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Conversion of C2C12 Myoblast into Adipoblast with Thiazolidinediones - A Possible Basis for Intramuscular Fat Generation in Meat Animals

  • Singh, N.K. (Product and Utility Division, National Livestock Research Institute) ;
  • Chae, H.S. (Product and Utility Division, National Livestock Research Institute) ;
  • Hwang, I.H. (Department of Animal Resources and Biotechnology, Chonbuk National University) ;
  • Yoo, Y.M. (Product and Utility Division, National Livestock Research Institute) ;
  • Ahn, C.N. (Product and Utility Division, National Livestock Research Institute) ;
  • Lee, H.J. (Nutrition and physiology, National Livestock Research Institute) ;
  • Park, H.J. (Nutrition and physiology, National Livestock Research Institute) ;
  • Chung, H.Y. (Animal Genomics and Bioinformatics Division, National Livestock Research Institute)
  • 투고 : 2006.06.12
  • 심사 : 2006.10.09
  • 발행 : 2007.03.01

초록

Thiazolidinediones (TZDs) act as potent activators of the adipose differentiation program in established preadipose cell lines. TZD's have also been investigated in diabetic patients and reported to act as PPAR-${\gamma}$ ligands. In this report, the effects of TZDs on the differentiation pathway of myoblasts have been investigated. C2C12 mouse myoblasts were grown in Dulbecco's Modified Eagles medium for 4-5 days until they reached almost 100% confluency. Post-confluent cells (day 0) were further exposed to adipogenic induction medium along with TZDs for 48 hours. Thereafter, cells were exposed only to TZDs every 48 h until day 10. The control was provided with differentiation medium without any treatment. Alterations in the cells during the differentiation programme were analyzed on the basis of fusion index, oil-red-o staining, adipocyte index, adipocyte stain uptake measurement, immuno-histochemistry and western blotting. Exposure of C2C12 mouse myoblasts to TZDs prevented the expression of myosin heavy chain with parallel increase in the expression of C/EBP-${\alpha}$ and PPAR-${\gamma}$ and acquisition of adipocyte morphology, thus abolishing the formation of multinucleated myotubes. TZDs exert their adipogenic effects only in non-terminally differentiated myoblasts; myotubes were insensitive to the compound. Continuous exposure (at least 4-5 doses) to inducers after the growth arrest was essential to provide a sustained environment to the cells converting to fully matured adipoctyes. The results indicate that TZDs specifically converted the differentiation pathway of myoblasts into that of adipoblasts.

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