• Asian-Australasian Journal of Animal Sciences
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• v.18 no.1
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• pp.133-140
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• 2005

Although amino acids are substrates for the synthesis of proteins and nitrogen-containing compounds, it has become more and more clear over the years that these nutrients are also extremely important as regulators of body protein turnover. The branched-chain amino acids (BCAAs) together or simply leucine alone stimulate protein synthesis and inhibit protein breakdown in skeletal muscle. However, it was only recently that the mechanism(s) involved in the regulation of protein turnover by BCAAs has begun to be defined. The acceleration of protein synthesis by these amino acids seems to occur at the level of peptide chain initiation. Oral administration of leucine to food-deprived rats enhances muscle protein synthesis, in part, through activation of the mRNA binding step of translation initiation. Despite our knowledge of the induction of protein synthesis by BCAAs, there are few studies on the suppression of protein degradation. The recent findings that oral administration of leucine rapidly reduced $N^{\tau}$-methylhistidine (3-methylhistidine; MeHis) release from isolated muscle, an index of myofibrillar protein degradation, indicate that leucine suppresses myofiblilar protein degradation. The details of the molecular mechanism by which leucine inhibits proteolysis is just beginning to be elucidated. The purpose of this report was to review the current understanding of how BCAAs act as regulators of protein turnover.

• Proceedings of the Korean Society for Food Science of Animal Resources Conference
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• 1996.11a
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• pp.12-19
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• 1996

• Korean Journal of Exercise Nutrition
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• v.17 no.2
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• pp.35-42
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• 2013

The purpose of this study was to identify the effects of gene expression of endoplasmic reticulum (ER) stress in skeletal muscle and adipose tissue on acute exhaustive exercise. Thirty-five Sparague Dawley male rats were divided into a control group (CON, n = 7) and a exhaustive exercise group (n = 28), immediately after exhaustive exercise group (n = 7), after 30 minutes exhaustive exercise group (n = 7), after 60 minutes exhaustive exercise group (n = 7), after 180 minutes exhaustive exercise group (n = 7). As a result, changes in the composition of the blood serum triglyceride concentration increased significantly in immediately after exhaustive exercise group, On the contrary, blood glucose showed a significantly decreased (p < .05). Homeostasis of energy metabolism due to exhaustive exercise as a result of the mechanism of action of skeletal muscle in the glycogenolysis and absorption, which indicates that the process of means. On the other hand, a result of examining changes in endoplasmic reticulum stress-related proteins in skeletal muscle and adipose tissue, JNK1 except in skeletal muscle BiP, ATF4, CHOP, GRP78 mRNA increased significantly immediately after exercise, and after 30 minutes returned to normal levels that could be confirmed (p < .05). BiP mRNA in adipose tissue show a similar pattern and skeletal muscle increased significantly immediately after exercise, but other changes in the specificity of the endoplasmic reticulum stress-related proteins also did not appear. In conclusion, Exercise applies and exercise training duration and exercise intensity as well as research on the interaction of the endoplasmic reticulum stress-related genes should be study continuously, to be more clear.

• BMB Reports
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• v.47 no.6
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• pp.348-353
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• 2014

The speed of sound (SOS) value is an indicator of bone mineral density (BMD). Previous genome-wide association (GWA) studies have identified a number of genes, whose variations may affect BMD levels. However, their biological implications have been elusive. We re-analyzed the GWA study dataset for the SOS values in skeletal sites of 4,659 Korean women, using a gene-set analysis software, GSA-SNP. We identified 10 common representative GO terms, and 17 candidate genes between these two traits (PGS < 0.05). Implication of these GO terms and genes in the bone mechanism is well supported by the literature survey. Interestingly, the significance levels of some member genes were inversely related, in several gene-sets that were shared between two skeletal sites. This implies that biological process, rather than SNP or gene, is the substantial unit of genetic association for SOS in bone. In conclusion, our findings may provide new insights into the biological mechanisms for BMD.

• IMMUNE NETWORK
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• v.11 no.4
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• pp.223-226
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• 2011

Although exercise-induced growth factors such as Insulin-like growth factor-I (IGF-I) are known to affect various aspects of physiology in skeletal muscle cells, the molecular mechanism by which IGF-I modulates anti-inflammatory effects in these cells is presently unknown. Here, we showed that IGF-I stimulation suppresses the expression of toll-like receptor 4 (TLR4), a key innate immune receptor. A pharmacological inhibitor study further showed that PI3K/Akt signaling pathway is required for IGF-I-mediated negative regulation of TLR4 expression. Furthermore, IGF-I treatment reduced the expression of various NF-${\kappa}B$-target genes such as TNF-${\alpha}$ and IL-6. Taken together, these findings indicate that the anti-inflammatory effect of exercise may be due, at least in part, to IGF-I-induced suppression of TLR4 and subsequent downregulation of the TLR4-dependent inflammatory signaling pathway.

• Korean Journal of Exercise Nutrition
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• v.16 no.1
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• pp.35-41
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• 2012

We investigated the role of fatty acid availability on skeletal muscle AMPK activity and adenine nucleotide content. To investigate the chronic effects of elevated fatty acid in vivo Sprague-Dawley rats were fed a chow diet (15% fat) or a diet high in saturated (SAFA, 52% fat) or polyunsaturated (PUFA, 52% fat) fat for eight weeks. High fat diets increased (P < 0.05) plasma FFA levels by 25%. AMPK activity was increased in SAFA and PUFA rats and occurred in the absence of changes in ATP, AMP, phosphocreatine and glycogen content. These results suggest that increasing fatty acid availability increases AMPK activity independent of changes in the cellular energy charge, and implicate the regulation of AMPK by a covalent mechanism. These data also support the contention that increasing fatty acid availability can increase subsequent fatty acid oxidation by an AMPK-mediated process.

• Molecules and Cells
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• v.28 no.6
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• pp.589-593
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• 2009

In this study, the roles of the p38 MAPK, ERK1/2 and JNK signaling pathway in IGF-I-induced AR induction and activation were examined. C2C12 cells were treated with IGF-I in the absence or presence of various inhibitors of p38 MAPK (SB203580), ERK1/2 (PD98059), and JNK (SP600125). Inhibition of the MAPK pathway with SB203580, PD98059, or SP600125 significantly decreased IGF-I-induced AR phosphorylation and total AR protein expression. IGF-I-induced nuclear fraction of total AR and phosphorylated AR were significantly inhibited by SB203580, PD98059, or SP600125. Furthermore, IGF-I-induced AR mRNA and skeletal ${\alpha}-actin$ mRNA were blocked by those inhibitors in dose-dependent manner. Confocal images showed that IGF-I-induced AR nuclear translocation from cytosol was significantly blocked by SB203580, PD98059, or SP600125, suggesting that the MAPK pathway regulates IGF-I-induced AR nuclear localization in skeletal muscle cells. The present results suggest that the MAPK pathways are required for the ligand-independent activation of AR by IGF-I in C2C12 skeletal muscle cells.

• Journal of Acupuncture Research
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• v.31 no.1
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• pp.7-21
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• 2014

Objectives : To observe the regenerative effects of indirect moxibustion, a traditional Korean medical treatment on skeletal muscles using mouse model of skeletal muscle adiposity. Methods : Twenty seven ICR male mice were randomly assigned into Intact control(n=3), glycerol treatment together without moxibustion(n=12), and glycerol treatment together with moxibustion (n=12) groups. Mice of glycerol treatment groups were injected with 50 ${\mu}l$ DW(distilled water) containing 50 % of glycerol into the two tibialis anterior. After injection, moxibustion was applied at 'Shenshu'($BL_{23}$) and 'Zusanli'($ST_{36}$) acupoints three times per each session, every days for twelve days(total 12 treatments). Phospho-Erk1/2, Myostatin protein levels were analyzed by western blotting and immunofluo-rescence staining techniques for tissues of the tibialis anterior muscle. Smad, phospho-Smad were analyzed by immunofluorescence staining. Results : 1. Histological analysis of sections from injected TA muscles showed that glycerol induced rapidly muscle necrosis, with a maximum at day 3. 6 days and 9 days after injection, muscle was regenerating. 2. According to western blotting and immunofluorescence staining, phospho-Erk1/2 protein signals in glycerol treatment with moxibustion group were stronger compared to Intact and glycerol treatment without moxibustion group. 3. According to western blotting and immunofluorescence staining, myostatin protein signals in glycerol treatment without moxibustion group were stronger compared to Intact and glycerol treatment with moxibustion group. 4. According to immunofluorescence staining, Smad protein signals in glycerol treatment without moxibustion group were stronger compared to Intact and glycerol treatment with moxibustion group. 5. According to immunofluorescence staining, phospho-Smad protein signals in glycerol treatment without moxibustion group were stronger compared to Intact and glycerol treatment with moxibustion group. Conclusions : These results confirm that indirect moxibustion of 'Shenshu'($BL_{23}$) and 'Zusanli'($ST_{36}$) influences muscle regeneration in mouse models of skeletal muscle adiposity. Further discussion, and the establishment of moxibustion mechanism will prompt clinical application of moxibustion.

• Journal of Yeungnam Medical Science
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• v.18 no.1
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• pp.94-100
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• 2001

Background: It is doubtful that aging causes deteriorated glucose metabolism and insulin resistance of skeletal muscle. Some researchers had different results about it. So we have studied the mechanism responsible for the abnormal glucose tolerance associated with aging in rapidly growing and matured rats. Materials and Methods: Animals were used S.D. rats. Growing rats were 7 weeks old (BW: 160-190 gm) and matured rats were 28 weeks old (BW: 420-525 gm). Results: Fasting blood glucose and plasma insulin levels were significantly elevated in matured rat compared with growing rats. And during oral glucose tolerance test the glucose level was also significantly elevated in matured rats. These results confirmed an insulin resistant state of aging. Insulin levels at 30 minutes of oral glucose tolerance test was significantly elevated in growing rat. But at 120 minutes it was maintained at higher level in matured rats than in growing rats. It suggested the possibility of increased insulin secretion by initial stimulation of beta-cells in growing rats, and increased secretion and decreased catabolic rate of insulin in matured rats. Glucose uptake rate of soleus muscle in matured rats was lower than that of growing rats, but the difference was not statistically significant. The dose(insulin)-responsive(glucose uptake) curve of soleus muscle was only slightly deviated to the right side. Conclusion: Glucose metabolism of rat skeletal muscle was worsened by aging. The data of glucose uptake experiments suggested the possibility of insulin resistance of skeletal muscle in matured rats. but the mechanism of insulin resistance of skeletal muscle need further studies.

• Biomedical Science Letters
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• v.16 no.3
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• pp.151-159
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• 2010

The peroxisome proliferator-activated receptor $\alpha$ (PPAR$\alpha$) is a nuclear transcription factor that plays a central role in lipid metabolism and obesity. Exercise also is a powerful modifier of the manifestations of the lipid metabolism and obesity in animal models and humans with obesity and metabolic syndrome. However, effects of exercise on lipid metabolism and obesity in normal-weight younger female subjects, having functional ovaries and not metabolic disease, remain unexplained. To explore the effects of exercise on the development of obesity and its molecular mechanism in high fat diet-fed female C57BL/6J mice, we experimented the effects of swim training on body weight, adipose tissue mass, serum lipid levels, morphological changes of adipocytes and the expression of PPAR$\alpha$ target genes involved in fat oxidation in skeletal muscle tissue of female C57BL/6J mice. Swim-trained mice had significantly decreased body weight, adipose tissue mass, serum triglycerides compared with female control mice. Histological studies showed that swim training significantly decreased the average size of adipoctyes in parametrial adipose tissue. Swim training did not affect the expression of PPAR$\alpha$ mRNA in skeletal muscle. Concomitantly, swim training did not increase mRNA levels of PPAR$\alpha$ target genes responsible for fatty acid $\beta$-oxidation, such as carnitine palmitoyltransferase 1, medium chain acyl-CoA dehydrogenase, enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase, and thiolase in skeletal muscle. In conclusion, these results indicate that swim training regulates lipid metabolism and obesity in high fat diet fed-female mice although swim training did not increase mRNA levels of PPAR$\alpha$ target genes involved in fatty acid $\beta$-oxidation in skeletal muscle, suggesting that swim training may prevent obesity and improve fitness through other mechanisms in female with ovaries, not through the activation of skeletal muscle PPAR$\alpha$.