GSE106512
Transcriptome analyses reveal metabolic syndrome of adulthood with intrauterine growth restriction in a pig model
Epidemiological data indicated intrauterine growth retardation (IUGR) is a risk factors for adult metabolic syndrome. However, the genetic mechanism underlying the phenotype in adulthood is not well characterized. Here, the present study employed adult normal and IUGR pigs as models to survey the difference of global gene expression in the liver using transcriptome sequence. The trancriptome libraries generated 104.54 gigabases data, 16,948 and 17,078 genes were expressed in normal and IUGR pigs, repectively. A total of 1,322 differentially expreesion genes (DGEs) were identified. An enrichment analysis of DGEs presented the top overrepresented GO terms and pathway were related to oxidoreductase activity, ATPase activity, amino catabolic process, glucose metabolism and Insulin signaling pathway. Finally, combined their phenotypes and gene expression patterns, we proved the adult IUGR pigs would obstruct the process of mitochondrial biogenesis and oxidative phosphorylation, which induced high oxidation press in adult IUGR. The increased gluconeogenic and decreased glycogen synthesis in liver resulted in reducing the capacity of glucose intolerance in IUGR. The decreased expression of insulin signaling genes (such as PI3K and AKT) implied a risk of diabetes in adult IUGR. Moreover, the capacity of fatty acid oxidation decreased in IUGR liver leaded to high content of triglyceride and free fatty acid in IUGR. Together, these findings provide a comprehensive understanding of the molecular mechanisms of adult IUGR pigs and valuable information for future studies of therapeutic intervention in IUGR metabolic syndrome. Overall design: Liver mRNA profiles of adult IUGR and normal pigs were generated by deep transcriptome sequencing, in triplicate, using  HiSeq 2000 platform.