Evidence map›Paper›PMID 21167066›Full record

ArticleBMC genomics2010

Genetic and genomic analysis of hyperlipidemia, obesity and diabetes using (C57BL/6J × TALLYHO/JngJ) F2 mice.

Taryn P Stewart, Hyoung Yon Kim, Arnold M Saxton, Jung Han Kim

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 46 citations in OpenAlex.

  1. Tachol1 QTL on mouse chromosome 1 is responsible for hypercholesterolemia and diet-induced obesity.Mammalian genome : official journal of the International Mammalian Genome Society · 2024
    Article
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  4. DEPP Deficiency Contributes to Browning of White Adipose Tissue.International journal of molecular sciences · 2022
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  12. Congenic mice demonstrate the presence of QTLs conferring obesity and hypercholesterolemia on chromosome 1 in the TALLYHO mouse.Mammalian genome : official journal of the International Mammalian Genome Society · 2017
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  15. Genotype-dependent Metabolic Responses to Semi-Purified High-Sucrose High-Fat Diets in the TALLYHO/Jng vs. C57BL/6 Mouse during the Development of Obesity and Type 2 Diabetes.Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association · 2016
    Article
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  19. The genetic basis of obesity-associated type 2 diabetes (diabesity) in polygenic mouse models.Mammalian genome : official journal of the International Mammalian Genome Society · 2014
    Review
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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

4 authors at 2 institutions in 1 country.

Taryn P StewartDepartment of Pharmacology, Physiology and Toxicology, Joan C, Edwards School of Medicine, Marshall University, Huntington, WV 25755, USA.
Hyoung Yon Kim
Arnold M Saxton
Jung Han Kim
Marshall University · USUniversity of Tennessee at Knoxville · US

Funding

WVU &MU NEW FACULTY GRANTSP20RR016477 · NCRR · MARSHALL UNIVERSITY · PI RANKIN, GARY O · 2001 to 2011
$35.5M
Transcription Factors in CancerP20RR020180 · NCRR · MARSHALL UNIVERSITY · PI NILES, RICHARD M. · 2004 to 2009
$9.5M
Genetics of diet-induced obesity in a new mouse modelR01DK077202 · NIDDK · UNIVERSITY OF TENNESSEE KNOXVILLE · PI KIM, JUNG HAN · 2008 to 2012
$1.4M
NCRR NIH HHS RR016477NCRR NIH HHS RR020180NIDDK NIH HHS R01DK077202
6 · The paper itself

Abstract

backgroundType 2 diabetes (T2D) is the most common form of diabetes in humans and is closely associated with dyslipidemia and obesity that magnifies the mortality and morbidity related to T2D. The genetic contribution to human T2D and related metabolic disorders is evident, and mostly follows polygenic inheritance. The TALLYHO/JngJ (TH) mice are a polygenic model for T2D characterized by obesity, hyperinsulinemia, impaired glucose uptake and tolerance, hyperlipidemia, and hyperglycemia.

resultsIn order to determine the genetic factors that contribute to these T2D related characteristics in TH mice, we interbred TH mice with C57BL/6J (B6) mice. The parental, F1, and F2 mice were phenotyped at 8, 12, 16, 20, and 24 weeks of age for 4-hour fasting plasma triglyceride, cholesterol, insulin, and glucose levels and body, fat pad and carcass weights. The F2 mice were genotyped genome-wide and used for quantitative trait locus (QTL) mapping. We also applied a genetical genomic approach using a subset of the F2 mice to seek candidate genes underlying the QTLs. Major QTLs were detected on chromosomes (Chrs) 1, 11, 4, and 8 for hypertriglyceridemia, 1 and 3 for hypercholesterolemia, 4 for hyperglycemia, 11 and 1 for body weight, 1 for fat pad weight, and 11 and 14 for carcass weight. Most alleles, except for Chr 3 and 14 QTLs, increased phenotypic values when contributed by the TH strain. Fourteen pairs of interacting loci were detected, none of which overlapped the major QTLs. The QTL interval linked to hypercholesterolemia and hypertriglyceridemia on distal Chr 1 contains Apoa2 gene. Sequencing analysis revealed polymorphisms of Apoa2 in TH mice, suggesting Apoa2 as the candidate gene for the hyperlipidemia QTL. Gene expression analysis added novel information and aided in selection of candidates underlying the QTLs.

conclusionsWe identified several genetic loci that affect the quantitative variations of plasma lipid and glucose levels and obesity traits in a TH × B6 intercross. Polymorphisms in Apoa2 gene are suggested to be responsible for the Chr 1 QTL linked to hypercholesterolemia and hypertriglyceridemia. Further, genetical genomic analysis led to potential candidate genes for the QTLs.

Indexed as

Crosses, GeneticAdipose TissueAnimalsApolipoprotein A-IIBase SequenceBlood GlucoseBody WeightCholesterolDiabetes Mellitus, ExperimentalEpistasis, GeneticFemaleGenomeGenome-Wide Association StudyHyperlipidemiasInsulinMaleApolipoprotein A-IIBlood GlucoseCholesterolInsulinTriglycerides

Identifiers

PMID21167066
PMCPMC3022919
OpenAlexW2078524200

What OpenQuestion holds

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LicenceCC BY
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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.