Department of Human Health and Nutritional Sciences, Animal Science and Nutrition Building, University of Guelph, Guelph, ON N1G 2W1, Canada.
Appl Physiol Nutr Metab. 2010 Dec;35(6):783-9. doi: 10.1139/H10-076.
Adiponectin, a protein secreted from adipose tissue, has been shown to have anti-diabetic and anti-inflammatory effects, but its regulation is not completely understood. Long-chain n-3 fatty acids eicosapentaenoic acid (20:5n-3; EPA) and docosahexaenoic acid (22:6n-3; DHA) may be involved in adiponectin regulation as they are potential ligands for peroxisome proliferator-activated receptor-γ (PPARγ), a key transcription factor for the adiponectin gene. To examine this, 3T3-L1 adipocytes were incubated with 125 µmol·L-1 EPA, DHA, palmitic, or oleic acids complexed to albumin, or with albumin alone (control) for 24 h. Adipocytes were also incubated for 24 h with EPA and DHA plus bisphenol-A-diglycidyl ether (BADGE), a PPARγ antagonist. Both EPA and DHA increased (p < 0.05) secreted adiponectin concentration compared with the control (44% and 102%, respectively), but did not affect cellular adiponectin protein content. Incubation with BADGE and DHA inhibited increases in secreted adiponectin protein, suggesting that DHA may act through a PPARγ-dependent mechanism. However, BADGE had no effect on EPA-induced increases in secreted adiponectin protein. Only DHA enhanced (p < 0.05) PPARγ and adiponectin mRNA expression compared wtih the control. Our results demonstrate that DHA increases cellular adiponectin mRNA and secreted adiponectin protein in 3T3-L1 adipocytes, possibly by a mechanism involving PPARγ. Moreover, DHA increased adiponectin concentration to a greater extent (40% more, p < 0.05) compared with EPA, emphasizing the need to consider the independent actions of EPA and DHA in adipocytes.
脂联素是一种由脂肪组织分泌的蛋白质，具有抗糖尿病和抗炎作用，但它的调节机制尚不完全清楚。长链 n-3 脂肪酸二十碳五烯酸（20:5n-3；EPA）和二十二碳六烯酸（22:6n-3；DHA）可能参与脂联素的调节，因为它们是过氧化物酶体增殖物激活受体-γ（PPARγ）的潜在配体，PPARγ 是脂联素基因的关键转录因子。为了研究这一点，将 3T3-L1 脂肪细胞与结合白蛋白的 125 μmol·L-1 EPA、DHA、棕榈酸或油酸或单独用白蛋白（对照）孵育 24 h。脂肪细胞还与 EPA 和 DHA 与双酚 A 二缩水甘油醚（BADGE）孵育 24 h，BADGE 是一种 PPARγ 拮抗剂。与对照相比，EPA 和 DHA 均增加（p < 0.05）分泌的脂联素浓度（分别增加 44%和 102%），但不影响细胞内脂联素蛋白含量。与 BADGE 和 DHA 孵育抑制了分泌的脂联素蛋白的增加，表明 DHA 可能通过一种依赖 PPARγ 的机制起作用。然而，BADGE 对 EPA 诱导的分泌的脂联素蛋白增加没有影响。只有 DHA 与对照相比增加了 PPARγ 和脂联素 mRNA 的表达（p < 0.05）。我们的结果表明，DHA 增加 3T3-L1 脂肪细胞中细胞内脂联素 mRNA 和分泌的脂联素蛋白，可能通过一种涉及 PPARγ 的机制。此外，与 EPA 相比，DHA 增加脂联素浓度的幅度更大（增加 40%，p < 0.05），这强调了在脂肪细胞中需要考虑 EPA 和 DHA 的独立作用。
