS compared to subjects with high (EQ4) energy intake, irrespective of their NAFLD status (p < 0.0001). However, the HGS did not differ based on the level of protein or fat intake ratio. Additionally, the effect of energy intake on HGS was more pronounced in men than in women. Conclusion: Energy intake was associated with the risk of weak HGS in men with NAFLD. The results indicate that energy intake may be a key factor in nutrition care for NAFLD patients with low muscle function.

• Korean Journal of Exercise Nutrition
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• v.23 no.3
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• pp.50-55
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• 2019

[Purpose] The purpose of this study was to identify the relationships between muscle mass, muscle strength, and physical and cognitive functions and to examine the effects of resistive Theraband® exercise on sarcopenia-associated variables in the older population. [Methods] A total of 28 elderly women (age: 69.90 ± 0.8 years) participated in this study, 15 of whom underwent elastic band exercise for 1 hour per day, twice per week for 8 weeks. The correlation analysis was conducted to identify the associations between body composition, skeletal muscle mass indices, grip strength, and physical and cognitive functions. All variables were assessed at baseline and post-exercise. [Results] Skeletal muscle mass was significantly associated with grip strength and physical function. Gait speed was positively correlated with grip strength and physical function, but not with cognitive function. Theraband® exercise significantly improved gait speed and physical function. [Conclusion] The present data suggest that skeletal muscle mass is highly correlated with grip strength and physical function. Eight weeks of resistive Theraband® exercise favorably affects sarcopenia by improving gait speed and mobility of elderly women.

• Biomedical Science Letters
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• v.15 no.4
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• pp.301-307
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• 2009

Whole-body insulin resistance results largely from impaired insulin-stimulated glucose disposal in skeletal muscle. Our previous studies using differential display and quantitative real-time RT-PCR have shown that a novel cDNA band (DD23) had a higher level of expression in insulin resistant skeletal muscle and it was correlated with whole-body insulin action, independent of age, sex, and percent body fat. In this study, we cloned and characterized DD23. The DD23 sequence is part of the 3'UTR region of the RNA binding motif, single stranded interacting protein (RBMS3). We have cloned the full length cDNA for RBMS3 and identified two splice variants. These variants named DD23-L and DD23-S have 15 and 14 exons respectively and differ from RBMS3 in the 3'UTR significantly. Northern blot analyses showed that an ~8.8 kb mRNA transcript of DD23 was predominantly expressed in skeletal muscle and to a lesser extent in placenta, but not in heart, brain, lung, liver, or kidney, unlike RBMS3. Elevated expression levels of these novel alternatively spliced variants of RBMS3 in skeletal muscle may play a role in whole body insulin resistance.

• Journal of Ginseng Research
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• v.48 no.1
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• pp.52-58
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• 2024

Background: Skeletal muscle denervation leads to motor neuron degeneration, which in turn reduces muscle fiber volumes. Recent studies have revealed that apoptosis plays a role in regulating denervation-associated pathologic muscle wasting. Korean red ginseng (KRG) has various biological activities and is currently widely consumed as a medicinal product worldwide. Among them, ginseng has protective effects against muscle atrophy in in vivo and in vitro. However, the effects of KRG on denervation-induced muscle damage have not been fully elucidated. Methods: We induced skeletal muscle atrophy in mice by dissecting the sciatic nerves, administered KRG, and then analyzed the muscles. KRG was administered to the mice once daily for 3 weeks at 100 and 400 mg/kg/day doses after operation. Results: KRG treatment significantly increased skeletal muscle weight and tibialis anterior (TA) muscle fiber volume in injured areas and reduced histological alterations in TA muscle. In addition, KRG treatment reduced denervation-induced apoptotic changes in TA muscle. KRG attenuated p53/Bax/cytochrome c/Caspase 3 signaling induced by nerve injury in a dose-dependent manner. Also, KRG decreases protein kinase B/mammalian target of rapamycin pathway, reducing restorative myogenesis. Conclusion: Thus, KRG has potential protective role against denervation-induced muscle atrophy. The effect of KRG treatment was accompanied by reduced levels of mitochondria-associated apoptosis.

• Journal of Life Science
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• v.27 no.3
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• pp.361-369
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• 2017

Mitochondrial homeostasis is tightly regulated by two major processes: mitochondrial biogenesis and mitochondrial degradation by autophagy (mitophagy). Research in mitochondrial biogenesis in skeletal muscle in response to endurance exercise training has been well established, while the mechanisms regulating mitophagy and the relationship between mitochondrial biogenesis and degradation following endurance exercise training are not yet well defined. Studies have demonstrated that endurance exercise training increases the expression levels of mitochondrial biogenesis-, dynamics-, mitophagy-related genes in skeletal muscle. However, the increased levels of mitochondrial biogenesis marker proteins such as Cox IV and citrate synthase, by endurance exercise training were abolished when autophagy/mitophagy was inhibited in skeletal muscle. This suggests that both autophagy/mitophagy plays an important role in mitochondrial biogenesis/homeostasis and the coordination between the opposing processes may be important for skeletal muscle adaptation to endurance exercise training to improve metabolic function and endurance exercise performance. It is considered that endurance exercise training regulates each of these processes, mitochondrial biogenesis, fusion and fission events and autophagy/mitophagy, ensuring a relatively constant mitochondrial population. Exercise training may also have contributed to mitochondrial quality control which replaces old and/or unhealthy mitochondria with new and/or healthy ones in skeletal muscle. In this review paper, the molecular mechanisms regulating mitochondrial biogenesis and mitophagy and the coordination between the opposing processes is involved in the cellular adaptation to endurance exercise training in skeletal muscle will be discussed.