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).