Pharmacological agents targeting the mTOR complexes are used clinically as immunosuppressants and anticancer agents, and can extend lifespan in model organisms. An undesirable side effect of these drugs is hyperlipidemia. Raptor and Rictor are essential component of mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) and 2 (mTORC2), respectively. Despite multiple roles that have been described for mTOR complex 1 (mTORC1) in lipid metabolism, the etiology of hyperlipidemia remains incompletely understood. The objective of this study was to determine the influence of adipocyte mTORC1 signaling in systemic lipid homeostasis in vivo. We characterized systemic lipid metabolism in mice lacking the mTORC1 subunit raptor (RaptoraKO), the key lipolytic enzyme ATGL (ATGLaKO), or both (ATGL-RaptoraKO) in adipocytes. Mice lacking mTORC1 activity in adipocytes failed to completely suppress lipolysis in the fed state and displayed prominent hypertriglyceridemia and hypercholesterolemia. Blocking lipolysis in adipose tissue restored normal levels of triglycerides and cholesterol in the fed state, as well as the ability to clear triglycerides in an oral fat tolerance test. Unsuppressed adipose lipolysis in the fed state interferes with triglyceride clearance and contributes to hyperlipidemia. Adipose tissue mTORC1 activity is necessary for appropriate suppression of lipolysis and for the maintenance of systemic lipid homeostasis. Loss of mTORC1 signaling in adipose is sufficient to disrupt lipid homeostasis, resulting in hyperlipidemia caused by unrestrained lipolysis. However, studies to date examining the role of deletion of this complex, complex 2 or both in adipose tissue in combination with rapamycin have yet to be investigated. Here, we report the consequences of Raptor, Rictor or both deleted specifically in mature adipocytes driven by Adiponectin-Cre (RaptoraKO, RictoraKO, Raptor-RictoraKO). Concordant with the RaptoraKO mice, RictoraKO mice display pronounced hyperlipidemia and both KO models have a further increase in plasma lipids with rapamycin treatment. Genetic inhibition of lipolysis in mice with loss of mTORC1 (ATGL-RaptoraKO) treated with rapamycin prevents the further increase in plasma lipids seen in Raptorako mice treated with rapamycin. We propose a hypothetical mechanism that in the fed state, rapamycin inhibition of adipose mTORC1 leads to decreased C/EBP transcriptional activity. This decreased transcriptional activity results in decreased expression of perilipin and subsequent unrestrained lipolysis, leading to hyperlipidemia. Here we show that enhanced lipolysis upon refeeding increases plasma triglyceride levels in the context of rapamycin treatment and that both complexes are involved in regulating this lipolytic process. However, mTORC1, not mTORC2, is required for proper adipocyte lipolysis to maintain circulating plasma lipid levels. Additionally, we provide evidence that loss of adipocyte mTOR signaling is not solely responsible for the rapamycin induced hyperlipidemia.