Master of Science (MS)
CPT1, drosophila, fetal alcohol spectrum disorder, fetal alcohol syndrome, lipid metabolism, withered
Exposure to ethanol during development causes a variety of physical, developmental, and cognitive abnormalities. In humans, these symptoms are referred to as fetal alcohol syndrome (FAS) or fetal alcohol spectrum disorder (FASD). Previously, we established a Drosophila melanogaster model of FASD and showed that developmental ethanol exposure causes oxidative stress, and that this is a primary cause of the developmental lethality and delay associated with ethanol exposure. In this study, we investigate the role of fatty acid metabolism and lipid accumulation in connection to FASD. Here, we show that developmental ethanol exposure leads to dysregulation of fatty acid metabolism and lipid accumulation. Flies reared in ethanol-containing food had increased fat storage and had increased expression of withered, a lipid metabolism gene. Further, we saw a novel synergistic interaction between ethanol and a long-chain saturated fatty acid (palmitic acid), which strongly indicates that they both have the same molecular target in the cell. Our results show that one of the mechanisms by which ethanol induces oxidative stress is through dysregulation of fatty acid metabolism. These data suggest that dietary changes may prevent some aspects of FASD.
Khodabakhshi, Payam, "Mitochondrial dysfunction and lipid metabolism play a major role in the lethality caused by developmental alcohol exposure" (2015). Master's Theses. 4643.