| Summary: | Fructose-rich diets, an experimental model of induced metabolic syndrome (MS), affects pregnant and lactating rat dams, and moreover, it leads to an imbalance in their offspring’s metabolic profile. Selenium (Se) homeostasis and body distribution is also altered. Selenoproteins: Glutathione peroxidase (GPx) and selenoprotein P (SelP) appear to play a role in MS. To evaluate selenoproteins’ implication in the transmission of this pathology to the progeny, hepatic Se deposits, GPx activity, biomolecular oxidation and selenoproteins and AMPK expression were measured in the offspring of dams exposed to a fructose-rich diet (65%). Se intake and liver selenoproteins are affected by fructose exposition during early nutrition. Female fructose pups show a repletion of Se and oxidation in liver, higher GPx activity and expression of hepatic GPx1 and SelP, related to a lower activation of AMPK and serum insulin levels. Fructose exposure during early nutrition negatively alters selenoproteins, oxidation and metabolism in female pups.
|
|---|
