4.1 Maternal fructose consumption increases their own and their offsprings’ caloric intake, while exercise reduces it
In our study, the fructose serum concentration of the mothers in the groups treated with fructose was higher compared to those consuming water, confirming proper uptake of the fructose by the body, and a decrease was observed in the groups doing voluntary physical exercise. The higher exposure to fructose before and during pregnancy increased the liquid consumption of the mothers, and that intervention with voluntary physical exercise was able to reduce this 20%/L fructose liquid consumption, especially in the groups FRU+VPE/Water+VPE and FRU+VPE/Water. Food consumption seemed to be more associated with doing exercise, as only slight non-significant increases were observed for the fructose only group (G3) compared to the water only group (G1). However, caloric intake did increase significantly in the fructose consuming groups during all the study periods.
Corroborating with our results, Magenis et al. (2020) observed that fructose consumption at 10 and 20%/L in mice can lead to an increase in food and caloric intake in female mice during pregnancy, as well as, increase in food consumption in offspring of mothers that were exposed to fructose. Clayton et al. (2015) suggest that maternal fructose (10%) consumption may alter maternal responsiveness to leptin and lead to impaired signaling in the fetus, thus altering food consumption. The imbalance of this hormone can affect appetite regulation and lead to insufficient satiety, increasing food intake (Kao et al., 2021). It is further suggested that fructose consumption may be a significant factor in the obesity epidemic since human studies using fructose concentrations ranging from 7.5% to 25% of caloric intake have demonstrated that its long-term consumption may be associated with the development of hyperlipidemia and insulin resistance (Vos et al., 2008; Stanhope et al., 2015).
Physical exercise can bring benefits in food control as observed in this study. Platt et al. (2015) observed that the physical exercise of the voluntary wheel did not change the caloric consumption of pregnant females, as in our study. Hsu et al. (2021) evaluated the effects of aquatic exercise in mice fed with a high-fructose diet and observed that fructose increases food consumption and that physical exercise decreases this consumption when associated with fructose.
In the offspring (male and female), an increase in serum fructose concentration was observed during the lactation, showing that maternal fructose exposure passes via the placental barrier and that exposure continues via breast milk to offspring. However, upon reaching adulthood and without maternal exposure, levels returned to normal. These results prove that fructose was taken up by the mothers, and that the offspring were exposed to fructose via the mothers during pregnancy and lactation. When fructose was consumed in combination with voluntary physical exercise, these levels decreased. As suggested by Egli et al. (2016) exercise performed immediately after fructose ingestion increases fructose oxidation and suppresses fructose and glycogen storage.
Indeed, we observed that food consumption, and caloric intake (especially for the males), was lower in the FRU+VPE/Water+VPE intervention compared to the FRU group, showing that stopping fructose and continuing to practice physical exercise during pregnancy has better regulation of food consumption in the offspring. Interestingly, the uterine environment may influence taste preferences and healthy eating in offspring. The flavors of the maternal diet are found in the amniotic fluid and consequently ingested by the fetus, thus flavors experienced in the intrauterine period determine a preference that persists into childhood or even into adulthood, along with possible complications such as type 2 diabetes mellitus and obesity (Trout and Effinger, 2012). Koo et al. (2021) have observed the negative effects of maternal fructose intake during pregnancy and lactation on their offspring, leading to the appearance of metabolic syndrome, suggesting that nutritional status and food intake during pregnancy and lactation may affect fetal programming (Koo et al., 2021).