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Metabolic Rebalancing of CR6 Interaction Factor 1-Deficient Mouse Embryonic Fibroblasts: A Mass Spectrometry-Based Metabolic Analysis

  • Tadi, Surendar (Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine) ;
  • Kim, Soung Jung (Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine) ;
  • Ryu, Min Jeong (Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine) ;
  • Park, Taeseong (Korea Basic Science Institute) ;
  • Jeong, Ji-Seon (Korea research Institute of standards and Science) ;
  • Kim, Young Hwan (Korea Basic Science Institute) ;
  • Kweon, Gi Ryang (Department of Biochemistry, Chungnam national University School of Medicine) ;
  • Shong, Minho (Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine) ;
  • Yim, Yong-Hyeon (Korea research Institute of standards and Science)
  • Received : 2012.08.13
  • Accepted : 2012.10.04
  • Published : 2013.01.20

Abstract

Metabolic analysis of CR6 interacting factor 1 (Crif1) deficient mouse embryonic fibroblasts with impaired oxidative phosphorylation has been carried out using LC-MS/MS and GC-MS methods. Metabolic profiles of the Crif1 deficient cells were comprehensively obtained for the first time. Loss of oxidative phosphorylation functions in mitochondria resulted in cancer-like metabolic reprogramming with consumption of majority of glucose carbon from up-regulated glycolysis to produce lactate, suppressed utilization of glucose carbon in the TCA cycle, increased amounts of amino acids. The changes in metabolic profile of the Crif1 deficient cells are most probably a consequence of metabolic reprogramming to meet the needs of energy balance and anabolic precursors in compensation for the loss of major oxidative phosphorylation functions.

Keywords

References

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