No evidence for mutations in a putative subunit of the β-cell ATP-sensitive potassium channel (K-ATP Channel) in Japanese NIDDM patients

Kazuki Yasuda, Hiroshi Sakura, Yasumichi Mori, Keiji Iwamoto, Kohtaro Shimokawa, Hiroko Kadowaki, Ryoko Hagura, Yasuo Akanuma, John P. Adelman, Yoshio Yazaki, Frances M. Ashcroft, Takashi Kadowaki

Research output: Contribution to journalArticle

6 Scopus citations

Abstract

The ATP-sensitive K channel (K-ATP channel) in pancreatic β cells is believed to play a crucial role in glucose stimulated insulin release. We investigated whether defects in the recently cloned gene for a putative subunit of this channel (KATP-2) could be a cause of diabetes in Japanese patients. The coding region of this β-cell type channel gene was investigated in 192 diabetics with a family history of the disorder by single-stranded conformational polymorphism (SSCP) analysis. Two silent polymorphisms were found and confirmed by sequencing, but no missense or nonsense mutations were detected. The allele frequency of the polymorphisms was compared with 96 control subjects without a family history of the disease, and no clear difference was found. These results indicate that genetic defects of the KATP-2 channel may not be a major cause of diabetes in Japan.

Original languageEnglish (US)
Pages (from-to)1036-1040
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume211
Issue number3
DOIs
StatePublished - Jun 26 1995

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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    Yasuda, K., Sakura, H., Mori, Y., Iwamoto, K., Shimokawa, K., Kadowaki, H., Hagura, R., Akanuma, Y., Adelman, J. P., Yazaki, Y., Ashcroft, F. M., & Kadowaki, T. (1995). No evidence for mutations in a putative subunit of the β-cell ATP-sensitive potassium channel (K-ATP Channel) in Japanese NIDDM patients. Biochemical and Biophysical Research Communications, 211(3), 1036-1040. https://doi.org/10.1006/bbrc.1995.1915