Affordable Access

Access to the full text

Eicosapentaenoic Acid Regulates Inflammatory Pathways through Modulation of Transcripts and miRNA in Adipose Tissue of Obese Mice

Authors
  • Ramalho, Theresa1
  • Pahlavani, Mandana1, 2
  • Kalupahana, Nishan1, 2, 3
  • Wijayatunga, Nadeeja1
  • Ramalingam, Latha1, 2
  • Jancar, Sonia
  • Moustaid-Moussa, Naima1, 2
  • 1 (L.R.)
  • 2 Obesity Research Institute, Texas Tech University, Lubbock, TX 79409, USA
  • 3 Department of Physiology, Faculty of Medicine, University of Peradeniya, Peradeniya 20400, Sri Lanka
Type
Published Article
Journal
Biomolecules
Publisher
MDPI AG
Publication Date
Sep 07, 2020
Volume
10
Issue
9
Identifiers
DOI: 10.3390/biom10091292
PMID: 32906847
PMCID: PMC7564513
Source
PubMed Central
Keywords
License
Green

Abstract

This study aims to investigate the global profiling of genes and miRNAs expression to explore the regulatory effects of eicosapentaenoic acid (EPA) in visceral adipose tissue (VAT) of obese mice. We used male mice, fed either a high-fat diet (HF) or HF supplemented with EPA (HF-EPA), for 11 weeks. RNA, and small RNA profiling, were performed by RNAseq analysis. We conducted analyses using Ingenuity Pathway Analysis software (IPA®) and validated candidate genes and miRNAs related to lipid mediators and inflammatory pathways using qRT-PCR. We identified 153 genes differentially downregulated, and 62 microRNAs differentially expressed in VAT from HF-EPA compared to HF. Genes with a positive association with inflammation, chemotaxis, insulin resistance, and inflammatory cell death, such as Irf5 , Alox5ap , Tlrs , Cd84 , Ccr5 , Ccl9 , and Casp1 , were downregulated by EPA. Moreover, EPA significantly reduced LTB4 levels, a lipid mediator with a central role in inflammation and insulin resistance in obesity. The pathways and mRNA/microRNA interactions identified in our study corroborated with data validated for inflammatory genes and miRNAs. Together, our results identified key VAT inflammatory targets and pathways, which are regulated by EPA. These targets merit further investigation to better understand the protective mechanisms of EPA in obesity-associated inflammation.

Report this publication

Statistics

Seen <100 times