Type 2 diabetes: Evidence for linkage on chromosome 20 in 716 Finnish affected sib pairs

Soumitra Ghosh(Public Health Institute), Richard M. Watanabe(Public Health Institute), Elizabeth R. Hauser(Public Health Institute), Timo T. Valle(Public Health Institute), Victoria L. Magnuson(Public Health Institute), Michael R. Erdos(Public Health Institute), Carl D. Langefeld(Public Health Institute), James E. Balow(Public Health Institute), Delphine S. Ally(Public Health Institute), Kimmo Kohtamäki(Public Health Institute), Peter S. Chines(Public Health Institute), Gunther Birznieks(Public Health Institute), Hong-Shi Kaleta(Public Health Institute), Anjene Musick(Public Health Institute), Catherine Te(Public Health Institute), Joyce Tannenbaum(Public Health Institute), William Eldridge(Public Health Institute), Shane A. Shapiro(Public Health Institute), Colin Martin(Public Health Institute), Alyson Witt(Public Health Institute), Alistair So(Public Health Institute), Jennie Chang(Public Health Institute), Ben Shurtleff(Public Health Institute), Rachel Porter(Public Health Institute), Kristina Kudelko(Public Health Institute), Arun M. Unni(Public Health Institute), Leonid Segal(Public Health Institute), Ravi Sharaf(Public Health Institute), Jillian Blaschak‐Harvan(Public Health Institute), Johan G. Eriksson(Public Health Institute), Tuula Tenkula(Public Health Institute), Gabriele Vidgrén(Public Health Institute), Christian Ehnholm(Public Health Institute), Eva Tuomilehto‐Wolf(Public Health Institute), William Hagopian(Public Health Institute), Thomas A. Buchanan(Public Health Institute), Jaakko Tuomilehto(Public Health Institute), Richard N. Bergman(Public Health Institute), Francis S. Collins(Public Health Institute), Michael Boehnke(Public Health Institute)
Proceedings of the National Academy of Sciences
March 2, 1999
Cited by 232Open Access

Abstract

We are conducting a genome scan at an average resolution of 10 centimorgans (cM) for type 2 diabetes susceptibility genes in 716 affected sib pairs from 477 Finnish families. To date, our best evidence for linkage is on chromosome 20 with potentially separable peaks located on both the long and short arms. The unweighted multipoint maximum logarithm of odds score (MLS) was 3.08 on 20p (location, chi = 19.5 cM) under an additive model, whereas the weighted MLS was 2.06 on 20q (chi = 57 cM, recurrence risk,lambda(s) = 1. 25, P = 0.009). Weighted logarithm of odds scores of 2.00 (chi = 69.5 cM, P = 0.010) and 1.92 (chi = 18.5 cM, P = 0.013) were also observed. Ordered subset analyses based on sibships with extreme mean values of diabetes-related quantitative traits yielded sets of families who contributed disproportionately to the peaks. Two-hour glucose levels in offspring of diabetic individuals gave a MLS of 2. 12 (P = 0.0018) at 9.5 cM. Evidence from this and other studies suggests at least two diabetes-susceptibility genes on chromosome 20. We have also screened the gene for maturity-onset diabetes of the young 1, hepatic nuclear factor 4-a (HNF-4alpha) in 64 affected sibships with evidence for high chromosomal sharing at its location on chromosome 20q. We found no evidence that sequence changes in this gene accounted for the linkage results we observed.


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