Effect of Eicosapentaenoic Acid Supplementation on Murine Preadipocytes 3T3-L1 Cells Activated with Lipopolysaccharide and/or Tumor Necrosis Factor-α.

Anna Zając-Grabiec,Karoline Bartusek,Katarzyna Sroczyńska,Joanna Gdula-Argasińska,Tadeusz Librowski

doi:10.3390/life11090977

Anna Zając-Grabiec, Karoline Bartusek + Show 3 more

Open Access

https://doi.org/10.3390/life11090977

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Journal: Life	Publication Date: Sep 16, 2021
Citations: 2	License type: CC BY 4.0

Affiliation: Jagiellonian University, University of Bonn

Abstract

The beneficial effect of n-3 fatty acids can be related to anti-inflammatory properties. The aim of the study was to analyzed the effect of eicosapentaenoic acid (EPA) on 3T3-L1 cells (murine embryonic fibroblasts‒preadipocytes) activated with inflammatory factors (IF). Cells were incubated with 50 µmol of EPA for 48 h, and then activated with lipopolysaccharide (LPS) or tumor necrosis factor-α (TNF-α). The level of cycloxygenase-2 (Prostaglandin-Endoperoxide Synthase 2, PTGS2, COX-2), cytosolic prostaglandin synthase E2 (cPGES), fatty acid binding protein 4 (FABP4), toll-like receptor 4 (TLR4), glucose receptor type 4 (GLUT-4), and cannabinoid receptor 2 (CB2) was determined using Western blot analysis. The phospholipase A2 (Pla2g4a), and prostaglandin-Endoperoxide Synthase 2 (Ptgs2) gene expression was analyzed by real-time qPCR. After EPA and IF activation, a significant decrease in the COX-2, cPGES, and TRL4 protein levels was observed. Incubation of cells with EPA and IF resulted in a decrease in Ptgs2 and an increase in the Pla2g4a gene. A significant increase in the CB2 protein was observed in adipocytes co-treated with EPA and IF. The results indicated an anti-inflammatory properties of EPA. Interestingly, the activation of the GLUT4 receptor by EPA suggests an unique role of this FA in the regulation of the adipocyte metabolism and prevention of insulin resistance.

Highlights

Adipose tissue has insulating, shock-absorbing, and above all, energy storage functions
Many of the major contributors to inflammation are well known with the likes of transcription factors such as nuclear factor kappa B (NF-κB); pro-inflammatory cytokines, including interleukins (IL-1 and IL-6) and tumor necrosis factor alpha (TNF-α); products of cyclooxygenase and lipoxygenase; and lipid mediators, including prostaglandins and leukotrienes [1,2,8,9,10,11]
The current evidence suggests that the inflammation process is much more complex as many other molecules coordinate the entire process in an interrelated network

Summary

Introduction

Shock-absorbing, and above all, energy storage functions. De novo adipocyte differentiation in response to excess energy supply acts as an adaptive mechanism by increasing the size of adipose tissue and affects the proper functions of adipocytes [1,2,3,4]. This adaptive mechanism prevents systemic lipid overload, which is the leading cause of insulin resistance. One of the major regulators of adipogenesis is peroxisome proliferator-activated receptor γ (PPARγ), which is responsible for the differentiation and phenotype of adipocytes [2,3]

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