A meta-analysis study of gene expression datasets in mouse liver under PPARα knockout

Abstract

Gene expression profiling of peroxisome-proliferator-activated receptor α (PPARα) has been used in several studies, but there were no consistent results on gene expression patterns involved in PPARα activation in genome-wide due to different sample sizes or platforms. Here, we employed two published microarray datasets both PPARα dependent in mouse liver and applied meta-analysis on them to increase the power of the identification of differentially expressed genes and significantly enriched pathways. As a result, we have improved the concordance in identifying many biological mechanisms involved in PPARα activation. We suggest that our analysis not only leads to more identified genes by combining datasets from different resources together, but also provides some novel hepatic tissue-specific marker genes related to PPARα according to our re-analysis.

Effect of oleoylethanolamide on diet-induced nonalcoholic fatty liver in rats

“…Peroxisome proliferator-activated receptor alpha (PPAR-a) is predominantly distributed in the active metabolic tissues, such as liver, kidney, heart and skeletal muscle, in which modulates the lipid metabolism and energy balance. PPAR-a activation not only up-regulates the expression levels of carnitine palmitoyl transferase 1 (CPT1) to promote fatty acid b-oxidation and reduces triglyceride deposition in vivo, but also inhibits the signal transduction mediated by AP-1 and NF-kB to relieve inflammation (3). Fatty acid oxidases in the mitochondria, peroxisomes and microsomes expressed abnormally in PPAR-a knockout (KO) mice, leading to increase of free fatty acids in plasma and excessive accumulation of lipids in liver (4).…”