Systemic pharmacological blockade of Ang II activity with ACE inhibitors or angiotensin receptor blockers (ARBs), or global genetic deletion of AT1a receptors (AT1aR), protects male rodents against development of HFD-induced obesity and dyslipidemia by increasing energy expenditure and improving glucose tolerance and insulin sensitivity [57, 58, 129]. This evidence concerns the gene AGT and obesity due to melanocortin 4 receptor deficiency.