ArticleDiabetologia2010
Direct evidence for susceptibility genes for type 2 diabetes on mouse chromosomes 11 and 14.
Article in Diabetologia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Contribution of animal models to diabetes research: Its history, significance, and translation to humans.Journal of diabetes investigation · 2023Review
- Novel loci for hyperglycemia identified by QTL mapping of longitudinal phenotypes and congenic analysis.Scientific reports · 2023Article
- β-Cell failure in diabetes: Common susceptibility and mechanisms shared between type 1 and type 2 diabetes.Journal of diabetes investigation · 2021Review
- Type 2 diabetes susceptibility genes on mouse chromosome 11 under high sucrose environment.BMC genetics · 2020Article
- Verification That Mouse Chromosome 14 Is Responsible for Susceptibility to Streptozotocin in NSY Mice.International journal of endocrinology · 2018Article
- Genetic dissection of susceptibility genes for diabetes and related phenotypes on mouse chromosome 14 by means of congenic strains.BMC genetics · 2014Article
- Article
- Dose effect and mode of inheritance of diabetogenic gene on mouse chromosome 11.Journal of diabetes research · 2013Article
- The liver X receptor agonist T0901317 protects mice from high fat diet-induced obesity and insulin resistance.The AAPS journal · 2013Article
- Chromosome substitution strains: gene discovery, functional analysis, and systems studies.Mammalian genome : official journal of the International Mammalian Genome Society · 2012Review
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisDiabetogenic loci for type 2 diabetes have been mapped to mouse chromosome (Chr) 11 and 14 in the Nagoya-Shibata-Yasuda (NSY) mouse, an animal model of type 2 diabetes. We aimed to obtain direct evidence of these genes on each chromosome and to clarify their function and interaction in conferring susceptibility to type 2 diabetes.
methodsWe established three consomic strains homozygous for diabetogenic NSY-Chr11, NSY-Chr14 or both on the control C3H background (C3H-11(NSY), C3H-14(NSY) and C3H-11(NSY)14(NSY), respectively), and monitored diabetes-related phenotypes longitudinally. The glucokinase gene was sequenced as a positional candidate gene on Chr11.
resultsC3H-11(NSY) mice showed hyperglycaemia associated with impaired insulin secretion and age-dependent insulin resistance without obesity. C3H-14(NSY) mice exhibited hyperglycaemia mainly due to insulin resistance, with a slight increase in percentage body fat. C3H-11(NSY)14(NSY) double consomic mice showed marked hyperglycaemia and obesity, which was not observed in single consomic strains. Sequences of the glucokinase gene were allelically variant between NSY and C3H mice. CONCLUSIONS/
interpretationThese data provide direct evidence that Chr11 and Chr14 harbour major susceptibility genes for type 2 diabetes. These two chromosomes interact to cause more severe hyperglycaemia and obesity, which was not observed with the presence of either single chromosome, indicating different modes of gene-gene interaction depending on the phenotype. Marked changes in the phenotypes retained in the consomic strains will facilitate fine mapping and the identification of the responsible genes and their interaction with each other, other genes and environmental factors.
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