Lipins constitute an evolutionarily conserved family of proteins found from yeast to mammals. The Lipin1 gene was first identified in mice as the gene mutated in fatty liver dystrophy. Lipins have dual activity as enzymes and transcriptional coregulators. I characterized the single lipin ortholog in Drosophila melanogaster ( dLipin), and showed that dLipin is required for fat body development and triglyceride storage. dLipin mutants were developmentally delayed and displayed high larval and pupal lethality. Larvae lacking dLipin had reduced fat tissue mass and lipid droplets in fat body cells were smaller. Consequently, overall triglyceride stores were diminished in these animals and adults showed reduced survival upon starvation. Individual fat body cells were enlarged and rounded. Electron microscopy revealed ultrastructural defects affecting mitochondria, autophagosomes, and the cell nucleus. In addition, mutant cells contained putative lipophagosomes, suggesting that dLipin may be required for the suppression of lipid breakdown by lipophagy. Genetic interaction studies revealed that dLipin cooperates with the Drosophila Target of Rapamycin (dTOR) kinase in the regulation of adipogenesis and growth. Fat body and lipid storage defects were exacerbated in animals lacking both dTOR and dLipin, and the systemic growth defect observed with dTOR mutants was enhanced, suggesting mutual interdependence between the two proteins. Finally, I showed that dLipin is upregulated during starvation and may promote starvation resistance. Taken together, the results indicate that dLipin has essential functions in lipid and energy metabolism, and establish Drosophila as a genetic model for further studies of conserved functions of lipin proteins.