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.

富含果糖的饮食是诱发性代谢综合征（MS）的实验模型，会影响怀孕和哺乳期的大鼠大坝，而且还会导致其后代的代谢状况失衡。硒（Se）稳态和身体分布也发生了改变。硒蛋白：谷胱甘肽过氧化物酶（GPx）和硒蛋白P（SelP）似乎在MS中起作用。为了评估硒蛋白在这种疾病向子代的传播中的作用，在暴露于富含果糖饮食（65％）的大坝的后代中测量了肝硒沉积，GPx活性，生物分子氧化和硒蛋白以及AMPK的表达。早期营养期间，果糖暴露会影响硒的摄入量和肝脏硒蛋白含量。雌性果糖幼犬肝脏中硒的含量增加并被氧化，GPx活性更高，肝GPx1和SelP的表达也增加，与较低的AMPK活化和血清胰岛素水平有关。早期营养期间的果糖暴露会对雌性幼犬的硒蛋白，氧化和代谢产生负面影响。