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Rapid Publications

Sequence Variants in the Sulfonylurea Receptor (SUR) Gene Are Associated With NIDDM in Caucasians

  1. Hiroshi Inoue,
  2. Jorge Ferrer,
  3. Cris M Welling,
  4. Steven C Elbein,
  5. Michael Hoffman,
  6. Rachel Mayorga,
  7. Margaret Warren-Perry,
  8. Yun Zhang,
  9. Helen Millns,
  10. Robert Turner,
  11. Mike Province,
  12. Joseph Bryan,
  13. M Alan Permutt and
  14. Lydia Aguilar-Bryan
  1. Division of Metabolism, Diabetes and Endocrinology, Washington University School of Medicine St. Louis, Missouri
  2. Department of Internal Medicine, Department of Biostatistics, Washington University School of Medicine St. Louis, Missouri
  3. Metabolism Division, Department of Internal Medicine, Veterans Affairs Medical Center and University of Utah Salt Lake City, Utah
  4. Diabetes Research Laboratories, University of Oxford Oxford, U.K.
  5. Department of Cell Biology and Medicine, Baylor College of Medicine Houston, Texas
  1. Address correspondence and reprint requests to Dr. M. Alan Permutt, Metabolism Division, Washington University School of Medicine, 660 S. Euclid, Box 8127, St. Louis, MO 63110. E-mail: apermutt{at}imgate.wustl.edu
Diabetes 1996 Jun; 45(6): 825-831. https://doi.org/10.2337/diab.45.6.825
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Abstract

NIDDM is a common heterogeneous disorder, the genetic basis of which has yet to be determined. The sulfonylurea receptor (SUR) gene, now known to encode an integral component of the pancreatic β-cell ATP-sensitive potassium channel, IKATP, was investigated as a logical candidate for this disorder. The two nucleotide-binding fold (NBF) regions of SUR are known to be critical for normal glucose regulation of insulin secretion. Thus, singlestrand conformational polymorphism analysis was used to find sequence changes in the two NBF regions of the SUR gene in 35 NIDDM patients. Eight variants were found; and three were evaluated in two Northern European white populations (Utah and the U.K.): 1) a missense mutation in exon 7 (S1370A) was found with equal frequency in patients (n = 223) and control subjects (n = 322); 2) an ACC→ACṮ silent variant in exon 22 (T761T) was more common in patients than in control subjects (allele frequencies 0.07 vs. 0.02, P = 0.0008, odds ratio (OR) 3.01, 95% CI 1.54–5.87); and 3) an intronic t→c change located at position –3 of the exon 24 splice acceptor site was also more common in patients than in control subjects (0.62 vs. 0.46, P < 0.0001, OR 1.91, 95% Cl 1.50–2.44). The combined genotypes of exon 22 C/T or T/T and intron 24 –3c/–3c occurred in 8.9% of patients and 0.5% of control subjects (P < 0.0001, OR 21.5,95% CI 2.91–159.6). These results suggest that defects at the SUR locus may be a major contributor to the inherited basis of NIDDM in Northern European Caucasians.

  • Received January 4, 1996.
  • Revision received March 4, 1996.
  • Accepted March 4, 1996.
  • Copyright © 1996 by the American Diabetes Association
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June 1996, 45(6)
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Sequence Variants in the Sulfonylurea Receptor (SUR) Gene Are Associated With NIDDM in Caucasians
Hiroshi Inoue, Jorge Ferrer, Cris M Welling, Steven C Elbein, Michael Hoffman, Rachel Mayorga, Margaret Warren-Perry, Yun Zhang, Helen Millns, Robert Turner, Mike Province, Joseph Bryan, M Alan Permutt, Lydia Aguilar-Bryan
Diabetes Jun 1996, 45 (6) 825-831; DOI: 10.2337/diab.45.6.825

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Sequence Variants in the Sulfonylurea Receptor (SUR) Gene Are Associated With NIDDM in Caucasians
Hiroshi Inoue, Jorge Ferrer, Cris M Welling, Steven C Elbein, Michael Hoffman, Rachel Mayorga, Margaret Warren-Perry, Yun Zhang, Helen Millns, Robert Turner, Mike Province, Joseph Bryan, M Alan Permutt, Lydia Aguilar-Bryan
Diabetes Jun 1996, 45 (6) 825-831; DOI: 10.2337/diab.45.6.825
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