Related Experiment Videos
Effects of ethanol on fetal fuels and brain growth in rats
S P Singh1, G L Pullen, A K Snyder
1Department of Medicine, Chicago Medical School, IL.
Insights
Maternal alcoholism causes fetal brain growth retardation by altering fetal fuel metabolism. Ethanol-fed fetuses showed decreased glucose and increased lactate, suggesting aberrant fuel mixtures contribute to impaired brain development.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Maternal alcoholism is a leading cause of preventable birth defects.
- The precise mechanisms underlying fetal brain growth retardation due to alcohol exposure remain incompletely understood.
Purpose of the Study:
- To investigate the relationship between maternal ethanol consumption and fetal brain growth retardation.
- To analyze fuel concentrations in fetal brain and blood samples from ethanol-exposed rats.
Main Methods:
- Rats were fed ethanol during pregnancy; offspring body and brain weights were compared to pair-fed and ad libitum-fed controls.
- Concentrations of glucose, pyruvate, lactate, and ketone bodies were measured in maternal and fetal blood and brain tissues.
- Correlations between fuel concentrations and fetal brain weight were analyzed.
Main Results:
- Ethanol-fed offspring exhibited significantly reduced body and brain weights.
- Ethanol-fed fetuses displayed decreased plasma glucose and pyruvate, elevated lactate, and an increased lactate-to-pyruvate ratio.
- Fetal brain glucose levels were lower, while lactate and ketone concentrations were higher in ethanol-exposed fetuses, correlating negatively with brain weight.
Conclusions:
- Aberrant fetal fuel metabolism, characterized by altered glucose, lactate, and ketone levels, likely contributes to fetal brain growth retardation in maternal alcoholism.
- These metabolic changes may disrupt normal brain development during gestation.
Abstract:
The mechanism of fetal brain growth retardation caused by maternal alcoholism is unclear. In this study we examined fuel concentrations in brain and blood samples and their relationship to brain growth in term fetuses of rats fed ethanol during pregnancy. The offspring of ethanol-fed (EF) rats showed a significant decrease in body and brain weights compared with those of pair-fed (PF) control rats and control rats given free access to food (ad libitum fed) (AF). The EF and PF rats consumed nearly 20% less food than the AF rats, and both groups showed a slight but significant reduction of the maternal blood glucose level. In PF rats, beta-hydroxybutyrate concentration was increased in maternal as well as in fetal blood and brain samples, but no adverse effect of this magnitude of maternal undernutrition was observed on fetal body or brain weights. In EF fetuses, plasma glucose and pyruvate levels were decreased and lactate levels were increased, resulting in a nearly twofold increase in the lactate-to-pyruvate ratio when compared with levels in control fetuses. The beta-hydroxybutyrate--to-acetoacetate ratio was increased because of low plasma acetoacetate concentration. In EF fetuses, brain glucose and pyruvate levels were decreased. Fetal brain weight showed a positive correlation with brain glucose concentration and a negative correlation with the brain concentrations of lactate or ketones. It is surmised that an aberrant fetal fuel mixture may play a role in the fetal growth retardation associated with maternal alcoholism.