In summary, data from our present study suggested that aging and the leptin deficientob/ob obesity compromise cardiac contractile function andintracellular Ca2+ homeostasis via comparable mechanismsinvolving NADPH oxidase-dependent O2− production,phosphorylation of Akt, eNOS as well as the stress signaling molecules p38, JNK andNFκB. The gene discussed is FMO5; the disease is obesity disorder.