Fetal alcohol spectrum disorder (FASD) is the leading cause of congenital intellectual disabilities in the Western World, with a worldwide prevalence of 2-11% of all births. FASD is preventable but recent epidemiological studies suggest that public awareness campaigns have reached the limits of their effectiveness. Therefore, research is shifting from prevention to treatment and mitigation of symptoms. No biological treatments for FASD exist, due in part to the fact the cellular mechanisms of alcohol toxicity are not well-understood. Developmental alcohol exposure (DAE) causes a variety of deleterious effects in both vertebrates and invertebrates, including increased mortality, slow growth, learning and memory deficits, and behavioral changes including feeding abnormalities. In this study, we use the common fruit fly, Drosophila melanogaster, as a model to study the effects of developmental alcohol exposure (DAE) on feeding behavior. We have previously shown that DAE causes feeding dysfunction in fly larvae, consistent with phenotypes seen in mammalian models, and that these effects are mediated by the reward molecule neuropeptide F (NPF). In addition, we have shown that DAE reduced insulin signal transduction. Here, we investigate the interaction between reduced insulin signaling and feeding changes in flies exposed to ethanol during development.
"Insulin signal transduction mediates ethanol-induced feeding dysfunction in a fly model of Fetal Alcohol Spectrum Disorder,"
McNair Research Journal SJSU: Vol. 15
, Article 7.
Available at: https://scholarworks.sjsu.edu/mcnair/vol15/iss1/7