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Statements

Subject Item
n2:RIV%2F00023001%3A_____%2F12%3A00055966%21RIV13-MZ0-00023001
rdf:type
n6:Vysledek skos:Concept
rdfs:seeAlso
http://www.nature.com/hdy/journal/v109/n1/full/hdy201214a.html
dcterms:description
Deficiency of fatty acid translocase Cd36 has been shown to have a major role in the pathogenesis of metabolic syndrome in the spontaneously hypertensive rat (SHR). We have tested the hypothesis that the effects of Cd36 mutation on the features of metabolic syndrome are contextually dependent on genomic background. We have derived two new congenic strains by introgression of limited chromosome 4 regions of SHR origin, both including the defective Cd36 gene, into the genetic background of a highly inbred model of insulin resistance and dyslipidemia, polydactylous (PD) rat strain. We subjected standard diet-fed adult males of PD and the congenic PD.SHR4 strains to metabolic, morphometric and transcriptomic profiling. We observed significantly improved glucose tolerance and lower fasting insulin levels in PD.SHR4 congenics than in PD. One of the PD.SHR4 strains showed lower triglyceride concentrations across major lipoprotein fractions combined with higher levels of low-density lipoprotein cholesterol compared with the PD progenitor. The hepatic transcriptome assessment revealed a network of genes differentially expressed between PD and PD.SHR4 with significant enrichment by members of the circadian rhythmicity pathway (Arntl (Bmal1), Clock, Nfil3, Per2 and Per3). In summary, the introduction of the chromosome 4 region of SHR origin including defective Cd36 into the PD genetic background resulted in disconnected shifts of metabolic profile along with distinct changes in hepatic transcriptome. The synthesis of the current results with those obtained in other Cd36-deficient strains indicates that the eventual metabolic effect of a deleterious mutation such as that of SHR-derived Cd36 is not absolute, but rather a function of complex interactions between environmental and genomic background, upon which it operates. Heredity (2012) 109, 63-70; doi:10.1038/hdy.2012.14; published online 4 April 2012 Deficiency of fatty acid translocase Cd36 has been shown to have a major role in the pathogenesis of metabolic syndrome in the spontaneously hypertensive rat (SHR). We have tested the hypothesis that the effects of Cd36 mutation on the features of metabolic syndrome are contextually dependent on genomic background. We have derived two new congenic strains by introgression of limited chromosome 4 regions of SHR origin, both including the defective Cd36 gene, into the genetic background of a highly inbred model of insulin resistance and dyslipidemia, polydactylous (PD) rat strain. We subjected standard diet-fed adult males of PD and the congenic PD.SHR4 strains to metabolic, morphometric and transcriptomic profiling. We observed significantly improved glucose tolerance and lower fasting insulin levels in PD.SHR4 congenics than in PD. One of the PD.SHR4 strains showed lower triglyceride concentrations across major lipoprotein fractions combined with higher levels of low-density lipoprotein cholesterol compared with the PD progenitor. The hepatic transcriptome assessment revealed a network of genes differentially expressed between PD and PD.SHR4 with significant enrichment by members of the circadian rhythmicity pathway (Arntl (Bmal1), Clock, Nfil3, Per2 and Per3). In summary, the introduction of the chromosome 4 region of SHR origin including defective Cd36 into the PD genetic background resulted in disconnected shifts of metabolic profile along with distinct changes in hepatic transcriptome. The synthesis of the current results with those obtained in other Cd36-deficient strains indicates that the eventual metabolic effect of a deleterious mutation such as that of SHR-derived Cd36 is not absolute, but rather a function of complex interactions between environmental and genomic background, upon which it operates. Heredity (2012) 109, 63-70; doi:10.1038/hdy.2012.14; published online 4 April 2012
dcterms:title
CD36-deficient congenic strains show improved glucose tolerance and distinct shifts in metabolic and transcriptomic profiles CD36-deficient congenic strains show improved glucose tolerance and distinct shifts in metabolic and transcriptomic profiles
skos:prefLabel
CD36-deficient congenic strains show improved glucose tolerance and distinct shifts in metabolic and transcriptomic profiles CD36-deficient congenic strains show improved glucose tolerance and distinct shifts in metabolic and transcriptomic profiles
skos:notation
RIV/00023001:_____/12:00055966!RIV13-MZ0-00023001
n6:predkladatel
n12:ico%3A00023001
n4:aktivita
n13:V n13:Z
n4:aktivity
V, Z(MSM0021620807)
n4:cisloPeriodika
1
n4:dodaniDat
n11:2013
n4:domaciTvurceVysledku
n17:3973425
n4:druhVysledku
n18:J
n4:duvernostUdaju
n15:S
n4:entitaPredkladatele
n16:predkladatel
n4:idSjednocenehoVysledku
126169
n4:idVysledku
RIV/00023001:_____/12:00055966
n4:jazykVysledku
n9:eng
n4:klicovaSlova
transcriptomics; animal model; metabolic syndrome; functional genomics
n4:klicoveSlovo
n5:functional%20genomics n5:animal%20model n5:transcriptomics n5:metabolic%20syndrome
n4:kodStatuVydavatele
GB - Spojené království Velké Británie a Severního Irska
n4:kontrolniKodProRIV
[265F20F1E062]
n4:nazevZdroje
Heredity
n4:obor
n20:FB
n4:pocetDomacichTvurcuVysledku
1
n4:pocetTvurcuVysledku
10
n4:rokUplatneniVysledku
n11:2012
n4:svazekPeriodika
109
n4:tvurceVysledku
Šedová, L. Kazdová, Ludmila Tremblay, J. Liska, F. Seda, O. Hamet, P. Krupkova, M. Kren, V. Corbeil, G. Krenova, D.
n4:wos
000305366700010
n4:zamer
n7:MSM0021620807
s:issn
0018-067X
s:numberOfPages
8
n19:doi
10.1038/hdy.2012.14