ArticleMammalian genome : official journal of the International Mammalian Genome Society2006
Mapping diabetes QTL in an intercross derived from a congenic strain of the Brown Norway and Goto-Kakizaki rats.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 14 citations in OpenAlex.
- Topological analysis of metabolic networks integrating co-segregating transcriptomes and metabolomes in type 2 diabetic rat congenic series.Genome medicine · 2016Article
- Fine-mapping diabetes-related traits, including insulin resistance, in heterogeneous stock rats.Physiological genomics · 2012Article
- Chromosomal mapping of pancreatic islet morphological features and regulatory hormones in the spontaneously diabetic (Type 2) Goto-Kakizaki rat.Mammalian genome : official journal of the International Mammalian Genome Society · 2010Article
- Genes unlinked to the leptin receptor influence urinary albumin excretion in obese Zucker rats.Physiological genomics · 2010Article
- Fine-mapping a locus for glucose tolerance using heterogeneous stock rats.Physiological genomics · 2010Article
- Pathophysiological, genetic and gene expression features of a novel rodent model of the cardio-metabolic syndrome.PloS one · 2008Article
- Genetic control of plasma lipid levels in a cross derived from normoglycaemic Brown Norway and spontaneously diabetic Goto-Kakizaki rats.Diabetologia · 2006Article
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8 authors at 2 institutions in 1 country.
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Abstract
Genetic studies in experimental crosses derived from the inbred Goto-Kakizaki (GK) rat model of spontaneous diabetes mellitus have identified quantitative trait loci (QTL) for diabetes phenotypes in a large region of rat Chromosome (RNO) 1. To test the impact of GK variants on QTL statistical and biological features, we combined genetic and physiologic studies in a cohort of F(2) hybrids derived from a QTL substitution congenic strain (QTLSCS) carrying a 110-cM GK haplotype of RNO1 introgressed onto the genetic background of the Brown Norway (BN) strain. Glucose intolerance and altered insulin secretion in QTLSCS rats when compared with BN controls were consistent with original QTL features in a GK x BN F(2) cross. Segregating GK alleles in the QTLSCS F(2) cross account for most of these phenotypic differences between QTLSCS and BN rats. However, significant QTL for diabetes traits in both the QTLSCS and GK x BN F(2) cohorts account for a similar small proportion of their variance. Comparing results from these experimental systems provides indirect estimates of the contribution of genetic interactions and environmental factors to QTL architecture as well as locus and biological targets for future post-QTL mapping studies in congenic substrains.
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