• 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.

• The Journal of the Korea Contents Association
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• v.9 no.4
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• pp.355-363
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• 2009

Increased oxidative stress by abnormal mitochondrial function can damage cell signal transduction and gene expression, and induce insulin resistance or diabetes. Autophagy, however, improve insulin resistance by clearance of malfunctioning mitochondria. Exercise also recovers the muscle dysfunction and degeneration by activating mitochondrial biogenesis. As it seems that exercise and autophagy might act as an orchestrated network to induce mitochondrial biogenesis, we investigated whether autophagy is involved in AMPK signal pathway stimulated by exercise or AICAR to increase mitochondrial biogenesis. And it showed that PGC-1 and mtTFA, but not autophagy marker LC3 mRNA expression were significantly increased by 6 hr of acute exercise. On the other hand, PGC-1 and mtTFA mRNA expression were upregulated by AICAR treatment to C2C12 myotube. However these genes were not inhibited by LC3 siRNA transfection. These results provide the evidence that autopahgy affects on mitochondrial biogenesis through different signal pathway from AMPK signal transduction.

• Journal of Life Science
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• v.28 no.12
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• pp.1455-1460
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• 2018

Due to a rapidly expanding aging population, the incidence of degenerative bone disease has increased, and efforts to handle the issue using regenerative medicine have become more important. In order to control various bone diseases such as osteoarthritis and osteoporosis, regenerative medicine utilizing adult stem cells has been extensively studied. And it is now clear that the mitochondrial energy metabolism, oxidative phosphorylation, is important for the process of stem cell differentiation. Interestingly, a recent study reported that salicylate promotes mitochondrial biogenesis by regulating the expression of $PGC-1{\alpha}$ in murine cells. However, the possible effects of salicylate on osteogenic differentiation through increased mitochondrial biogenesis in stem cells remain unknown. Thus, here we investigated whether salicylate could influence osteogenic differentiation and mitochondrial biogenesis of periosteum-derived mesenchymal stem cells (POMSCs). We found that salicylate treatments of POMSCs undergoing osteogenic differentiation increased the activity of alkaline phosphatase, a well-known early marker of bone cell differentiation. In addition, we observed that mitochondrial mass was increased by salicylate treatments in POMSCs. Together, these results indicate that salicylate can enhance osteogenic differentiation and mitochondrial biogenesis in POMSCs. Therefore, the findings in this study suggest that small molecules augmenting mitochondrial function such as salicylate can be a novel modulator for osteogenic differentiation and regenerative medicine.

• Journal of Life Science
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• v.29 no.8
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• pp.837-845
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• 2019

The purpose of this study was to analyze the effects of aerobic exercise and resveratrol supplementation on mitochondrial biogenesis in skeletal muscle of high-fat diet-induced obese mice. In this study, 4-wk-old C57BL/6 male mice were divided into four groups, with 10 animals in each group: a normal diet group (NC), high-fat diet group (HC), high-fat diet group with resveratrol supplementation (HRe), and high-fat diet GROUP with exercise (HE). Aerobic exercise was performed on a treadmill for 40~60 min/d at 10~14 m/min, 0% grade, 4 d/wk for 16 wk. Resveratrol (25 mg/kg bodyweight) was administrated once a day, 4 d/wk for 16 wk. There was a significance difference in COX-IV mRNA expression in the NC group versus that in the HC group (p<0.05). The expression of the SIRT-3, PGC-1a, and COX-IV mRNA genes in the HE group increased significantly as compared with the expression of these genes in the HC and HRe groups (p<0.05). These results indicated that high- fat diet-induced obesity did not affect mitochondria biogenesis gene expression in skeletal muscle. In contrast, aerobic exercise training increased the expression of mitochondria biogenesis gene expression in skeletal muscle in high-fat diet-induced obese mice. These findings suggested that aerobic exercise but not resveratrol supplementation had a positive effect on mitochondrial biogenesis in skeletal muscle in high-fat diet-induced obese mice.

• 한국체육학회지인문사회과학편
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• v.51 no.3
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• pp.353-362
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• 2012

The purpose of this research was to find effects of high fat diet and endurance exercise on mitochondria biosynthesis and insulin resistance in male Wister rat. Th rats were randomly separated into 4 groups: A, Isocaloric high fat diet group (50% of calories from fat), B. Chow group, C. Isocaloric high fat diet with endurance exercise (treadmill running, slop 8%, 23 m/min, 120 min/day, 5 days per week), D. Chow group with endurance exercise. Both Isocaloric high fat diet group and chow group were given an equal caloric composition with 3.2kcal/g. equal amount of food were checked every day and given to both groups. 4 weeks of high fat diet did not show any change in body weight and amount of body fat. Further the level of glucose and insulin in blood, and insulin-stimuilated glucose transport rate in epitrochlearis muscle was not affected by Isocaloric high fat diet. However, the endurance exercise showed statistically significant change in the level of insulin in blood. Although either Isocaloric high fat diet or endurance exercise alone did not change on mitochondria biogenesis marker, Isocaloric high fat diet with endurance exercise could induce the increased level of marker (p<0.05). Also, plasma free fatty acids were increased in this group. From this investigation, Isocaloric high fat diet with moderate-intensity endurance exercise is effective way to induce mitochondrial biogenesis.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.38 no.3
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• pp.237-245
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• 2012

Coumestrol is one of phytoalexins synthesized in response to environmental stress, and commonly found in natural foods such as alfalfa sprouts, clovers, and soybean. In the present study, we investigated the mechanism underlying protective effect of coumestrol against UVB-induced photoaging in human dermal fibroblasts. We found that pretreatment with coumestrol enhanced the UVB-suppressed mitochondrial biogenesis through regulation of Sirt1 expression and activity, and its downstream gene regulation such as PGC-$1{\alpha}$, NRF1, and TFAM. Moreover, the ATP and ROS production was restored to normal status and the formation of advanced glycation endproducts leading to skin photoaging in skin fibroblasts was blocked by coumestrol pretreatment before UVB irradiation. These findings indicate that coumestrol might potentially prevent skin photoaging induced by mitochondrial damage and glycated protein production in dermal fibroblasts.

• Korean Journal of Food Science and Technology
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• v.49 no.6
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• pp.685-692
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• 2017

Mitochondrial biogenesis-a process that leads to an increment in the number and density of mitochondria, improves physical performance and body health by enhancing exercise capacity. In the present study, we investigated the stimulatory effect of Ashitaba and red ginseng complex (ARC) on exercise capacity in L6 skeletal muscle cells and mice. In L6 skeletal muscle cells, ARC increased the mitochondrial contents and ATP production by activating AMP-activated protein kinase (AMPK), sirtuin 1 (SIRT1), and peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-$1{\alpha}$) and up-regulating the mRNA expression of nuclear respiratory factor-1 (NRF-1) and mitochondrial transcription factor A (TFAM). In the animal experiments, mice treated with ARC showed an increment in exercise capacity as compared with mice treated with Ashitaba extract or red ginseng extract alone. These studies indicate that ARC might serve as a potential natural candidate for enhancing exercise capacity by stimulation of mitochondrial biogenesis.

• Journal of Life Science
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• v.21 no.7
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• pp.997-1003
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• 2011

Menopause and obesity are associated with metabolism. The purpose of this study was to examine the changes of PPAR${\gamma}$, PGC-1(${\alpha},\;{\beta}$), NRf-1 and TFAM mRNA and mitochondria biogenesis in adipocytes and investigate the effect of swimming exercise for 6weeks on ovariectomized rats. Rats were randomly assigned to 3 groups: (1) ovariectomized rats fed with a control diet (C, n=4), (2) ovariectomized rats fed with high fat diet (H, n=4), and (3) ovariectomized rats trained to exercise and fed with high fat diet (H+EX, n=4). Exercise was performed by swimming for 5 days/wk, with a progressive increase in exercise over the course of 6 weeks. Results showed that the fat tissue weight in the H group was markedly increased (p<0.01) compared to other groups, however, regular exercise significantly decreased fat weight. The PPAR-${\gamma}$ (p<0.05), PGC-$1{\alpha}$ (p<0.01), -$1{\beta}$ (p<0.05), NRf-1 (p<0.01) and TFAM (p<0.05) mRNA expression in the adipocytes of H+EX were higher than in the H group. These results suggest that regular exercise for 6 weeks might exert positive effects by increasing PPAR-${\gamma}$, PGC-1 (${\alpha},\;{\beta}$), NRf-1 and TFAM mRNA expression and mitochondria in adipocytes. Thus, regular exercise may be helpful in the improvement of mitochondria biogenesis function in obese, ovariectomized rats.

• Microbiology and Biotechnology Letters
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• v.50 no.3
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• pp.414-421
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• 2022

In this study, we isolated Weizmannia ginsengihumi LGHNH (KCTC 14462BP) from 30-year-old wild Panax ginseng C.A. Meyer and elucidated the characteristics of the isolated bacterium and its industrial potential as an anti-aging material. W. ginsengihumi LGHNH was investigated to produce indole-3-acetic acid (IAA), a plant growth-promoting hormone (1.38 ㎍/ml to 2.22 ㎍/ml). We also confirmed the existence of bioconversion activity via the comparison of the ginsenoside content before and after fermentation. As for the converted minor ginsenoside, Rg2(R), Rg4, Rg6, Rg3(S), Rg3(R), Rk1, Rg5, Rh1(R), Rk3 and Rh4 are known to have high bioavailability and various skin effects. We measured mitochondrial membrane potential and ATP biosynthesis to elucidate W. ginsengihumi LGHNH cultured product (WCP) as an anti-aging material. As a result, the mitochondrial membrane potential in HaCaT cells with UVB decreased to 39.3% compared to the unirradiated group, but was recovered to 57.3% and 58.1% by 0.001% (v/v) and 0.01% (v/v) WCP, respectively. In addition, we measured mitochondrial ATP biosynthesis. It decreased to 94.3% compared to the unirradiated group with UVB, but was recovered to 105.3% and 105.7% by 0.001% (v/v) and 0.01% (v/v) WCP.

• Journal of the Korean Applied Science and Technology
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• v.37 no.4
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• pp.744-754
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• 2020

We investigated the whether endurance exercise and MitoQ intake mediated neuroprotection are associated with mitochondrial function in 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine(MPTP) -induced mice model of Parkinson's disease. C57BL/6 male mice were randomly assigned to five groups: Normal Conrol(NC, n=10), MPTP Control(MC, n=10), MPTP +MitoQ(MQ, n=10), MPTP + Exercise(ME, n=10) and MPTP + MitoQ + Exercise(MQE, n=10). Exercise intervention groups performed the treadmill exercise for 5days/week for 5 weeks with gradual increase of intensity. MitoQ intake groups consumed the MitoQ at a concentration of 250μmol by dissolving with water during experiment period. Our data demonstrated that ME and MQE group restored MPTP-induced motor dysfunction. In addition, treatment groups(MQ, ME and MQE) increased tyrosine hydroxylase levels, and suppressed the accumulation of α-synuclein levels. Futhermore, treatment groups modulated the mitochondrial function such as upregulated mitochondrial biogenesis, increased antioxidant enzyme, enhanced a anti-apoptotic protein(e.g., BCL2), and reduced a pro-apoptotic protein(e.g., BAX). Taken together, these results suggested that endurance exercise and MitoQ intake-mediated increase in mitochondrial function contributes to improvement of aggravated dopaminergic neuronal, resulting in attenuation of motor function of Parkinson's disease.