ArticleDiabetes2007
A novel susceptibility locus on rat chromosome 8 affects spontaneous but not experimentally induced type 1 diabetes.
Article in Diabetes, 2007. 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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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Contribution of animal models to diabetes research: Its history, significance, and translation to humans.Journal of diabetes investigation · 2023Review
- Genetic dissection of Iddm26 in the spontaneously diabetic BBDP rat.Genes and immunity · 2014Article
- IL-7- and IL-15-mediated TCR sensitization enables T cell responses to self-antigens.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
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- Genetic dissection reveals diabetes loci proximal to the gimap5 lymphopenia gene.Physiological genomics · 2009Article
- Analysis of the rat Iddm14 diabetes susceptibility locus in multiple rat strains: identification of a susceptibility haplotype in the Tcrb-V locus.Mammalian genome : official journal of the International Mammalian Genome Society · 2009Article
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
objectiveThe biobreeding diabetes-prone (BBDP) rat spontaneously develops type 1 diabetes. Two of the genetic factors contributing to this syndrome are the major histocompatibility complex (Iddm1) and a Gimap5 mutation (Iddm2) responsible for a T-lymphopenia. Susceptibility to experimentally induced type 1 diabetes is widespread among nonlymphopenic (wild-type Iddm2) rat strains provided they share the BBDP Iddm1 allele. The question follows as to whether spontaneous and experimentally induced type 1 diabetes share susceptibility loci besides Iddm1. Our objectives were to map a novel, serendipitously discovered Iddm locus, confirm its effects by developing congenic sublines, and assess its differential contribution to spontaneous and experimentally induced type 1 diabetes. RESEARCH DESIGN AND
methodsAn unexpected reduction in spontaneous type 1 diabetes incidence (86 to 31%, P < 0.0001) was observed in a BBDP line congenic for a Wistar Furth-derived allotypic marker, RT7 (chromosome 13). Genome-wide analysis revealed that, besides the RT7 locus, a Wistar Furth chromosome 8 fragment had also been introduced. The contribution of these intervals to diabetes resistance was assessed through linkage analysis using 134 F2 (BBDP x double congenic line) animals and a panel of congenic sublines. One of these sublines, resistant to spontaneous type 1 diabetes, was tested for susceptibility to experimentally induced type 1 diabetes.
resultsBoth linkage analysis and congenic sublines mapped a novel locus (Iddm24) to the telomeric 10.34 Mb of chromosome 8, influencing cumulative incidence and age of onset of spontaneous type 1 diabetes but not insulitis nor experimentally induced type 1 diabetes.
conclusionsThis study has identified a type 1 diabetes susceptibility locus that appears to act after the development of insulitis and that regulates spontaneous type 1 diabetes exclusively.
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