Elimination of KATP channels in mouse islets results in elevated [U-13C]glucose metabolism, glutaminolysis, and pyruvate cycling but a decreased gamma-aminobutyric acid shunt.

@article{Li2008EliminationOK,
  title={Elimination of KATP channels in mouse islets results in elevated [U-13C]glucose metabolism, glutaminolysis, and pyruvate cycling but a decreased gamma-aminobutyric acid shunt.},
  author={Changhong Li and Itzhak Nissim and Pan Chen and Carol W. Buettger and Habiba Najafi and Yevgeny Daikhin and Ilana B Nissim and H. W. Collins and Marc Yudkoff and Charles A. Stanley and Franz M. Matschinsky},
  journal={The Journal of biological chemistry},
  year={2008},
  volume={283 25},
  pages={17238-49}
}
Pancreatic beta cells are hyper-responsive to amino acids but have decreased glucose sensitivity after deletion of the sulfonylurea receptor 1 (SUR1) both in man and mouse. It was hypothesized that these defects are the consequence of impaired integration of amino acid, glucose, and energy metabolism in beta cells. We used gas chromatography-mass spectrometry methodology to study intermediary metabolism of SUR1 knock-out (SUR1(-/-)) and control mouse islets with d-[U-(13)C]glucose as substrate… CONTINUE READING