The metabolism of proliferating cancer cells not only generates energy, but also synthesizes the biomolecules required for growth. In response to these metabolic demands, cancer cells rely on a metabolic program known as aerobic glycolysis, which synthesizes biomass from carbohydrates. Drosophila also uses aerobic glycolysis to support the nearly 200-fold increase in body size that occurs during larval development and we are now using the fly to understand how the inhibition of aerobic glycolysis affects growth and physiology. Our initial studies have focused on the Drosophila Lactate Dehydrogenase gene (Ldh; also known as ImpL3), which encodes the hallmark enzyme of aerobic glycolysis. We have confirmed that LDH is widely expressed in larval tissues, with notably high levels occurring in the muscle and brain. Furthermore, this expression occurs independent of oxygen availability; however, LDH expression in the salivary glands and imaginal discs is enhanced under hypoxic conditions. Furthermore, we have generated Ldh loss-of-function mutations with the goal of understanding how this enzyme influences growth and biosynthesis. Our preliminary metabolic characterization reveals that Ldh mutants accumulate excessive glycogen stores and exhibit a 95% decrease in lactate production. However, despite these metabolic defects, Ldh mutants grow at a normal rate and experience an impenetrant lethal phase during the mid-L3. These relatively mild phenotypes suggest that larval metabolism can compensate for loss of LDH activity. To test this possibility, we analyzed the Ldh mutants using a combination of GC-MS-based metabolomics and RNAseq. These analyses revealed several putative compensatory metabolic networks that are activated in Ldh mutants. For example, loss of LDH activity induces a significant increase in glycerol-3-phosphate (G3P) metabolism, as mutant larvae exhibit a 300% increase in glycerol-3-phosphate levels and 4-fold increase in glycerol-3-phosphate dehydrogenase gene expression. Overall, these studies represent a unique opportunity to both understand how the disruption of aerobic glycolysis affects biosynthesis and to explore the metabolic plasticity that underlies larval growth.