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<p>Type 2 diabetes is a common and chronic disease caused by interactions between genetic and environmental factors. The Goto-Kakizaki (GK) rat is a well-established genetic model of type 2 diabetes. Since several aspects of the pathophysiology of diabetes are shared between human and GK rats, we used this model to perform the first genome-wide scan for quantitative trait locus (QTL) of type 2 diabetes.</p><p>A genetic linkage map with 530 microsatellite markers was constructed in a (GK x F344)F2 intercross. The map covers the whole rat genome evenly, and has a total length of 1827 centimorgans (cM), an average interval of 3 cM between markers and the maximum interval less than 20 cM. Subsequently, this map was used as a framework for the integration of 6 linkage maps and 2 radiation hybrid maps of the rat. The unified map comprises the majority of available rat markers (a total of 8627 markers) in a single map, allowing us to assemble a comparative genetic map for ty
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<p>Type 2 diabetes is a common and chronic disease caused by interactions between genetic and environmental factors. The Goto-Kakizaki (GK) rat is a well-established genetic model of type 2 diabetes. Since several aspects of the pathophysiology of diabetes are shared between human and GK rats, we used this model to perform the first genome-wide scan for quantitative trait locus (QTL) of type 2 diabetes.</p><p>A genetic linkage map with 530 microsatellite markers was constructed in a (GK x F344)F2 intercross. The map covers the whole rat genome evenly, and has a total length of 1827 centimorgans (cM), an average interval of 3 cM between markers and the maximum interval less than 20 cM. Subsequently, this map was used as a framework for the integration of 6 linkage maps and 2 radiation hybrid maps of the rat. The unified map comprises the majority of available rat markers (a total of 8627 markers) in a single map, allowing us to assemble a comparative genetic map for ty
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