Disruption of the Igf2 gene alters hepatic lipid homeostasis and gene expression in the newborn mouse

American Journal of Physiology. Endocrinology and Metabolism
M F LopezJoel N Hirschhorn

Abstract

Newborns with intrauterine growth-restriction are at increased risk of mortality and life-long comorbidities. Insulin-like growth factor-II (IGF2) deficiency in humans, as well as in mice, leads to intrauterine growth restriction and decreased neonatal glycogen stores. The present study aims to further characterize the metabolic and transcriptional consequences of Igf2 deficiency in the newborn. We found that, despite being born significantly smaller than their wild-type ( Igf2+/+) littermates, brain size was preserved in Igf2 knockout ( Igf2-/-), consistent with nutritional deficiency. Histological and triglyceride analyses of newborn livers revealed that Igf2-/- mice are born with hepatic steatosis. Gene expression analysis in Igf2-/- newborn livers showed an alteration of genes known to be dysregulated in chronic caloric restriction, including the most upregulated gene, serine dehydratase. Multiple genes connected with lipid metabolism and/or hepatic steatosis were also upregulated. Ingenuity Pathway Analysis confirmed that the biological functions most altered in livers of Igf2-/- newborns are related to lipid metabolism, with the top upstream regulator predicted to be the peroxisome proliferator-activated receptor alpha, a...Continue Reading

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Methods Mentioned

BETA
PCR
biopsies

Software Mentioned

Bioconductor Lumi
Ingenuity Pathway Analysis ( IPA )
Ingenuity Pathway Analysis
R
Primer
Bioconductor
Limma Bioconductor
IPA
BLAST

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