In view of the influence of AT1R activation on cardiac function by affecting cardiac metabolism, the effects of Ang II on cardiac energy metabolism in experimental models of hypertrophy and diastolic dysfunction have been demonstrated to be associated with marked reduction in cardiac glucose and lactate oxidation without any change in glycolysis or fatty acid β-oxidation in Ang II-treated mice [87]. The gene discussed is AGTR1; the disease is cardiac hypertrophy.