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Diabetes 53:3307-3312, 2004
© 2004 by the American Diabetes Association, Inc.

Linkage Analysis of Diabetes Status Among Hypertensive Families

The Hypertension Genetic Epidemiology Network Study

Christy L. Avery1, Barry I. Freedman2, Gerardo Heiss1, Aldi Kraja3, Treva Rice3, Donna Arnett4, Michael B. Miller4, James S. Pankow4, Cora E. Lewis5, Richard H. Myers6, Steven C. Hunt7, Laura Almasy8, and Kari E. North1

1 Department of Epidemiology, University of North Carolina Chapel Hill, Chapel Hill, North Carolina
2 Department of Internal Medicine, Wake Forest University, Winston Salem, North Carolina
3 Division of Biostatistics, Washington University School of Medicine, St. Louis, Missouri
4 Division of Epidemiology, University of Minnesota, Minneapolis, Minnesota
5 Department of Preventive Medicine, University of Alabama Birmingham, Birmingham, Alabama
6 Section of Neurogenetics, Boston University, Boston, Massachusetts
7 Cardiovascular Genetics Division, University of Utah, Salt Lake City, Utah
8 Department of Genetics, Southwest Foundation for Biomedical Research, San Antonio, Texas

Type 2 diabetes susceptibility is determined by multiple genetic and environmental factors. Genome-wide linkage scans have localized common regions, possibly harboring susceptibility genes on chromosomes 1, 2, 12, and 20. Variability in linkage findings underscores the probable genetic heterogeneity of type 2 diabetes. Thus, we conducted a genome scan of diabetes status using maximum likelihood methods that model affection status by a liability threshold model. Hypertensive sibships and their offspring and/or parents in the Hypertension Genetic Epidemiology Network study were recruited from five field centers. The diabetes phenotype was derived using the World Health Organization criteria and adjusted for race/study center, age, age2, sex, and with and without percent body fat. In total, 567 diabetic participants were identified in 437 families. Variance component linkage analysis was performed among 1,545 Caucasians and 1,608 African Americans using race-specific marker allele frequencies. We detected a quantitative trait loci (QTLs) influencing diabetes variance (logarithm of odds = 3.4) on chromosome 22, which overlaps a positive type 2 diabetes finding among Canadian Oji-Cree Indians. We also observed suggestive evidence for linkage on chromosomes 1, 2, 5, 8, 14, 17, and 19. The identification and replication of type 2 diabetes QTLs will bring us closer to the detection of functional genes that influence diabetes susceptibility.

Address correspondence and reprint requests to Kari E. North, PhD, Department of Epidemiology, CB no. 8050, Suite 306, Bank of America, University of North Carolina Chapel Hill, Chapel Hill, NC 27514. E-mail: kari_north{at}unc.edu


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Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 2004 by the American Diabetes Association.