Evidence map›Paper›PMID 18698428›Full record

ArticlePloS one2008

Pathophysiological, genetic and gene expression features of a novel rodent model of the cardio-metabolic syndrome.

Robert H Wallis, Stephan C Collins, Pamela J Kaisaki, Karène Argoud, Steven P Wilder, Karin J Wallace, Massimiliano Ria, Alain Ktorza, Patrik Rorsman, Marie-Thérèse Bihoreau and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.4field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 26 citations in OpenAlex.

  1. Creatine Kinase Equilibration and ΔGInternational journal of molecular sciences · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 2 countries.

Robert H WallisThe Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom.
Stephan C Collins
Pamela J Kaisaki
Karène Argoud
Steven P Wilder
Karin J Wallace
Massimiliano Ria
Alain Ktorza
Patrik Rorsman
Marie-Thérèse Bihoreau
Dominique Gauguier
University of Oxford · GBCentre for Human Genetics · GBCentre National de la Recherche Scientifique · FROxford Centre for Diabetes, Endocrinology and Metabolism · GB

Funding

Wellcome TrustWellcome Trust 057733Wellcome Trust 066780
6 · The paper itself

Abstract

backgroundComplex etiology and pathogenesis of pathophysiological components of the cardio-metabolic syndrome have been demonstrated in humans and animal models. METHODOLOGY/PRINCIPAL

findingsWe have generated extensive physiological, genetic and genome-wide gene expression profiles in a congenic strain of the spontaneously diabetic Goto-Kakizaki (GK) rat containing a large region (110 cM, 170 Mb) of rat chromosome 1 (RNO1), which covers diabetes and obesity quantitative trait loci (QTL), introgressed onto the genetic background of the normoglycaemic Brown Norway (BN) strain. This novel disease model, which by the length of the congenic region closely mirrors the situation of a chromosome substitution strain, exhibits a wide range of abnormalities directly relevant to components of the cardio-metabolic syndrome and diabetes complications, including hyperglycaemia, hyperinsulinaemia, enhanced insulin secretion both in vivo and in vitro, insulin resistance, hypertriglyceridemia and altered pancreatic and renal histological structures. Gene transcription data in kidney, liver, skeletal muscle and white adipose tissue indicate that a disproportionately high number (43-83%) of genes differentially expressed between congenic and BN rats map to the GK genomic interval targeted in the congenic strain, which represents less than 5% of the total length of the rat genome. Genotype analysis of single nucleotide polymorphisms (SNPs) in strains genetically related to the GK highlights clusters of conserved and strain-specific variants in RNO1 that can assist the identification of naturally occurring variants isolated in diabetic and hypertensive strains when different phenotype selection procedures were applied.

conclusionsOur results emphasize the importance of rat congenic models for defining the impact of genetic variants in well-characterised QTL regions on in vivo pathophysiological features and cis-/trans- regulation of gene expression. The congenic strain reported here provides a novel and sustainable model for investigating the pathogenesis and genetic basis of risks factors for the cardio-metabolic syndrome.

Indexed as

AnimalsArginineBasal MetabolismBlood GlucoseBlood PressureBody WeightChromosome MappingDiabetes Mellitus, Type 2Disease Models, AnimalGlucoseHyperglycemiaHyperinsulinismInsulinInsulin SecretionIslets of LangerhansLipidsArginineBlood GlucoseGlucoseInsulinLipids

Identifiers

PMID18698428
PMCPMC2500170
OpenAlexW2010064539

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.