No evidence for mutations in a putative β-cell ATP-sensitive K+ channel subunit in MODY, NIDDM, or GDM

Yun Zhang, Margaret Warren-Perry, Hiroshi Sakura, John Adelman, Markus Stoffel, Graeme I. Bell, Frances M. Ashcroft, Robert C. Turner

Research output: Contribution to journalArticlepeer-review

20 Scopus citations


The β-cell ATP-sensitive K+ (K-ATP) channel has a major role in glucose- induced insulin secretion. Screening the entire coding sequence of the gene for a putative β-cell K-ATP channel subunit, K-ATP2, with single-strand conformation polymorphism did not show any mutations associated with diabetes in white Caucasian diabetic patients, including five pedigrees with maturity onset diabetes of the young (MODY), 25 patients with non-insulin-dependent diabetes mellitus (NIDDM) selected for marked β-cell deficiency, 25 selected for mild diabetes presenting before age 50 years with fasting plasma glucose levels <10 mmol/l, 25 unselected NIDDM patients, and 25 subjects with gestational diabetes mellitus (GDM) and subsequent raised fasting plasma glucose. In five large MODY pedigrees, linkage analysis with simple tandem- repeat polymorphisms (STRPs) near the K-ATP2 gene excluded linkage. In a population association study, no linkage disequilibrium for the STRP was found between 237 unselected white Caucasian NIDDM patients and 104 geographically matched and age-matched white Caucasian nondiabetic subjects. In addition, two silent polymorphisms were found with similar frequency in nondiabetic and diabetic subjects. Mutations in the gene for K-ATP2 are unlikely to be a major cause of MODY, NIDDM, or GDM.

Original languageEnglish (US)
Pages (from-to)597-600
Number of pages4
Issue number5
StatePublished - 1995

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism


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