Fig. 3

A fatty cell model was induced using sodium oleate (OA) and accompanied by enhanced fatty acid transport via the PPAR signaling pathway, similar to that of lower Menin expression. A. Sodium oleate (OA, 0.25 mM) was used to induce mouse hepatocytes into a fat-deposited cell model. Red oil staining indicated significantly increased TG (Additional file 2: Figure S2B), and lipid droplets accumulated in hepatocytes upon OA treatment. B. Both mRNA and protein levels of Menin were elevated in fatty hepatocytes upon OA induction. C. Gene ontology analysis of differentially expressed genes detected using RT². Profiler PCR Array in OA-induced fatty hepatocytes. D. Protein–protein interaction network analysis of differentially expressed genes indicates fat deposition in hepatocytes upon OA treatment was accompanied by dysregulations in signaling pathways associated with fatty liver disease or disorder in glycolipid metabolism, such as NAFLD, PPAR signaling pathway, insulin signaling pathway, etc. E. The enhanced expression of a series of target genes suggested OA-induced fat accumulation in hepatocytes was regulated via the PPARγ signaling pathway, similar to that of Menin knockdown experiments, except for the elevated fatty acid transport genes Fabp3/4/5, which were supposed to be inhibited by elevated Menin. *P < 0.05, **P < 0.01, ***P < 0.001