Fig. 1

Menin knockdown in hepatocytes facilitated the expression of fatty acid transport-associated genes via the PPAR signaling pathway. A. Knockdown of Men1 mRNA was detected in mouse hepatocytes (NCTC-1469) at 24 h after transfection with Men1-specific siRNA (si-Men1) or non-specific negative control siRNA (Ctrl). B. Menin protein was suppressed in hepatocytes, as shown in the representative Western blot images presented in the inserted panel. C. Protein–protein interaction network analysis of differentially expressed genes detected using RT². Profiler PCR Array in Menin lower-expressed hepatocytes indicates that lower Menin cause fatty liver disease or disorder in glycolipid metabolism via enriched signaling pathways such as NAFLD, AMPK signaling pathway, insulin signaling pathway, etc. D. Genes involved in the PI3K/Akt/mTOR, AMPK, and PPAR signaling pathways were regulated upon inhibition of Menin expression, which are downstream targets of Menin, such as enhanced Fabp3, Fabp4, and Cd36. E. Lower Menin expression in hepatocytes led to elevated protein expressions of PPARγ, FABP3, FABP4, and FABP5