Evidence map›Paper›PMID 15164172›Full record

ArticleDiabetologia2004

Enhanced insulin secretion and cholesterol metabolism in congenic strains of the spontaneously diabetic (Type 2) Goto Kakizaki rat are controlled by independent genetic loci in rat chromosome 8.

R H Wallis, K J Wallace, S C Collins, M McAteer, K Argoud, M T Bihoreau, P J Kaisaki, D Gauguier

Open access · bronzeAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in Diabetologia, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.7field-weighted citation impact, top 10% of its field
1 · What the graph read from it

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3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 31 citations in OpenAlex.

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  10. Mapping diabetes QTL in an intercross derived from a congenic strain of the Brown Norway and Goto-Kakizaki rats.Mammalian genome : official journal of the International Mammalian Genome Society · 2006
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4 · The record

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5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

R H WallisThe Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Headington, Oxford OX3 7BN, UK.
K J Wallace
S C Collins
M McAteer
K Argoud
M T Bihoreau
P J Kaisaki
D Gauguier
University of Oxford · GBCentre for Human Genetics · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisGenetic investigations in the spontaneously diabetic (Type 2) Goto Kakizaki (GK) rat have identified quantitative trait loci (QTL) for diabetes-related phenotypes. The aims of this study were to refine the chromosomal mapping of a QTL ( Nidd/gk5) identified in chromosome 8 of the GK rat and to define a pathophysiological profile of GK gene variants underlying the QTL effects in congenics.

methodsGenetic linkage analysis was carried out with chromosome 8 markers genotyped in a GKxBN F2 intercross previously used to map diabetes QTL. Two congenic strains were designed to contain GK haplotypes in the region of Nidd/gk5 transferred onto a Brown Norway (BN) genetic background, and a broad spectrum of diabetes phenotypes were characterised in the animals.

resultsResults from QTL mapping suggest that variations in glucose-stimulated insulin secretion in vivo, and in body weight are controlled by different chromosome 8 loci (LOD3.53; p=0.0004 and LOD4.19; p=0.00007, respectively). Extensive physiological screening in male and female congenics at 12 and 24 weeks revealed the existence of GK variants at the locus Nidd/gk5, independently responsible for significantly enhanced insulin secretion and increased levels of plasma triglycerides, phospholipids and HDL, LDL and total cholesterol. Sequence polymorphisms detected between the BN and GK strains in genes encoding ApoAI, AIV, CIII and Lipc do not account for these effects. CONCLUSIONS/

interpretationWe refined the localisation of the QTL Nidd/gk5 and its pathophysiological characteristics in congenic strains derived for the locus. These congenic strains provide novel models for testing the contribution of a subset of GK alleles on diabetes phenotypes and for identifying diabetes susceptibility genes.

Indexed as

Disease Models, AnimalAnimalsAnimals, CongenicBlood GlucoseBody WeightCholesterolChromosome MappingChromosomes, MammalianDiabetes Mellitus, Type 2FemaleGenetic LinkageGenetic Predisposition to DiseaseGenomeGenotypeInsulinInsulin SecretionBlood GlucoseCholesterolInsulinLipids

Identifiers

PMID15164172
OpenAlexW1994892275

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.