IL-1β and TNFα inhibit GPR120 (<i>FFAR4</i>) and stimulate GPR84 (<i>EX33</i>) and GPR41 (<i>FFAR3</i>) fatty acid receptor expression in human adipocytes: implications for the anti-inflammatory action of <i>n</i>-3 fatty acids

<p>Regulation of the expression of GPCR fatty acid receptor genes has been examined in human adipocytes differentiated in culture. TNFα and IL-1β induced a marked reduction in <i>GPR120</i> expression, mRNA level falling 17-fold at 24 h in adipocytes incubated with TNFα. In contrast, GPR84 mRNA was dramatically increased by these cytokines (>500-fold for IL-1β at 4 h); <i>GPR41</i> expression was also stimulated. Rosiglitazone did not affect <i>GPR84</i> expression, but <i>GPR120</i> and <i>GPR41</i> expression increased. Dexamethasone, insulin, linoleic and docosahexaenoic acids (DHA), and TUG891 (GPR120 agonist) had little effect on <i>GPR120</i> and <i>GPR84</i> expression. TUG891 did not attenuate the pro-inflammatory actions of TNFα and IL-1β. DHA slightly countered the actions of IL-1β on <i>CCL2</i>, <i>IL6</i> and <i>ADIPOQ</i> expression, though not on secretion of these adipokines. <i>GPR120</i> and <i>GP84</i> gene expression in human adipocytes is highly sensitive to pro-inflammatory mediators; the inflammation-induced inhibition of <i>GPR120</i> expression may compromise the anti-inflammatory action of GPR120 agonists.</p