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

¹ Genometrics Section, National Institutes of Health/National Human Genome Research Institute, Baltimore, Maryland
² Laboratory of Epidemiology, Demography and Biometry, National Institute of Aging, Bethesda, Maryland
³ Molecular Genetics Unit, National Institute of Aging, Bethesda, Maryland
⁴ Laboratory of Clinical Investigation, National Institute of Aging, Baltimore, Maryland
⁵ Laboratory of Immunology, National Institute of Aging, Baltimore, Maryland
⁶ Department of Geriatric Medicine, John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawaii
⁷ Pacific Health Research Institute, Honolulu, Hawaii
⁸ Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington, Seattle, Washington

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

Abbreviations: GENNID, Genetics of NIDDM; HFDS, Hawaii Family Diabetes Study; HHP, Honolulu Heart Program; IDB, identical by descent; LOD, logarithm of odds

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.

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