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Eicosapentaenoic acid prevents high fat diet‐induced metabolic disorders: Genomic and metabolomic analyses of underlying mechanisms
Author(s) -
LeMieux Monique,
Kalupahaishan,
Xin Wenting,
Thanamool Catthareeya,
Voorhees Victor,
Siriwardhalin,
Claycombe Kate,
MoustaidMoussa Naima
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.865.7
Subject(s) - eicosapentaenoic acid , adipose tissue , polyunsaturated fatty acid , metabolomics , beta oxidation , adipogenesis , medicine , lipid metabolism , insulin resistance , endocrinology , carbohydrate metabolism , fatty acid metabolism , cd36 , biology , glucose homeostasis , fatty acid , adipocyte , adiponectin , chemistry , biochemistry , metabolism , insulin , bioinformatics , gene
Previously our lab demonstrated eicosapenaenoic acid (EPA)'s ability to prevent high‐fat (HF) diet‐induced obesity by decreasing insulin resistance, glucose intolerance and inflammation. In the current study, we used genomic and metabolomic approaches to further investigate the molecular basis for these effects. Gene (microarrays and RT‐PCR) and protein expression studies (immunoassays) revealed changes in levels of genes/proteins associated with cell proliferation, apoptosis, adipocyte differentiation and glucose metabolism. Specifically, expression of lipogenic/adipogenic markers (Fasn, Srebf1, Cebpa, Ncoa2, Wnt signaling) were decreased by EPA. Metabolomic analyses confirmed enrichment of adipose tissue in n‐3 polyunsaturated fatty acids (PUFAs) and a decrease in n‐6 PUFAs in both visceral and subcutaneous fat. These studies also indicated increased oxidation of stored fatty acid and increased fatty acid oxidation related‐metabolites such as acetylcarnitine. Together the genomic and metabolomic findings were in‐line with other metabolic and physiologic outcomes including decreased adiposity and fat cell size and increased lipid oxidation. In conclusion, our studies demonstrate that EPA ameliorates glucose homeostasis at least in part by reducing adipose tissue inflammation and lipid accumulation and increasing fatty acid oxidation. Grant Funding Source : UT AgResearch and College of Human Sciences / Texas Tech University