Document Type


Publication Date

January 2015


fetal alcohol syndrome, reactive oxygen species, lipid accumulation, withered, carnitine transporter


Biology | Genetics and Genomics


Ethanol exposure during development causes an array of developmental abnormalities, both physiological and behavioral. In mammals, these abnormalities are collectively known as Fetal Alcohol Effects (FAE) or Fetal Alcohol Spectrum Disorder (FASD). We have established a Drosophila melanogaster model of FASD, and have previously shown that developmental ethanol exposure in flies leads to reduced expression of insulin like peptides (dILPs) and their receptor. In this work, we link that observation to dysregulation of fatty acid metabolism and lipid accumulation. Further, we show that developmental ethanol exposure in Drosophila causes oxidative stress, that this stress is a primary cause of the developmental lethality and delay associated with ethanol exposure, and, finally, that one of the mechanisms by which ethanol increases oxidative stress is through abnormal fatty acid metabolism. These data suggest a previously uncharacterized mechanism by which ethanol causes the symptoms associated with FASD.


This article originally appeared in G3, volume 5, issue 1, 2015 and can be found online at this link:
This is an open-access article distributed under the terms of the Creative Commons Attribution Unported License (, which permits unrestricted use, distribution, and reproduction in anymedium, provided the original work is properly cited.
Supporting files and data are available online at

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution 3.0 License.