AKT1 and Insulin resistance: Further studies showed that sEH blocker t-AUCB potently ameliorated inflammation, cardiac remodeling, and hypertrophy in a model of insulin resistance, which was related to decreased infiltration of CD45- and F4/80-positive cells, downregulated expression of p-AKT, sEH, NF-κB, NOX4, and reduced fibrosis related proteins [105].