Figure S5.
PML loss promotes differences in lipid metabolic reprogramming between body fat and the liver in liver-specific HBsAg-transgenic mice.PML-/-HBsAgtg/0 male mice were fed a high-fat diet for 11 months. (A) Weight changes in body fat and liver. Error bars indicate mean ± SD (n = 10-20 for each time point). (B) Representative histology of white body fat mass and liver. Note the continuous fat accumulation in the liver in contrast to the gradual browning and wasting of the body fat. (C) Common and divergent alterations in liver proteomics between 7-month-old and 11-month-old PML-/-HBsAgtg/0 mice. The enriched genes, whose expression was 2-fold up-regulated or down-regulated in more than 50% of the tested mice compared to the average expression of the same genes in sex- and age-matched wild-type mice (n = 5-10 for each group), were categorized by gene ontology (GO) analysis. Note that energy metabolism and cell growth control are the major affected GO pathways.