Further scrutiny depicted thataging and obesity independently decreased the phosphorylation of Akt and itsdownstream signaling molecule eNOS, stimulated JNK and IκB phosphorylationas well as inhibited p38 phosphorylation without overt interactions between the two.Consistent with its responsiveness to mechanical function,O2− production andp47phox expression,physiological levels of leptin effectively restored leptin deficiency-inducedchanges in the phosphorylation of Akt, eNOS, JNK, IκB and p38 in young butnot aging ob/ob mice. This evidence concerns the gene AKT1 and obesity disorder.