Maresin 1 inhibits TNF‐alpha‐induced lipolysis and autophagy in 3T3‐L1 adipocytes

Obesity is associated with high pro-inflammatory cytokine levels like tumor necrosis factor-alpha (TNF-α), which promotes inflammation in adipose tissue. The omega-3 PUFAs, and their derived lipid mediators, such as Maresin 1 (MaR1) have anti-inflammatory effects on adipose tissue. This study aimed to analyze if MaR1 may counteract alterations induced by TNF-α on lipolysis and autophagy in mature 3T3-L1 adipocytes. Our data revealed that MaR1 (1-100 nM) inhibited the TNF-α-induced glycerol release after 48 h, which may be related to MaR1 ability of preventing the decrease of lipid droplet-coating protein perilipin and G0/G1 Switch 2 protein expression. MaR1 also reversed the decrease on total hormone sensitive lipase (total HSL), and the ratio of phosphoHSL at Ser-565/total HSL, while preventing the increased ratio of phosphoHSL at Ser-660/total HSL and phosphorylation of extracellular signal-regulated kinase 1/2 induced by TNF-α. Moreover, MaR1 counteracted the cytokine-induced decrease of p62 protein, a key autophagy indicator, and also prevented the induction of LC3II/LC3I, an important autophagosome formation marker. Current data suggest that MaR1 may ameliorate TNF-α-induced alterations on lipolysis and autophagy in adipocytes. This might also contribute to the beneficial actions of MaR1 on adipose tissue and insulin sensitivity in obesity. This article is protected by copyright. All rights reserved