• 한국동물학회지
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• 제34권2호
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• pp.131-141
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• 1991

TPA나 PDGF를 처리로 인한 Protein Kinase C의 신호전달은 힌산화에 의해 일어난다. 그렇지만, PKC에 의해 인산화 되어지는 targeting protein은 TAP나 PDGF 처리시에는 분자량이 서로 다른 단백질들이 인산화가 되어졌다. TPA처리한 myoblast에서 분자량 20,000의 단백질이 인산화되었다. PDGF처리한 세포에서는 분자량 40,000의 단백질이 인산화된 반면에 TPA처리로 인산화 되었던 분자량 20,000의 단백질은 탈인산화 되었다. 이러한 결과들은 TPA와 PDGF가 신호전달계의 활성에 있어서 다를 뿐만 아니라 그들은 장시간의 처리동안 PKC의 down regulation에 관계되어 짐을 암시한다. 그러나 PDGF는 TPA의 경우에서 보다 빠른 down regulation을 유도하였다. 면역세포 화학적인 연구에서 PKC의 동위효소인 PKC II는 세포질에, PKC III는 세포질과 인에 각각 분포하고 있었다. Myoblast에 있어서 PCK두가지 형태의 동위효소의 발현은 이들 동위효소들이 signal transduction이나 down regulation의 각기 다른 경로에 개입되어 진다는 것을 암시한다.

• Journal of Nutrition and Health
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• 제55권4호
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• pp.462-475
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• 2022

본 연구는 팔미트산으로 인슐린 저항성을 유도한 C2C12 근육세포주에서 ADLE의 인슐린 저항성개선효과를조사하고이에대한조절기전을확인하고자하였다. C2C12 근육세포주에 ADLE를 처리 시, AMPK의 활성화를 통해 포도당흡수 (glucose uptake)가 증가되었으며, 이는 미토콘드리아-매개 에너지 생합성 조절단백질인 PGC1α, UCP3, CS 활성을 증가시킴과 동시에 지방산 합성인자인 ACC, FAS, SREBP-1의 발현을 억제함을 알 수 있었다. 세포주에서 확인된 결과들을 고지방식이 유도 당뇨마우스의 근육조직에서 조사한 결과, 고지방식이와 ADLE를 동시에 처리한 그룹에서 AMPK 활성화, GLUT4 발현증가와 미토콘드리아 에너지 대사증가, 지방산 합성 감소효과를 보였다. 이상의 결과들로, ADLE가 근육 내 에너지 대사 관련 경로의 상위유전자인 AMPK를 활성화하여 GLUT4의 세포막 이동을 증진시켜 당대사 조절에 관여하는 것을 관찰하였으며, AMPK의 인산화 증가는 PGC1α의 활성화에 관여하고, 이를 통해 열 발산 대사와 관련된 UCP3의 증가 및 CS 활성을 증가시키고, 지방산 합성 관련 유전자 발현을 억제시킴을 알 수 있었다. 본 결과로부터 ADLE는 대사증후군에서 공통적으로 나타나는 인슐린 저항성을 개선시킬 수 있으며, 이는 근육세포에서의 AMPK의 활성화를 통한 에너지생성기전과 관련이 있음을 알 수 있었다. ADLE는 비만, 당뇨 등의 다양한 부작용을 가진 약제와는 다른 안전성을 보장할 수 있는 이점을 가지고 있어 인슐린 저항성 및 제2형 당뇨병 치료를 위한 기능성 식품 소재로의 활용 가능성도 충분히 가지고 있음을 확인할 수 있었다.

• 한국가금학회지
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• 제48권4호
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• pp.255-265
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• 2021

지구 온난화와 여름철 고온 환경은 육계의 성장 능력뿐만 아니라 동물복지에도 큰 영향을 미친다. 성장과 근육발달 중심으로 선발된 육계는 열 스트레스를 완화시키는 심장과 폐와 같은 핵심 장기들은 비례적으로 성장하지 못하여 급격한 환경 온도 변화에 대처하기가 어렵다. 환경 온도의 변화는 배아 발달 기간 및 부화 초기까지 근육생성에 큰 영향을 준다. 위성세포 또한 고온 스트레스에 매우 민감하다. 고온스트레스는 위성세포의 증식 및 분화 활동에 영향을 주고, 위성세포의 운명뿐만 아니라, 근육 성장 및 구조에 영향을 미친다. 부화 기간의 정교한 온도조절과 부화 초기 사육 환경 온도의 관리는 육계의 성장과 근육 발달, 그리고 동물복지를 결정하는 데 가장 중요한 핵심 요소이다.

• The Korean Journal of Physiology
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• 제15권1호
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• pp.3-8
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• 1981

Studies have been conducted to test the effect of Ginseng alcohol extract on the membrane potentials of frog skeletal muscle. The gastrocnemius muscle was isolated and placed in a chamber containing the Clark-frog Ringer solution. Membrane potentials were recorded using microelectrodes filled with 3 M KCI and muscle was electrically stimulated to obtain action potential. Changes in both the action potential and the resting membrane potential were observed after adding an appropriate amount of Ginseng alcohol extract in the perfusing Ringer solution. The results obtained from 346 muscle cells are summarized as follows : 1) The average resting membrane potential of the normal frog gastrocnemius muscle cell was -92.8 mV and the peak of the action potential reached at 29.8 mV. 2) Both the resting membrane potential and the peak of the action potential decreased by Ginseng alcohol extract, the effect being proportional to the dose of Ginseng alcohol extract. 3) The resting membrane potential and the peak of the action potential continuously decreased until about 40 min after Ginseng addition and leveled off thereafter. The potentials recovered to its original value after Ginseng was washed out. 4) The resting membrane potential was more sensitive to the Ginseng alcohol extract than was the action potential. These results strongly suggest that Ginseng alcohol extract increases both the $Na^+$ and $K^+$ permeability in the skeletal muscle cell membrane.

• Asian-Australasian Journal of Animal Sciences
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• 제20권9호
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• pp.1349-1353
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• 2007

Calcineurin is a calmodulin dependent protein that functions as a regulator of muscle cell growth and function. Agents capable of interacting with calcineurin could have important applications in muscle disease treatment as well as in the improvement of livestock production. Calsarcins comprise a family of muscle-specific calcineurin binding proteins which play an important role in modulating the function of calcineurin in muscle cells. Recently, we described the first two members of the calsarcin family (calsarcin-1 and calsarcin-2) in the pig. Here, we characterized the third member of the calsarcin family, calsarcin-3, which is also expressed specifically in skeletal muscle. However, unlike calsarcin-1 and calsarcin-2, the calsarcin-3 mRNA expression in skeletal muscle kept rising throughout the prenatal and postnatal development periods. In addition, radiation hybrid mapping indicated that porcine calsarcin-3 mapped to the distal end of the q arm of pig chromosome 2 (SSC2). A C/T single nucleotide polymorphism site in exon 5 was genotyped using the denaturing high performance liquid chromatography (DHPLC) method and the allele frequencies at this locus were significantly different among breeds.

• International Neurourology Journal
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• 제22권4호
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• pp.260-267
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• 2018

Purpose: A major question remaining in approaches to tissue engineering and organ replacement is the role of native mobilized native cells in the regeneration process of damaged tissues and organs. The goal of this study was to compare the cell mobilizing effects of the chemokine CXCL12 and cell therapy on the urinary sphincter of nonhuman primates (NHP) with chronic intrinsic urinary sphincter dysfunction. Methods: Either autologous lenti-M-cherry labeled skeletal muscle precursor cells (skMPCs) or CXCL12 were injected directly into the sphincter complex of female NHPs with or without surgery-induced chronic urinary sphincter dysfunction (n=4/treatment condition). All monkeys had partial bone marrow transplantation with autologous lenti-green fluorescent protein (GFP) bone marrow cells prior to treatment. Labeled cells were identified, characterized and quantified using computer-assisted immunohistochemistry 6 months posttreatment. Results: GFP-labeled bone marrow cells (BMCs) were identified in the bone marrow and both BMCs and skMPCs were found in the urinary sphincter at 6-month postinjection. BMCs and skMPCs were present in the striated muscle, smooth muscle, and lamina propria/urothelium of the sphincter tissue. Sphincter injury increased the sphincter content of BMCs when analyzed 6-month postinjection. CXCL12 treatment, but not skMPCs, increased the number of BMCs in all layers of the sphincter complex (P<0.05). CXCL12 only modestly (P=0.15) increased the number of skMPCs in the sphincter complex. Conclusions: This dual labeling methodology now provides us with the tools to measure the relative number of locally injected cells versus bone marrow transplanted cells. The results of this study suggest that CXCL12 promotes mobilization of cells to the sphincter, which may contribute more to sphincter regeneration than injected cells.

• Journal of Animal Science and Technology
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• 제58권5호
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• pp.18.1-18.10
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• 2016

Muscle, studied mostly with respect to meat production, represents one of the largest protein reservoirs of the body. As gene expression profiling holds credibility to deal with the increasing demand of food from animal sources, excessive loss due to myopathies and other muscular dystrophies was found detrimental as it aggravates diseases that result in increased morbidity and mortality. Holding key point towards improving the developmental program of muscle in meat producing animals, elucidating the underlying mechanisms of the associated pathways in livestock animals is believed to open up new avenues towards enhancing the lean tissue deposition. To this end, identification of vital candidate genes having no known function in myogenesis, is believed to increase the current understanding of the physiological processes going on in the skeletal muscle tissue. Taking consequences of gene expression changes into account, knowledge of the pathways associated with their activation and as such up-regulation seems critical for the overall muscle homeostasis. Having important implications on livestock production, a thorough understanding of postnatal muscle development seems a timely step to fulfil the growing need of ever increasing populations of the world.

• Fisheries and Aquatic Sciences
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• 제26권6호
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• pp.406-422
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• 2023

Sarcopenia is an age-related, progressive skeletal muscle disorder involving the loss of muscle mass and strength. Previous studies have shown that γ-aminobutyric acid (GABA) from fermented oysters aids in regulatory T cells (Tregs) cell expansion and function by enhancing autophagy, and concomitantly mediate muscle regeneration by modulating muscle inflammation and satellite cell function. The fermentation process of oysters not only increases the GABA content but also enhances the content of branched amino acids and free amino acids that aid the level of protein absorption and muscle strength, mass, and repair. In this study, the effect of GABA-enriched fermented sarco oyster extract (FSO) on reduced muscle mass and functions via Treg modulation and enhanced autophagy in aged mice was investigated. Results showed that FSO enhanced the expression of autophagy markers (autophagy-related gene 5 [ATG5] and GABA receptor-associated protein [GABARAP]), forkhead box protein 3 (FoxP3) expression, and levels of anti-inflammatory cytokines (interleukin [IL]-10 and transforming growth factor [TGF]-β) secreted by Tregs while reducing pro-inflammatory cytokine levels (IL-17A and interferon [IFN]-γ). Furthermore, FSO increased the expression of IL-33 and its receptor IL-1 receptor-like 1 (ST2); well-known signaling pathways that increase amphiregulin (Areg) secretion and expression of myogenesis markers (myogenic factor 5, myoblast determination protein 1, and myogenin). Muscle mass and function were also enhanced via FSO. Overall, the current study suggests that FSO increased autophagy, which enhanced Treg accumulation and function, decreased muscle inflammation, and increased satellite cell function for muscle regeneration and therefore could decrease the loss of muscle mass and function with aging.

• 대한약침학회지
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• 제20권4호
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• pp.235-242
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• 2017

Irisin is a novel hormone like polypeptide that is cleaved and secreted by an unknown protease from fibronectin type III domain-containing protein 5 (FNDC5), a membrane-spanning protein and which is highly expressed in skeletal muscle, heart, adipose tissue, and liver. Since its discovery in 2012, it has been the subject of many researches due to its potent physiological role. It is believed that understanding irisin's function may be the key to comprehend many diseases and their development. Irisin is a myokine that leads to increased energy expenditure by stimulating the 'browning' of white adipose tissue. In the first description of this hormone, increased levels of circulating irisin, which is cleaved from its precursor fibronectin type III domain-containing protein 5, were associated with improved glucose homeostasis by reducing insulin resistance. Irisin is a powerful messenger, sending the signal to determine the function of specific cells, like skeletal muscle, liver, pancreas, heart, fat and the brain. The action of irisin on different targeted tissues or organs in human being has revealed its physiological functions for promoting health or executing the regulation of variety of metabolic diseases. Numerous studies focus on the association of irisin with metabolic diseases which has gained great interest as a potential new target to combat type 2 diabetes mellitus and insulin resistance. Irisin is found to improve insulin resistance and type 2 diabetes by increasing sensitization of the insulin receptor in skeletal muscle and heart by improving hepatic glucose and lipid metabolism, promoting pancreatic ${\beta}$ cell functions, and transforming white adipose tissue to brown adipose tissue. This review is a thoughtful attempt to summarize the current knowledge of irisin and its effective role in mediating metabolic dysfunctions in insulin resistance and type 2 diabetes mellitus.

• International Journal of Molecular Medicine
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• 제44권3호
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• pp.1161-1171
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• 2019

The present study investigated whether glucagon like peptide-1 (GLP-1) improves glucose uptake through glucose transporter type 4 (GLUT4), mediated by the activation of sirtuin 1 (SIRT1), in skeletal muscle cells with palmitate induced-insulin resistance. The levels of glucose uptake, GLUT4, protein kinase A (PKA), and cyclic adenosine monophosphate (cAMP) were determined in human skeletal muscle myotubes (HSMMs) exposed to palmitate and GLP-1. Then, to determine whether PKA/cAMP were downstream signals of GLP-1, a PKA inhibitor was used. To determine whether SIRT-1 contributes to GLP-1 action in HSMMs with palmitate-induced insulin resistance, the levels of peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α) deacetylation and SIRT-1 activity were assessed using a SIRT1 inhibitor and small interfering RNA (siRNA). The phosphorylation levels of protein kinase B (Akt) and insulin receptor substrate 1 (IRS-1) as insulin signaling pathways, were assessed in GLP-1-treated HSMMs exposed to palmitate. The influence of SIRT1 on the GLP-1-induced activation of insulin signaling pathway was determined using a SIRT1 inhibitor. GLP-1 restored the palmitate-induced reductions in the levels of glucose uptake, GLUT4 mRNA, GLUT4 promoter activity, and GLUT4 protein in HSMMs. PKA and cAMP, as GLP-1 downstream signals, played a role in this process. GLP-1 increased the deacetylation levels of PGC1α, and stimulated SIRT1 in HSMMs. Moreover, the SIRT1 inhibitor and siRNA of SIRT1 suppressed the effect of GLP-1 on GLUT4 expression in HSMMs exposed to palmitate. The SIRT1 inhibitor also prevented the GLP-1-induced phosphorylation of IRS-1 and Akt in palmitate-treated HSMMs. The present findings suggest that in palmitate-induced insulin-resistant HSMM, GLP-1 activates SIRT1 through the PKA/cAMP pathway, which in turn enhances glucose uptake through GLUT4 and the insulin signaling pathway.