Eicosapentaenoic acid regulates brown adipose tissue metabolism in high-fat-fed mice and in clonal brown adipocytes.
Brown adipose tissue (BAT) plays a key role in energy expenditure through its specialized thermogenic function. Therefore, BAT activation may help prevent and/or treat obesity. Interestingly, subcutaneous white adipose tissue (WAT) also has the ability to differentiate into brown-like adipocytes and may potentially contribute to increased thermogenesis. We have previously reported that eicosapentaenoic acid (EPA) reduces high-fat (HF)-diet-induced obesity and insulin resistance in mice. Whether BAT mediates some of these beneficial effects of EPA has not been determined. We hypothesized that EPA activates BAT thermogenic program, contributing to its antiobesity effects. BAT and WAT were harvested from B6 male mice fed HF diets supplemented with or without EPA. HIB 1B clonal brown adipocytes treated with or without EPA were also used. Gene and protein expressions were measured in adipose tissues and H1B 1B cells by quantitative polymerase chain reaction and immunoblotting, respectively. Our results show that BAT from EPA-supplemented mice expressed significantly higher levels of thermogenic genes such as PRDM16 and PGC1α and higher levels of uncoupling protein 1 compared to HF-fed mice. By contrast, both WATs (subcutaneous and visceral) had undetectable levels of these markers with no up regulation by EPA. HIB 1B cells treated with EPA showed significantly higher mRNA expression of PGC1α and SIRT2. EPA treatment significantly increased maximum oxidative and peak glycolytic metabolism in H1B 1B cells. Our results demonstrate a novel and promising role for EPA in preventing obesity via activation of BAT, adding to its known beneficial anti-inflammatory effects.
Department of Nutritional Sciences, Texas Tech University, Lubbock, TX; Obesity Research Cluster, Texas Tech University, Lubbock, TX.
Mandana
M
Pahlavani
Department of Nutritional Sciences, Texas Tech University, Lubbock, TX.
Fitia
F
Razafimanjato
Department of Nutritional Sciences, Texas Tech University, Lubbock, TX; Obesity Research Cluster, Texas Tech University, Lubbock, TX.
Latha
L
Ramalingam
Department of Nutritional Sciences, Texas Tech University, Lubbock, TX; Obesity Research Cluster, Texas Tech University, Lubbock, TX; Department of Physiology, University of Peradeniya, Peradeniya, Sri Lanka.
Nishan S
NS
Kalupahana
Obesity Research Cluster, Texas Tech University, Lubbock, TX; Department of Mechanical Engineering, Texas Tech University, Lubbock, TX.
Hanna
H
Moussa
Department of Nutritional Sciences, Texas Tech University, Lubbock, TX.
Shane
S
Scoggin
Department of Nutritional Sciences, Texas Tech University, Lubbock, TX; Obesity Research Cluster, Texas Tech University, Lubbock, TX. Electronic address: naima.moustaid-moussa@ttu.edu.
Naima
N
Moustaid-Moussa
D052437:Adipocytes, Brown / Q000187:drug effects* / Q000378:metabolism; D002001:Adipose Tissue, Brown / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D002460:Cell Line; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D059305:Diet, High-Fat; D015118:Eicosapentaenoic Acid / Q000494:pharmacology*; D005353:Fibronectins / Q000097:blood; D008297:Male; D051379:Mice; D009765:Obesity / Q000517:prevention & control; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha / Q000235:genetics / Q000378:metabolism; D022722:Thermogenesis / Q000187:drug effects / Q000235:genetics; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D000071256:Uncoupling Protein 1 / Q000235:genetics / Q000378:metabolism
D004268:DNA-Binding Proteins; C571428:FNDC5 protein, mouse; D005353:Fibronectins; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; C485290:Ppargc1a protein, mouse; C521133:Prdm16 protein, mouse; D014157:Transcription Factors; C000604372:Ucp1 protein, mouse; D000071256:Uncoupling Protein 1; D015118:Eicosapentaenoic Acid
Brown adipose tissue; Obesity; Omega 3 fatty acids; Thermogenic markers; UCP-1