Elevated circulating levels of aldosterone, either directly from adipocytes or released from the adrenal gland in response to leptin through the adipokines-cell-signaling molecules secreted (from central obesity or visceral adipose tissue), along with the attenuated anti-aldosterone effects from natriuretic peptides due to an increased neprilysin activity in obesity, may potentiate [50] the deleterious effect of neprilysin HF patients with obesity regardless of HF phenotypes [33]. The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.