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


Muredda, Laura, Kepczynska, Malgorzata A, Zaibi, Mohamed S, Alomar, Suliman Y and Trayhurn, Paul ORCID: 0000-0002-9940-283X (2018) 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. ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY, 124 (2). pp. 97-108.

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Abstract

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 GPR120 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); GPR41 expression was also stimulated. Rosiglitazone did not affect GPR84 expression, but GPR120 and GPR41 expression increased. Dexamethasone, insulin, linoleic and docosahexaenoic acids (DHA), and TUG891 (GPR120 agonist) had little effect on GPR120 and GPR84 expression. TUG891 did not attenuate the pro-inflammatory actions of TNFα and IL-1β. DHA slightly countered the actions of IL-1β on CCL2, IL6 and ADIPOQ expression, though not on secretion of these adipokines. GPR120 and GP84 gene expression in human adipocytes is highly sensitive to pro-inflammatory mediators; the inflammation-induced inhibition of GPR120 expression may compromise the anti-inflammatory action of GPR120 agonists.

Item Type: Article
Uncontrolled Keywords: Adipose tissue, docosahexaenoic acid, fatty acid sensors, inflammation
Depositing User: Symplectic Admin
Date Deposited: 28 Nov 2017 10:29
Last Modified: 10 Oct 2023 07:05
DOI: 10.1080/13813455.2017.1364774
Related URLs:
URI: https://livrepository.liverpool.ac.uk/id/eprint/3013063
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