No Evidence for Mutations in a Putative Subunit of the β-Cell ATP-Sensitive Potassium Channel (K-ATP Channel) in Japanese NIDDM Patients

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. T...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 1995-06, Vol.211 (3), p.1036-1040
Main Authors: 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.
Format: Article
Language:English
Subjects:
Adult
Asian Continental Ancestry Group - genetics
Base Sequence
Diabetes Mellitus, Type 2 - epidemiology
Diabetes Mellitus, Type 2 - etiology
Diabetes Mellitus, Type 2 - genetics
DNA Primers
Humans
Islets of Langerhans - cytology
Islets of Langerhans - physiology
Japan - epidemiology
Molecular Sequence Data
Mutation
Polymerase Chain Reaction
Potassium Channels - genetics
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Summary: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.
ISSN:0006-291X
1090-2104
DOI:10.1006/bbrc.1995.1915