We analyze three possible mechanisms underlying hypertension when the animals reach adulthood in both models: the first is through the effect of insulin, which inhibits endothelial nitric oxide synthase (eNOS) [21]; the second is through an elevation of free fatty acids, mainly oleic acid, which might diminish the activity of eNOS; and the third is through oxidative stress (OS), since uncoupled eNOS and other enzymes generate reactive oxygen species that react with NO, diminishing its bioavailability and therefore vessel relaxation [22]. The gene discussed is INS; the disease is hypertensive disorder.