GEICO-Study Group on Chronic Inflammation and Obesity, Platform 'Cyclotron Reunion Ocean Indien' CYROI, 2 Rue Maxime Rivière, Sainte-Clotilde, Reunion Island 97490, France.
Lipids Health Dis. 2012 Dec 21;11:175. doi: 10.1186/1476-511X-11-175.
On the basis that high fat diet induces inflammation in adipose tissue, we wanted to test the effect of dietary saturated and polysunsaturated fatty acids on human adipose tissue and adipocytes inflammation. Moreover we wanted to determine if TLR2 and TLR4 are involved in this pathway.
Human adipose tissue and adipocytes primary cultures were treated with endotoxin-free BSA conjugated with SFA (lauric acid and palmitic acid--LA and PA) and PUFA (eicosapentaeneic acid, docosahexaenoic acid and oleic acid--EPA, DHA and OA) with or without LPS. Cytokines were then assayed by ELISA (TNF-alpha, IL-6 and MCP-1). In order to determine if TLR2 and TLR4 are activated by fatty acid (FA), we used HEK-Blue cells transfected by genes from TLR2 or TLR4 pathways associated with secreted alkaline phosphatase reporter gene.
None of the FA tested in HEK-Blue cells were able to activate TLR2 or TLR4, which is concordant with the fact that after FA treatment, adipose tissue and adipocytes cytokines levels remain the same as controls. However, all the PUFA tested: DHA, EPA and to a lesser extent OA down-regulated TNF-alpha, IL-6 and MCP-1 secretion in human adipose tissue and adipocytes cultures.
This study first confirms that FA do not activate TLR2 and TLR4. Moreover by using endotoxin-free BSA, both SFA and PUFA tested were not proinflammatory in human adipose tissue and adipocytes model. More interestingly we showed that some PUFA exert an anti-inflammatory action in human adipose tissue and adipocytes model. These results are important since they clarify the relationship between dietary fatty acids and inflammation linked to obesity.
基于高脂肪饮食会引起脂肪组织炎症，我们想要测试饮食中饱和脂肪酸和多不饱和脂肪酸对人体脂肪组织和脂肪细胞炎症的影响。此外，我们还想确定 TLR2 和 TLR4 是否参与了这一途径。
用人内脂组织和原代脂肪细胞培养物，用脂多糖（LPS）处理不含内毒素的牛血清白蛋白（BSA）与饱和脂肪酸（月桂酸和棕榈酸-LA 和 PA）和多不饱和脂肪酸（二十碳五烯酸、二十二碳六烯酸和油酸-EPA、DHA 和 OA）的共轭物。然后通过 ELISA（TNF-α、IL-6 和 MCP-1）测定细胞因子。为了确定脂肪酸（FA）是否能激活 TLR2 和 TLR4，我们使用 TLR2 或 TLR4 途径基因转染的 HEK-Blue 细胞，检测与分泌碱性磷酸酶报告基因相关的基因。
在 HEK-Blue 细胞中测试的 FA 均不能激活 TLR2 或 TLR4，这与 FA 处理后脂肪组织和脂肪细胞细胞因子水平与对照相同的事实相符。然而，所有测试的多不饱和脂肪酸（PUFA）：DHA、EPA 以及在较小程度上的 OA，都能下调人脂肪组织和脂肪细胞培养物中 TNF-α、IL-6 和 MCP-1 的分泌。
本研究首次证实 FA 不能激活 TLR2 和 TLR4。此外，通过使用不含内毒素的 BSA，我们测试的所有饱和脂肪酸和多不饱和脂肪酸在人体脂肪组织和脂肪细胞模型中均无炎症作用。更有趣的是，我们发现一些多不饱和脂肪酸在人体脂肪组织和脂肪细胞模型中具有抗炎作用。这些结果很重要，因为它们阐明了饮食中脂肪酸与肥胖相关炎症之间的关系。
