The Finland-United States investigation of non-insulin-dependent diabetes mellitus genetics (FUSION) study. I. An autosomal genome scan for genes that predispose to type 2 diabetes

Soumitra Ghosh, Richard M. Watanabe, Timo T. Valle, Elizabeth R. Hauser, Victoria L. Magnuson, Carl D. Langefeld, Delphine S. Ally, Karen L. Mohlke, Kaisa Silander, Kimmo Kohtamaki, Peter Chines, James Balow, Gunther Birznieks, Jennie Chang, William Eldridge, Michael R. Erdos, Zarir E. Karanjawala, Julie I. Knapp, Kristina Kudelko, Colin MartinAnabelle Morales-Mena, Anjene Musick, Tiffany Musick, Carrie Pfahl, Rachel Porter, Joseph B. Rayman, David Rha, Leonid Segal, Shane Shapiro, Ravi Sharaf, Ben Shurtleff, Alistair So, Joyce Tannenbaum, Catherine Te, Jason Tovar, Arun Unni, Christian Welch, Ray Whiten, Alyson Witt, Jillian Blaschak Harvan, Julie A. Douglas, William L. Duren, Michael P. Epstein, Tasha E. Fingerlin, Hong Shi Kaleta, Ethan M. Lange, Chun Li, Richard C. McEachin, Heather M. Stringham, Edward Trager, Peggy P. White, Johan Eriksson, Liisa Toivanen, Gabriele Vidgren, Stella J. Nylund, Eva Tuomilehto-Wolf, Edna H. Ross, Elza Demirchyan, William A. Hagopian, Thomas A. Buchanan, Richard N. Bergman, Francis S. Collins, Michael Boehnke

Research output: Contribution to journalArticlepeer-review

211 Scopus citations

Abstract

We performed a genome scan at an average resolution of 8 cM in 719 Finnish sib pairs with type 2 diabetes. Our strongest results are for chromosome 20, where we observe a weighted maximum LOD score (MLS) of 2.15 at map position 69.5 cM from pter and secondary weighted LOD-score peaks of 2.04 at 56.5 cM and 1.99 at 17.5 cM. Our next largest MLS is for chromosome 11 (MLS = 1.75 at 84.0 cM), followed by chromosomes 2 (MLS = 0.87 at 5.5 cM), 10 (MLS = 0.77 at 75.0 cM), and 6 (MLS = 0.61 at 112.5 cM), all under an additive model. When we condition on chromosome 2 at 8.5 cM, the MLS for chromosome 20 increases to 5.50 at 69.0 cM (P =.0014). An ordered-subsets analysis based on families with high or low diabetes-related quantitative traits yielded results that support the possible existence of disease-predisposing genes on chromosomes 6 and 10. Genomewide linkage-disequilibrium analysis using microsatellite marker data revealed strong evidence of association for D22S423 (P =.00007). Further analyses are being carried out to confirm and to refine the location of these putative diabetes-predisposing genes.

Original languageEnglish (US)
Pages (from-to)1174-1185
Number of pages12
JournalAmerican journal of human genetics
Volume67
Issue number5
DOIs
StatePublished - 2000

ASJC Scopus subject areas

  • Genetics
  • Genetics(clinical)

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