Defective insulin secretion and enhanced insulin action in KATP channel-deficient mice.

@article{Miki1998DefectiveIS,
  title={Defective insulin secretion and enhanced insulin action in KATP channel-deficient mice.},
  author={Tohru Miki and Kazuaki Nagashima and Fumi Tashiro and Katsuhiro Kotake and Hideyuki Yoshitomi and Atsuko Tamamoto and Tohru Gonoi and Toshihiko Iwanaga and Jun ichi Miyazaki and Susumu Seino},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={1998},
  volume={95 18},
  pages={10402-6}
}
ATP-sensitive K+ (KATP) channels regulate many cellular functions by linking cell metabolism to membrane potential. We have generated KATP channel-deficient mice by genetic disruption of Kir6.2, which forms the K+ ion-selective pore of the channel. The homozygous mice (Kir6.2(-/-)) lack KATP channel activity. Although the resting membrane potential and basal intracellular calcium concentrations ([Ca2+]i) of pancreatic beta cells in Kir6.2(-/-) are significantly higher than those in control mice… CONTINUE READING
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Miki et al

  • I. A. Simpson, Cushman, +10 authors are seen also in the central region of the islets. The Biochemistry
  • Proc. Natl. Acad. Sci. USA 95
  • 1998
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