Since adipose-derived angiotensinogen in rodents contributes to one third of the circulating angiotensinogen [17] and diet-induced obesity does not alter angiotensinogen expression in the aorta, kidney, and liver [18], the increase in adipose-derived angiotensinogen is more likely to be responsible for both systemic and adipose RAS activation in stressed subjects. Here, AGT is linked to obesity due to melanocortin 4 receptor deficiency.