Taking ~5.4 Grams of actual EPA/DHA (from 8.4G Fish Oil) and 2 X a day Krillipid Balance. Thanks for the info All.
Actually, it looks as though it would be beneficial to keep it.
[h=1]Eicosapentaenoic acid promotes thermogenic and fatty acid storage capacity in mouse subcutaneous adipocytes[/h]
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DOI: 10.1016/j.bbrc.2014.07.010
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[h=2]Highlights[/h]•Chronic treatment of EPA induces the recruitment of brown-like adipocytes in inguinal SV cell cultures.
•EPA enhances mitochondrial function, glucose and fatty acid oxidation.
•EPA increases lipid storage and decreases lipolysis in inguinal adipocyte.
[h=2]Abstract[/h]In this study, we determined if eicosapentaenoic acid (EPA) promotes beneficial metabolic activities of subcutaneous adipocytes. Stromal-vascular (SV) cells were isolated from inguinal adipose tissue of C57BL/6 mice and induced to differentiate into adipocytes. EPA effect on thermogenic and mitochondrial gene expression and oxidative metabolism were assessed in inguinal adipocytes. When added to SV cell cultures during 8 day differentiation, EPA significantly increased the expression of thermogenic genes UCP1-3, CIDEA and VEGFα. Moreover, EPA increased mitochondrial DNA content and the expression of genes involved in mitochondrial biogenesis including PGC1α, Nrf1 and COXiv. However, this effect was not perceived when EPA was added to mature inguinal adipocytes for 24 h, suggesting that EPA exerts its browning effect via recruiting brite adipocytes. Consistently, long-term EPA treatment also upregulated AMPKα phosphorylation and CPT1 expression and increased glucose uptake and GLUT4 mRNA expression, suggesting improved mitochondrial oxidation. Additionally, EPA-treated adipocytes had enlarged lipid droplets and increased expression of triglyceride synthesis genes GPAT1 and GPAT3, while significantly decreased glycerol release and down-regulation of HSL and ATGL gene expression. We conclude that EPA enhances energy dissipation capacity by recruiting brite adipocytes to stimulate oxidative metabolism and reduces fatty acid release by facilitating fatty acid storage in subcutaneous adipocytes.
[h=2]rown adipose but not white adipose accumulate DHA in cultured cells provided with alpha-linolenic acid[/h]
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Xia Qin, ; J. Thomas Brenna, ; Kumar S. Kothapalli, ; Peter Lawrence, ; Lei Liu, ; Hiu Gyu Park, ; Jimmie Zhang, ;
Introduction. Adipose tissue has recently been recognized as a complex endocrine organ which coordinates numerous crucial biological functions including fatty acid metabolism, glucose metabolism, energy homeostasis, and immune function. White adipose tissue (WAT) stores energy, while brown adipose tissue (BAT) dissipates energy while producing heat.
Our aim was to compare the fatty acid profiles of undifferentiated and differentiated WAT and BAT/Beige transformed adipocytes provided with alpha-linolenic acid.
Methods. Murine 3T3 L1 fibroblasts (preWAT) or pre-BAT cells were grown in regular media to confluence, and differentiation were then induced to either WAT or BAT. At days 10, 12 and 14, cell were supplemented with 50 μM of albumin bound
alpha-
linolenic acid (ALA). Cells with no ALA supplementation were additional controls. Twenty-four hours after supplementation, fatty acid profiles of the cells were analyzed by GC and structural mass spectrometry.
Results and DIscussion. ALA supplementation caused an increase in cellular eicosapentaenoic acid (EPA, 20:5n-3) with no change in docosahexaenoic acid (DHA, 22:6n-3) levels in undifferentiated cells. WAT cells accumulated more EPA. Similarly, BAT cells accumulated EPA, however in contrast differentiated BAT cells also accumulate significant amounts of DHA when compared to undifferentiated preBAT cells. BAT adipocytes are characterized by a vast increase in mitochondria which require highly unsaturated fatty acids. DHA may be required for their function.
Conclusion. When provided with ALA, WAT cells accumulate EPA with no change in DHA; BATcells accumulate EPA and DHA. If BAT function similarly in vivo, they may serve as a source of DHA for other tissues.