Adverse conditions during early developmental stages permanently modify the metabolic function of organisms through epigenetic changes. Exposure to high sugar diets during gestation and/or lactation affects susceptibility to metabolic syndrome or hypertension in adulthood. The effect of a high sugar diet for shorter time lapses remains unclear. Here we studied the effect of short-term sucrose ingestion near weaning (postnatal days 12 and 28) (STS) and its effect after long-term ingestion, for a period of seven months (LTS) in rats. Rats receiving sucrose for seven months develop metabolic syndrome (MS). The mechanisms underlying hypertension in this model and those that underlie the effects of short-term exposure have not been studied. We explore NO and endothelin-1 concentration, endothelial nitric oxide synthase (eNOS) expression, fatty acid participation and the involvement of oxidative stress (OS) after LTS and STS. Blood pressure increased to similar levels in adult rats that received sucrose during short- and long-term glucose exposure. The endothelin-1 concentration increased only in LTS rats. eNOS and SOD2 expression determined by Western blot and total antioxidant capacity were diminished in both groups. Saturated fatty acids and arachidonic acid were only decreased in LTS rats. In conclusion, a high-sugar diet during STS increases the hypertension predisposition in adulthood to as high a level as LTS, and the mechanisms involved have similarities (participation of OS and eNOS and SOD expression) and differences (fatty acids and arachidonic acid only participate in LTS and an elevated level of endothelin-1 was only found in LTS) in both conditions. Changes in the diet during short exposure times in early developmental stages have long-lasting effects in determining hypertension susceptibility.
Keywords: critical window; endothelial nitric oxide synthase; fatty acids; hypertension; oxidative stress; sucrose.