Glucose modulation of ATP-sensitive K-currents in wild-type, homozygous and heterozygous glucokinase knock-out mice

@article{Sakura1998GlucoseMO,
  title={Glucose modulation of ATP-sensitive K-currents in wild-type, homozygous and heterozygous glucokinase knock-out mice},
  author={Hiroshl Sakura and Stephen J. H. Ashcroft and Yasuo Terauchi and Takashi Kadowaki and Frances M. Ashcroft},
  journal={Diabetologia},
  year={1998},
  volume={41},
  pages={654-659}
}
One type of maturity-onset diabetes of the young (MODY2) is caused by mutations in the glucokinase gene, a key glycolytic enzyme in the beta cell and liver. Glucose fails to stimulate insulin secretion in mice in which the glucokinase gene has been selectively knocked out in the beta cell. We tested the hypothesis that this effect results from defective metabolic regulation of beta cell ATP-sensitive potassium (KATP) channels. Glucose had little effect on KATP currents in homozygous (-/-) mice… CONTINUE READING

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Diabetes and insulin secretion: whither KATP?

American journal of physiology. Endocrinology and metabolism • 2002
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