All growth during the Drosophila life cycle is restricted to larval development, when animals increase their body size ~200-fold over the course of four days. To support this exponential growth, larvae rely aerobic glycolysis, a unique metabolic program ideally suited to synthesize biomolecules from carbohydrates. Our previous work demonstrated that aerobic glycolysis is transcriptionally-activated during embryogenesis, when the Drosophila ortholog of the Estrogen-Related Receptor (ERR) class of nuclear receptors coordinately up-regulates genes involved in glycolysis, the pentose phosphate pathway, and lactate production. We have discovered that dERR activity is not restricted to embryogenesis; rather, dERR also promotes aerobic glycolysis during larval development. Our preliminary analyses demonstrate that dERR protein is expressed in key metabolic tissues, including the fat body, intestine, and muscle. This expression pattern suggests that dERR coordinates glucose-derived biosynthesis with growth conditions. Consistent with this model, we have discovered that the dERR ligand-binding domain (LBD) is activated when larvae are fed a yeast-based diet but not sugar-only or starvation media. Furthermore, the addition of insulin to larval organ cultures fails to activate the dERR LBD, suggesting that dERR represents a novel mechanism for linking dietary conditions with sugar metabolism. We have also determined that dERR is covalently modified under starvation conditions, suggesting that a nutrient-sensitive enzyme controls dERR activity. Finally, we have demonstrated that many dERR target genes are transcriptionally down-regulated upon starvation, indicating that diet-induced changes in dERR activation are functionally significant. Overall, our studies indicate that dERR promotes aerobic glycolysis in response to dietary compounds and suggest that mammalian ERRs also act as nutrient sensors that coordinate biosynthesis with rapid growth.