A possible role of glucose has been proposed to explain these paradoxical results: in OLETF (Otsuka Long-Evans Tokushima Fatty) rats, a model of hypertension, high glucose levels might impair NRF2 pathway [176], and blocking AT1 might actually upregulate NRF2 and improve mitochondrial function, having antioxidant effects. The gene discussed is NFE2L2; the disease is hypertensive disorder.