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Obesity and its co-morbidities are a growing health epidemic. Interactions between genetic background, the environment and behavior (i.e. diet) greatly influence organismal energy balance. Previously, we described obesogenic mutations in the gene Split ends (Spen) in Drosophila melanogaster, and roles for Spen in fat storage and metabolic state. Lipid catabolism is impaired in Spen-deficient fat storage cells, accompanied by a compensatory increase in glycolytic flux and protein catabolism. Here we investigate gene-diet interactions t