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ATGL Is Not Required for Oleate Protection from Lipotoxicity in NIH3T3 Cells

The long chain, saturated fatty acid palmitate is toxic to cultured cells. However, co‐supplementation with monounsaturated oleate promotes storage of excess palmitate in lipid droplets and prevents cell death. We tested whether events downstream of lipid storage in lipid droplets contribute to oleate protection from lipotoxicity. Specifically, we asked whether protection from lipotoxicity requires adipose triglyceride lipase (ATGL) or sirtuin 1 (SIRT1) activity. We found that oleate continues to prevent palmitate induction of caspase 3/7 activity in NIH3T3 cells in the presence of ATGListatin, an inhibitor of ATGL. Moreover, oleate and palmitate co‐supplementation does not increase the activity of SIRT1, a transcriptional co‐activator downstream of ATGL, nor does it lead to ATGL‐dependent changes in expression of ACOT1, ACSL1, or CPT1α mRNA. Thus, our results fail to support a role for ATGL in oleate protection from lipotoxicity in NIH3T3 cells. Additional pathways through which oleate protects a cell from lipotoxicity should be explored.