Figure 8

A schematic summary of our hypotheses and obtained results. Angiotensin II, via redox-dependent mechanisms, promotes adipocyte growth and lipid accumulation. This involves the suppression of the Wnt-canonical pathway and leads to dysfunctional hypertrophic adipogenesis—characterized by increased visceral adiposity, increased inflammation and decreased adiponectin levels. A synthetic PPARδ-agonist binds to and activates the HO-1 promoter, with increased HO-1 expression as a consequence. Activation of this pathway stimulates the Wnt-canonical signaling cascade in adipose tissues, subjected to higher levels of Ang II and oxidative stress. Consequentially, preadipocyte maturation and lipid accumulation is retarded, leading to an increased number of smaller adipocytes with improved adipocytokine profile. Thus, PPARδ-agonist-mediated HO-1 activation prevents oxidative stress and associated dysfunctional adipogenesis in animals with an overactive renin–angiotensin system.