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Previous studies showed that insulin-like growth factor-binding protein 5 (IGFBP5) plays a role in non-alcoholic fatty liver disease; however, its expression and function in goose fatty liver remain unknown. To address this, we obtained a full-length mRNA sequence of the goose <i>IGFBP5</i> gene using a 5′-rapid amplification of cDNA ends assay and nested polymerase chain reaction (PCR). Additionally, using the newly acquired sequence of 5’-untraslated region, we determined the missing sequence of the first intron. Bioinformatics analysis revealed three exons and three introns in the goose <i>IGFBP5</i> gene. Quantitative PCR analysis indicated that the mRNA abundance of <i>IGFBP5</i> was significantly lower in goose fatty liver than in the normal liver. Comparison of transcriptomes of goose primary hepatocytes transfected with <i>IGFBP5</i> overexpression vector versus those transfected with empty vector identified 777 differentially expressed genes (DEGs). The enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways indicated the focal adhesion, ECM-receptor interaction, regulation of the actin cytoskeleton, mitogen-activated protein kinase (MAPK) signaling, and GnRH signaling pathways. Immunoblotting revealed the induction of the p38 MAPK pathway by <i>IGFBP5</i> overexpression, which is in line with the suppressed expression of <i>IGFBP5</i> and p38 MAPK in goose fatty liver than in normal liver. These findings suggest that IGFBP5 is involved in the development of goose fatty liver via the p38 MAPK pathway.