CD36-DEFICIENT CONGENIC STRAINS SHOW IMPROVED GLUCOSE TOLERANCE AND DISTINCT SHIFTS IN METABOLIC AND TRANSCRIPTOMIC PROFILES

ABSTRACT: Deficiency of fatty acid translocase Cd36 has been shown to play major role in pathogenesis of metabolic syndrome components in the spontaneously hypertensive rat (SHR). We have tested the hypothesis that effects of Cd36 mutation on 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 defective Cd36 gene, into genetic background of highly inbred model of insulin resistance and dyslipidemia, polydactylous (PD) rat strain. We have subjected standard diet-fed adult males of PD and the 2 congenic PD.SHR4 strains to metabolic, morphometric and transcriptomic (Affymetrix Rat 1.0 ST Exon array) profiling. We observed significantly improved glucose tol

ORGANISM(S): Rattus norvegicus

SUBMITTER: Ondrej Seda 

PROVIDER: E-GEOD-33597 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress