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No Association Between The Gly971 Arg Variant of the Insulin Receptor Substrate 1 Gene and NIDDM in the Taiwanese Population

  1. Lee-Ming Chuang, MD, PHD,
  2. Chuen-Shianf Lai, BS,
  3. Jih-I Yeh, PHD,
  4. Huey-Peir Wu, MD,
  5. Tong-Yuan Tai, MD, PHD and
  6. Boniface J Lin, MD
  1. Department of Internal Medicine and the Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University Taipei, Taiwan
  1. Address correspondence and reprint requests to Lee-Ming Chuang, MD, PhD, Department of Internal Medicine, National Taiwan University Hospital, 7 Chung-Shan South Rd., Taipei 10016, Taiwan. E-mail: leeming{at}ntumel.me.ntu.edu.tw

Abstract

OBJECTIVE To study the role of the Gly971 Arg variant of the insulin receptor substrate 1 (IRS-1) gene in the development of NIDDM in the Chinese population living in Taiwan.

RESEARCH DESIGN AND METHODS A total of 82 unrelated normal control subjects, 89 subjects with NIDDM, and 23 multiplex families were recruited in Taiwan. All of them were Han Chinese. Pedigree members without a history of diabetes were studies by the standard 75-g oral glucose tolerance test. Detection of the Gly971 Arg variant of the IRS-1 gene was performed by polymerase chain reaction and restriction fragment-length polymorphism analysis.

RESULTS The frequency of Gly971 Arg variant of the IRS-1 gene in the normal population was 1.2% which was lower than frequencies reported in white populations. The prevalence of the Gly971 Arg variant was not significantly increased in both the nonselected NIDDM population (1.1%) and the probands of the multiplex families (4.3%). More importantly, the Gly971 Arg variant of the IRS-1 gene did not cosegregate with BMI and NIDDM in these families,

CONCLUSIONS The Gly971 Arg variant of the IRS-1 gene is an infrequent normal allele among Taiwanese. This variant is neither associated nor cosegregated with NIDDM in the Taiwanese population and families. Gly971 Arg of IRS-1 gene does not play an important role in the development of NIDDM in this population.

  • Received September 12, 1995.
  • Revision received November 21, 1995.
  • Accepted November 21, 1995.
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