Fig. 6

Elevated Menin is also observed in biopsied fatty liver tissues of dairy cows, and Menin occupies promoter regions of FABPs, acting as a transcriptional regulatory factor in hepatic lipid metabolism via the PPARγ signaling pathway. A. Representative hepatic histology sections of biopsied liver tissues from prenatal dairy cows. An Oil Red O staining assa, as well as Hematoxylin–Eosin staining (top panel), was used for fat content assessment in cells, thereby being classified into normal liver (Norm) and fatty liver (FL). Blue dots indicate cell nucleus, while brown or red indicates lipid droplets in cells that dissolved Oil Red. The bottom panel is a high-powered magnification of the central area of the middle panel. B. Protein–protein interaction network analysis of the differentially expressed genes associated with fatty liver disease, indicating enrichment in the PPAR signaling pathway, as well as NAFLD, AMPK signaling pathway, insulin signaling pathway, etc. C. Upstream and downstream target genes of the PPAR signaling pathway were upregulated in fatty liver of dairy cows compared to healthy ones (Norm). D. Elevated Menin in liver tissue was found to interact with PPARγ and SIRT1 via a Menin-IP assay. E. Several amplicons (P1, P2, etc.) were designed to detect the indicated promoter regions of the FABP3, FABP4, and FABP5 genes for Menin-ChIP assays in liver tissues. TSS represents the transcription start site. F. Representative ChIP-PCR results of promoter regions of FABP3 (upper panel), FABP4 (middle panel), and FABP5 (lower panel) from anti-Menin ChIPs in fatty liver (FL) and/or normal liver (Norm) from dairy cattle