Nutrients, Год журнала: 2025, Номер 17(5), С. 812 - 812

Опубликована: Фев. 26, 2025

Background: Prenatal alcohol exposure (PAE) models can cause neurodevelopmental abnormalities like those observed in fetal spectrum disorder (FASD). Previous studies link experimental PAE effects the brain to impaired signaling through insulin/IGF and Notch pathways that mediate neuronal survival, growth, migration, energy metabolism, plasticity. Importantly, concurrent administration of peroxisome proliferator-activated receptor agonists or dietary soy prevented many aspects FASD due their insulin-sensitizing, anti-inflammatory, antioxidant properties. Objective: To determine if interventions during pregnancy would be sufficient normalize central nervous system structure function, we examined maternal gestation-limited on cerebellar postnatal development, motor critical pathways. Methods: Pregnant Long Evans rats were fed isocaloric liquid diets containing 0% 26% caloric ethanol with casein isolate as protein source. The feedings discontinued upon delivery. offspring subjected rotarod function tests, day 35, they sacrificed harvest cerebella for histological molecular studies. Results: Despite cessation exposure, chronic gestational reduced weight, caused hypoplasia, performance. Gestational ethanol-associated reduction weight largely restored integrity cerebellum but failed Ethanol withdrawal abolished impairments previously associated ongoing exposures, ethanol's inhibitory Wnt persisted. Soy significantly increased expression insulin IGF-1 receptors abrogated several signaling. Conclusions: Although gestation-restricted has significant positive neurodevelopment, optimum prevention FASD's long-term will likely require intervention periods even after exposures have ceased.

Язык: Английский