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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Healthy Body Weight Research » Research » Publications at this Location » Publication #293543
Title: Eicosapentaenoic acid prevents high fat diet-induced metabolic disorders: Genomic and metabolomic analyses of underlying mechanism

Author
item LEMIEUX, MONIQUE - Texas Tech University
item KALUPAHANA, NISHAN - University Of Peradeniya
item XIN, WENTING - University Of Tennessee
item THANAMOOL, CATTHAREEYA - University Of Tennessee
item VOORHEES, VICTOR - University Of Tennessee
item SIRIWARDHANA, NALIN - Texas Tech University
item Larson, Kate
item MOUSTAID-MOUSSA, NAIMA - Texas Tech University

Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: 10/5/2012
Publication Date: 9/9/2013
Citation: Lemieux, M., Kalupahana, N., Xin, W., Thanamool, C., Voorhees, V., Siriwardhana, N., Claycombe, K.J., Moustaid-Moussa, N. 2013. Eicosapentaenoic acid prevents high fat diet-induced metabolic disorders: Genomic and metabolomic analyses of underlying mechanism. Federation of American Societies for Experimental Biology Conference. 27:865.7.

Interpretive Summary:

Technical Abstract: 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