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AdipoR1 and AdipoR2 maintain membrane fluidity in most human cell types and independently of adiponectin

Journal article
Authors Mario Ruiz
Marcus Ståhlman
Jan Borén
Marc Pilon
Published in Journal of Lipid Research
Volume 60
Issue 5
Pages 995-1004
ISSN 0022-2275
Publication year 2019
Published at Wallenberg Laboratory
Department of Chemistry and Molecular Biology
Pages 995-1004
Language en
Keywords fatty acids, desaturases, phospholipids, metabolism, lipotoxicity, receptors, plasma membrane, protein-kinase, receptors, activation, expression, Biochemistry & Molecular Biology
Subject categories Cell and molecular biology


The FA composition of phospholipids must be tightly regulated to maintain optimal cell membrane properties and compensate for a highly variable supply of dietary FAs. Previous studies have shown that AdipoR2 and its homologue PAQR-2 are important regulators of phospholipid FA composition in HEK293 cells and Caenorhabditiselegans, respectively. Here we show that both AdipoR1 and AdipoR2 are essential for sustaining desaturase expression and high levels of unsaturated FAs in membrane phospholipids of many human cell types, including primary human umbilical vein endothelial cells, and for preventing membrane rigidification in cells challenged with exogenous palmitate, a saturated FA. Three independent methods confirm the role of the AdipoRs as regulators of membrane composition and fluidity: fluorescence recovery after photobleaching, measurements of Laurdan dye generalized polarization, and mass spectrometry to determine the FA composition of phospholipids. Furthermore, we show that the AdipoRs can prevent lipotoxicity in the complete absence of adiponectin, their putative ligand. We propose that the primary cellular function of AdipoR1 and AdipoR2 is to maintain membrane fluidity in most human cell types and that adiponectin is not required for this function.

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