Abstract
BackgroundSaturated fatty acids have been shown to cause insulin resistance and low-grade chronic inflammation, whereas unsaturated fatty acids suppress inflammation via G-protein coupled receptor 120 (GPR120) in macrophages. However, the anti-inflammatory effects of unsaturated fatty acids in adipocytes have yet to be elucidated. Hence, the aims of the present study were to evaluate the anti-inflammatory effects of eicosapentaenoic acid (EPA) via GPR120 in adipocytes.MethodsWe used 250 μM palmitate as a representative saturated fatty acid. 3T3-L1 adipocytes were used for in vitro studies. We further evaluated the effect of EPA supplementation in a high-fat/high-sucrose (HFHS) diet-induced adipose tissue inflammatory mouse model.ResultsEPA attenuated palmitate-induced increases in inflammatory gene expression and NF-κB phosphorylation in 3T3-L1 adipocytes. Silencing of GPR120 abolished the anti-inflammatory effects of EPA. In GPR120 downstream signal analysis, EPA was found to decrease palmitate-induced increases in TAK1/TAB1 complex expression. EPA supplementation suppressed HFHS-induced crown-like structure formation in epididymal adipose tissue and altered macrophage phenotypes from M1 to M2 in the stromal vascular fraction. Moreover, the EPA-containing diet attenuated increases in adipose p-JNK and phospho-p65 NF-κB levels.ConclusionsIn conclusion, the findings of the present study demonstrate that EPA suppresses palmitate-induced inflammation via GPR120 by inhibiting the TAK1/TAB1 interaction in adipocytes. EPA supplementation reduced HFHS diet-induced inflammatory changes in mouse adipose tissues. These results demonstrate adipose GPR120 as a potential therapeutic target for decreasing inflammation.
Highlights
Saturated fatty acids have been shown to cause insulin resistance and low-grade chronic inflammation, whereas unsaturated fatty acids suppress inflammation via G-protein coupled receptor 120 (GPR120) in macrophages
Oh et al demonstrated that docosanexaenoic acid (DHA), a ω-3 fatty acid, inhibits downstream nuclear factor-κB (NF-κB) signaling via tumor necrosis factor-α (TNF-α) receptor and toll-like receptor 4 (TLR4) activation in response to lipopolysaccharide (LPS) in macrophages [6, 7]
GPR120 expression was not observed in pre-adipocytes, and palmitate exposure and eicosapentaenoic acid (EPA) treatment had no effect on GPR120 protein expression levels (Additional file 1: Figure S1B)
Summary
Saturated fatty acids have been shown to cause insulin resistance and low-grade chronic inflammation, whereas unsaturated fatty acids suppress inflammation via G-protein coupled receptor 120 (GPR120) in macrophages. The anti-inflammatory effects of unsaturated fatty acids in adipocytes have yet to be elucidated. The aims of the present study were to evaluate the anti-inflammatory effects of eicosapentaenoic acid (EPA) via GPR120 in adipocytes. Fatty Acid Receptor 4: FFAR4) as a receptor for ω-3 fatty acids and demonstrated improved obesity-induced insulin resistance via GPR120 signaling in macrophages [6]. The aims of the present study were to determine the anti-inflammatory effects of EPA via GPR120 in cultured adipocytes, and to clarify the effects of EPA supplementation on high-fat/high-sucrose (HFHS) diet-induced inflammatory changes in adipose tissue
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