Maternal exposure to sucrose and maltodextrin alters metabolism and genotoxicity in mice offspring.

Early metabolic events during the intrauterine period can increase susceptibility to chronic diseases in adulthood. Fetal and neonatal nutrition rich in sugars may lead to disorders such as obesity, insulin resistance, and diabetes. This study evaluated the effects of maltodextrin and sucrose intake in Swiss female mice treated during gestation and lactation, as well as in their offspring. Sixty-day-old mating pairs were used, receiving nutritional interventions (maltodextrin 10%/L, sucrose 10%/L, or water) during mating, gestation, and lactation (7, 21, and 21 days, respectively), totaling 49 days. Genetic (comet assay, micronucleus test) and biochemical (glycemia and electron transport chain) analyses were performed in dams and in offspring of both sexes at postnatal days (PND) 21 and 30. In dams, food intake and body weight were monitored, whereas in offspring, anthropometric parameters were assessed. Results showed that both carbohydrates increased fluid and calorie intake without affecting maternal body weight. Sucrose raised fasting glucose significantly. Comet assay revealed increased DNA damage after gestation and lactation, especially in the cortex for maltodextrin (p < 0.05), with no changes in liver or hippocampus. The micronucleus test showed increased PCE micronuclei in the maltodextrin group (p < 0.05). Complex I activity increased in the liver with both carbohydrates, while Complex II-III decreased with sucrose. In the cortex, both carbohydrates increased Complex II and reduced Complex IV; in the hippocampus, Complex I increased with both, and Complex IV increased with maltodextrin. In the offspring, sucrose-exposed males had greater body weight at 21 days, and females showed increased glycemia at 30 days. Overall, findings suggest that maltodextrin and sucrose intake during pregnancy and lactation can induce long-term metabolic and genetic alterations in mothers and offspring.