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ATGL Is Not Required for Oleate Protection from Lipotoxicity in NIH3T3 Cells
Author(s) -
Roelike Lauren,
Plasek Leah,
Mashek Douglas G.,
Listenberger Laura L.
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1132.4
Subject(s) - lipotoxicity , adipose triglyceride lipase , lipid droplet , chemistry , microbiology and biotechnology , perilipin , medicine , lipolysis , biochemistry , adipose tissue , biology , insulin , insulin resistance
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. Support or Funding Information This research was funded by the Arnold and Mabel Beckman Foundation and St. Olaf College CURI.