Linkage and Association Analyses of Type 2 Diabetes/Impaired Glucose Metabolism and Adiponectin Serum Levels in Japanese Americans From Hawaii

  1. Ilija P. Kovac1,
  2. Richard J. Havlik2,
  3. Daniel Foley2,
  4. Rita Peila2,
  5. Dena Hernandez3,
  6. Fabienne Wavrant-De Vrièze3,
  7. Andrew Singleton3,
  8. Josephine Egan4,
  9. Dennis Taub5,
  10. Beatriz Rodriguez67,
  11. Kamal Masaki67,
  12. J. David Curb67,
  13. Wilfred Y. Fujimoto78 and
  14. Alexander F. Wilson1
  1. 1Genometrics Section, National Institutes of Health/National Human Genome Research Institute, Baltimore, Maryland
  2. 2Laboratory of Epidemiology, Demography and Biometry, National Institute of Aging, Bethesda, Maryland
  3. 3Molecular Genetics Unit, National Institute of Aging, Bethesda, Maryland
  4. 4Laboratory of Clinical Investigation, National Institute of Aging, Baltimore, Maryland
  5. 5Laboratory of Immunology, National Institute of Aging, Baltimore, Maryland
  6. 6Department of Geriatric Medicine, John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawaii
  7. 7Pacific Health Research Institute, Honolulu, Hawaii
  8. 8Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington, Seattle, Washington
  1. Address correspondence and reprint requests to Dr. Ilija Kovac, Department of Psychiatry, McGill University, Alan Memorial Institute, R&T Building, 1033 Pine Ave. West, Montreal H3A 1A1, Quebec, Canada. E-mail: ilija.kovac{at}mail.mcgill.ca

Abstract

Type 2 diabetes is a common disorder associated with obesity. Lower plasma levels of adiponectin were associated with type 2 diabetes. Candidate regions on chromosomes 1 (∼70 cM) and 14 (∼30 cM) were evaluated for replication of suggestive linkage results for type 2 diabetes/impaired glucose homeostasis in an independent sample of Japanese Americans. Replication of independent linkage evidence for serum levels of adiponectin on chromosome 14 was also evaluated. We investigated 529 subjects from 175 sibships who were originally part of the Honolulu Heart Program. Analyses included nonparametric linkage and association using SAGE (Statistical Analysis for Genetic Epidemiology) and FBAT (family-based test of association) programs and Monte Carlo simulation of Fisher’s exact test in SAS. For type 2 diabetes/impaired glucose metabolism, nominal linkage evidence (P < 0.02) followed-up by genotypic association (P = 0.016) was found with marker D14S297 at 31.8 cM; linkage analyses using only diabetes phenotype were also nominally significant at this marker (P < 0.02). Nominal evidence for genotypic association to adiponectin serum level phenotype (P = 0.04) was found with the marker D14S1032 at 23.2 cM. The present study was limited by relatively small sample size. Nevertheless, these results corroborate earlier studies, suggesting that further research is warranted in the candidate region ∼30 cM on chromosome 14.

Footnotes

  • The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    • Accepted November 13, 2006.
    • Received April 5, 2006.
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  1. doi: 10.2337/db06-0443 Diabetes February 2007 vol. 56 no. 2 537-540
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