Maternal high-fructose consumption provokes placental oxidative stress resulting in asymmetrical fetal growth restriction in rats.

We aimed to determine the impact of high-fructose intake during pregnancy on the fetal-placental unit in rats, which may be the initial mechanism of the programming effect of fructose. Pregnant Sprague-Dawley rats were randomly assigned to three groups and respectively provided tap water (n = 10), 10% (w/v) fructose solution (n = 10), and 10% (w/v) glucose solution (n = 10) from embryonic day 0 to 20. Compared with the control and glucose groups, significantly lower fetal length, fetal weight, placental weight, and fetus/placenta ratio were found in the fructose group on embryonic day 20 (all p<0.05). In parallel with markedly increased uric acid concentrations in the dams, significantly decreased antioxidant enzymes activities and mRNA expression levels were observed in placentas in the fructose group (all p<0.05). In the fructose group, placental mRNA and protein expression of nuclear factor erythroid 2-related factor 2 was markedly downregulated and kelch-like ECH-associated protein 1 was significantly upregulated (all p<0.05). In conclusion, high-fructose consumption during pregnancy drives augmented oxidative stress in rats. Placental insufficiency under oxidative stress contributes to asymmetrical fetal growth restriction.