Linkage but Not Association of Calpain-10 to Type 2 Diabetes Replicated in Northern Sweden
- Elisabet Einarsdottir1,
- Sofia Mayans1,
- Karin Ruikka2,
- Stefan A. Escher1,
- Petter Lindgren1,
- Åsa Ågren3,
- Mats Eliasson23 and
- Dan Holmberg1
- 1Division of Medical and Clinical Genetics, Department of Medical Biosciences, Umeå University, Umeå, Sweden
- 2Department of Medicine, Sunderby Hospital, Umeå, Sweden
- 3Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden
- Address correspondence and reprint requests to Dr. Dan Holmberg, Department of Medical Biosciences, Division of Medical and Clinical Genetics, Umeå University, SE-901 87 Umeå, Sweden. E-mail: dan.holmberg{at}medbio.umu.se
Abstract
We present data from a genome-wide scan identifying genetic factors conferring susceptibility to type 2 diabetes. The linkage analysis was based on 59 families from northern Sweden, consisting of a total of 129 cases of type 2 diabetes and 19 individuals with impaired glucose tolerance. Model-free linkage analysis revealed a maximum multipoint logarithm of odds score of 3.19 for D2S2987 at 267.7 cM (P = 0.00058), suggesting that a gene conferring susceptibility to type 2 diabetes in the northern Swedish population resides in the 2q37 region. These data replicate, in a European population, previously identified linkage of marker loci in this region to type 2 diabetes in Mexican Americans. In contrast, no evidence in support of association to the previously identified single nucleotide polymorphisms in the calpain-10 gene was observed in a case-control cohort derived from the same population.
- IGT, impaired glucose tolerance
- OGTT, oral glucose tolerance test
- SNP, single nucleotide polymorphism
Footnotes
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E.E. and S.M. contributed equally to this work.
Additional information for this article can be found in an online appendix at http://diabetes.diabetesjournals.org.
DOI: 10.2337/db05-1495
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- Accepted February 27, 2006.
- Received November 14, 2005.
- DIABETES
