Gene expression profiling in epidydimal fat from wild-type and macrophage-derived TNF-α deficient mice.

The pro-inflammatory cytokine, tumor necrosis factor-alpha (TNF-α), has been suggested to be a key factor in the induction of obesity-associated metabolic dysfunction. However, the role that macrophage-derived TNF-α has on regulating metabolic perturbations in obesity is not completely understood. Therefore, we utilized the TNF-αFlox/FLox (F/F), LyzMcre+/- mouse model to determine the impact that macrophage TNF-α deletion has on the development of high-fat-diet (HFD)-induced obesity. 20 total samples were analyzed. We performed a pairwise comparison of macrophage-derived TNF-α deficient (cre) and wild-type (wt) genotypes. Genes with a p-valued < 0.05 and a fold-change ≥ 1.5 were selected.