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운동수행에 따른 쥐의 골격근 형태별 UCP-3 mRNA의 변화
양대승,김철현,임예현,김문희,이승국,방상식,오유성,조준용,이규성 한국운동과학회 2003 운동과학 Vol.12 No.4
양대승, 김철현, 임예현, 김문희, 이승국, 방상식, 오유성, 조준용, 이규성. 운동과학, 제12권 제4호, 653-662, 2003. 운동수행에 따른 쥐의 골격근 형태별 UCP-3 mRNA의 변화. 이 연구는 비만 모델동물인 Obese Zucker Rat을 활용하여 12주간 지구성 운동이 골격근형태별 UCP-3 mRNA 발현, citrate synthase 활성도 및 혈청 지질 수준에 영향을 미치는가를 분자생물학적·생화학적 수준에서 평가한 결과, 장기간 지속적인 지구성 운동에 대한 골격근의 적응은 UCP-3 mRNA 발현량 감소 및 citrate synthase 활성도 증가와 혈청 지질(혈청 콜레스테롤, 중성지방, 저밀도 지단백 감소) 수준을 감소시키는 것으로 나타났다. 그러나 골격근의 UCP-3 유전자의 발현은 추위, 반응 산소종, 식이, 당뇨병 등과 같은 여러가지 요인과도 상관이 있기 때문에 운동과 관련된 보다 많은 연구들이 차후에 수행되어야 할 것이다. Yang, D.S., Kim, C.H, Leem, Y.H., Kim M.H., Lee, S.K,Bang, S.S., Oh, Y.S., Cho,J.Y., Lee, K.S. Thechanges of UCP-3 mRNA of obese Zucker rats during exercise training, Exercise Science, 12(4): 653-662, 2003. The factors that regulate gene expression of uncoupling protein-3 (UCP-3) in skeletal muscle are poorly understood, but uncoupling protein-3 gene is clearly responsive to the metabolic state of organism. There fore, We tested the hypothesis that chronic endurance exercise would alter UCP-3 gene expression. After 12wk endurance treadmill exercise, UCP-3 mRNA level of trained obese Zucker rat were decreased [vs. lean-type Zucker rat (100%) vs. obese Zucker rat control] in ail two tissues. in addition, cholesterol, triglyceride and LDL-C levels were significantly reduced in trained rats, whereas citrate synthase activites were significantly increased in trained rats. The results of this study show trot a need for a higher metabolic efficiency is associated with decreased mRNA expression of the uncoupling protein-3 (UCP-3) which would decrease energy dissipation in these tissues.
Endogenous Lipid-derived Ligands for Sensory TRP Ion Channels and Their Pain Modulation
방상수,유성재,Uhtaek Oh,황선욱 대한약학회 2010 Archives of Pharmacal Research Vol.33 No.10
Environmental or internal noxious stimuli excite the primary sensory nerves in our body. The sensory nerves relay these signals by electrical discharges to the brain, leading to pain perception. Six transient receptor potential (TRP) ion channels are expressed in the sensory nerve terminals and play a crucial role in sensing diverse noxious stimuli. Cation influx through activated TRP ion channels depolarizes the plasma membrane, resulting in neuronal excitation and pain. Natural and synthetic compounds have been found to act on these sensory TRP channels to alter the nociception. Evidence is growing that lipidergic substances are also cable of modifying TRP ion channel activity by direct binding. Here, we focus on endogenously generated lipids that modulate the sensory TRP activities. Unsaturated fatty acids or their metabolites via lipoxygenase, cyclooxygenase or epoxygenase are able to modulate (activate, inhibit or potentiate) the function of specific TRPs. Isoprene lipids, diacylglycerol, resolvin, and lysophospholipids also show distinct activities on sensory TRP channels. Outcomes caused by the interactions between sensory TRPs and lipid ligands are also discussed. The knowledge we collected here implicates that information on lipidergic ligands may contribute to our understanding of peripheral pain mechanism and provide an opportunity to design novel therapeutic strategies.