Liver inflammation caused by NASH, associated with the presence of pro-inflammatory mediators such as leptin, resistin, IL-6, and tumor necrosis factor-alpha (TNF-α) and intestinal lipopolysaccharides (bacterial endotoxins), creates an obstacle to insulin signaling pathways, impairing the insulin uptake of glucose in peripheral tissues and the inhibition of liver glucose production. Here, TNF is linked to metabolic dysfunction-associated steatohepatitis.