Extensive transcription mis-regulation and membrane defects in AdipoR2-deficient cells challenged with saturated fatty acids

How cells maintain vital membrane lipid homeostasis while obtaining most of their constituent fatty acids from a varied diet remains largely unknown. Here, we used transcriptomics, lipidomics, growth and respiration assays, property analyses in human HEK293 or umbilical vein endothelial (HUVEC) to show that the function AdipoR2 is respond rigidification by regulating many metabolism genes. We also AdipoR2-dependent critical for challenged with saturated acids. Additionally, found deficiency causes transcriptome cell physiological defects similar those observed SREBP-deficient upon SFA challenge. Finally, compared several genes considered important homeostasis, namely AdipoR2, SCD, FADS2, PEMT ACSL4, SCD are among these prevent excess saturation when exogenous SFAs. conclude one primary mechanisms protects against