The changes observed in SBP could be related to several factors: (a) chronic ingestion of sucrose that causes an increase of 10–15 mmHg the SBP in rats [32], (b) IR and hypertriglyceridemia which are associated with impaired endothelial nitric oxide synthase (eNOS) activity and increased production of endothelin-1 [33], (c) hyperinsulinemia that increases circulating levels of free fatty acids which participate in the development of endothelial dysfunction [34], and (d) the loss of E2 by ovariectomy. The gene discussed is EDN1; the disease is hyperinsulinism.