共查询到20条相似文献,搜索用时 93 毫秒
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PGC-1beta in the regulation of hepatic glucose and energy metabolism 总被引:14,自引:0,他引:14
Lin J Tarr PT Yang R Rhee J Puigserver P Newgard CB Spiegelman BM 《The Journal of biological chemistry》2003,278(33):30843-30848
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PGC-1alpha, a transcriptional coactivator involved in metabolism 总被引:1,自引:0,他引:1
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Defects in adaptive energy metabolism with CNS-linked hyperactivity in PGC-1alpha null mice 总被引:26,自引:0,他引:26
Lin J Wu PH Tarr PT Lindenberg KS St-Pierre J Zhang CY Mootha VK Jäger S Vianna CR Reznick RM Cui L Manieri M Donovan MX Wu Z Cooper MP Fan MC Rohas LM Zavacki AM Cinti S Shulman GI Lowell BB Krainc D Spiegelman BM 《Cell》2004,119(1):121-135
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Suppression of reactive oxygen species and neurodegeneration by the PGC-1 transcriptional coactivators 总被引:28,自引:0,他引:28
St-Pierre J Drori S Uldry M Silvaggi JM Rhee J Jäger S Handschin C Zheng K Lin J Yang W Simon DK Bachoo R Spiegelman BM 《Cell》2006,127(2):397-408
PPARgamma coactivator 1alpha (PGC-1alpha) is a potent stimulator of mitochondrial biogenesis and respiration. Since the mitochondrial electron transport chain is the main producer of reactive oxygen species (ROS) in most cells, we examined the effect of PGC-1alpha on the metabolism of ROS. PGC-1alpha is coinduced with several key ROS-detoxifying enzymes upon treatment of cells with an oxidative stressor; studies with RNAi or null cells indicate that PGC-1alpha is required for the induction of many ROS-detoxifying enzymes, including GPx1 and SOD2. PGC-1alpha null mice are much more sensitive to the neurodegenerative effects of MPTP and kainic acid, oxidative stressors affecting the substantia nigra and hippocampus, respectively. Increasing PGC-1alpha levels dramatically protects neural cells in culture from oxidative-stressor-mediated death. These studies reveal that PGC-1alpha is a broad and powerful regulator of ROS metabolism, providing a potential target for the therapeutic manipulation of these important endogenous toxins. 相似文献
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Ablation of PGC-1beta results in defective mitochondrial activity, thermogenesis, hepatic function, and cardiac performance
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Lelliott CJ Medina-Gomez G Petrovic N Kis A Feldmann HM Bjursell M Parker N Curtis K Campbell M Hu P Zhang D Litwin SE Zaha VG Fountain KT Boudina S Jimenez-Linan M Blount M Lopez M Meirhaeghe A Bohlooly-Y M Storlien L Strömstedt M Snaith M Oresic M Abel ED Cannon B Vidal-Puig A 《PLoS biology》2006,4(11):e369
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PGC-1alpha integrates insulin signaling, mitochondrial regulation, and bioenergetic function in skeletal muscle 总被引:1,自引:0,他引:1
Pagel-Langenickel I Bao J Joseph JJ Schwartz DR Mantell BS Xu X Raghavachari N Sack MN 《The Journal of biological chemistry》2008,283(33):22464-22472
The pathophysiology underlying mitochondrial dysfunction in insulin-resistant skeletal muscle is incompletely characterized. To further delineate this we investigated the interaction between insulin signaling, mitochondrial regulation, and function in C2C12 myotubes and in skeletal muscle. In myotubes elevated insulin and glucose disrupt insulin signaling, mitochondrial biogenesis, and mitochondrial bioenergetics. The insulin-sensitizing thiazolidinedione pioglitazone restores these perturbations in parallel with induction of the mitochondrial biogenesis regulator PGC-1alpha. Overexpression of PGC-1alpha rescues insulin signaling and mitochondrial bioenergetics, and its silencing concordantly disrupts insulin signaling and mitochondrial bioenergetics. In primary skeletal myoblasts pioglitazone also up-regulates PGC-1alpha expression and restores the insulin-resistant mitochondrial bioenergetic profile. In parallel, pioglitazone up-regulates PGC-1alpha in db/db mouse skeletal muscle. Interestingly, the small interfering RNA knockdown of the insulin receptor in C2C12 myotubes down-regulates PGC-1alpha and attenuates mitochondrial bioenergetics. Concordantly, mitochondrial bioenergetics are blunted in insulin receptor knock-out mouse-derived skeletal myoblasts. Taken together these data demonstrate that elevated glucose and insulin impairs and pioglitazone restores skeletal myotube insulin signaling, mitochondrial regulation, and bioenergetics. Pioglitazone functions in part via the induction of PGC-1alpha. Moreover, PGC-1alpha is identified as a bidirectional regulatory link integrating insulin-signaling and mitochondrial homeostasis in skeletal muscle. 相似文献
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PGC-1alpha deficiency causes multi-system energy metabolic derangements: muscle dysfunction, abnormal weight control and hepatic steatosis
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Leone TC Lehman JJ Finck BN Schaeffer PJ Wende AR Boudina S Courtois M Wozniak DF Sambandam N Bernal-Mizrachi C Chen Z Holloszy JO Medeiros DM Schmidt RE Saffitz JE Abel ED Semenkovich CF Kelly DP 《PLoS biology》2005,3(4):e101