Switch to anaerobic glucose metabolism with NADH accumulation in the beta-cell model of mitochondrial diabetes. Characteristics of betaHC9 cells deficient in mitochondrial DNA transcription.

@article{Noda2002SwitchTA,
  title={Switch to anaerobic glucose metabolism with NADH accumulation in the beta-cell model of mitochondrial diabetes. Characteristics of betaHC9 cells deficient in mitochondrial DNA transcription.},
  author={Mitsuhiko Noda and Shigeo Yamashita and Noriko Takahashi and Kazuhiro Eto and L Shen and Kazuo Izumi and Samira Daniel and Yoshiharu Tsubamoto and Tomomi Nemoto and Masamitsu Iino and Haruo Kasai and Geoffrey W. G. Sharp and Takashi Kadowaki},
  journal={The Journal of biological chemistry},
  year={2002},
  volume={277 44},
  pages={41817-26}
}
To elucidate the mechanism underlying diabetes caused by mitochondrial gene mutations, we created a model by applying 0.4 microg/ml ethidium bromide (EtBr) to the murine pancreatic beta cell line betaHC9; in this model, transcription of mitochondrial DNA, but not that of nuclear DNA, was suppressed in association with impairment of glucose-stimulated insulin release (Hayakawa, T., Noda, M., Yasuda, K., Yorifuji, H., Taniguchi, S., Miwa, I., Sakura, H., Terauchi, Y., Hayashi, J.-I., Sharp, G. W… CONTINUE READING

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