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首页> 外文期刊>Current opinion in lipidology >Toll-like receptor signaling links dietary fatty acids to the metabolic syndrome.
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Toll-like receptor signaling links dietary fatty acids to the metabolic syndrome.

机译：Toll样受体信号将饮食中的脂肪酸与代谢综合症联系起来。

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PURPOSE OF REVIEW: Dietary saturated fatty acids (SFAs) have been implicated in promoting the metabolic syndrome and atherosclerotic cardiovascular disease. Recent evidence suggests that SFAs promote the metabolic syndrome by activating Toll-like receptor 4 (TLR4). Here we examine emerging molecular evidence that SFAs directly engage pathways of innate immunity, thereby promoting inflammatory aspects of the metabolic syndrome. RECENT FINDINGS: Accumulation of SFA in the body is tightly regulated by stearoyl-CoA desaturase 1, an enzyme that converts endogenous SFA to monounsaturated fatty acids. Recent studies have demonstrated that the accumulation of SFA seen with genetic deletion or inhibition of stearoyl-CoA desaturase 1 promotes inflammation, TLR4 hypersensitivity, and accelerated atherosclerosis. Therefore, stearoyl-CoA desaturase 1 may play an unexpected role in suppressing inflammation by preventing excessive accumulation of endogenous SFA-derived TLR4 agonists. In parallel, several independent laboratories have demonstrated that TLR4 is necessary for dietary SFAs to induce obesity, insulin resistance, and vascular inflammation in rodent models. SUMMARY: The metabolic syndrome and atherosclerotic cardiovascular disease have long been linked to dietary SFA intake and inflammation. Recent mechanistic insights into how SFAs and downstream metabolites can potentiate inflammation-driven metabolic disease are discussed here.
机译：审查目的：饮食中的饱和脂肪酸（SFA）与促进代谢综合征和动脉粥样硬化性心血管疾病有关。最近的证据表明，SFA通过激活Toll样受体4（TLR4）促进代谢综合征。在这里，我们检查了新兴的分子证据，即SFA直接参与先天免疫的途径，从而促进了代谢综合征的炎症。最近的发现：体内的SFA的积累受到硬脂酰辅酶A去饱和酶1的严格控制，该酶将内源性SFA转化为单不饱和脂肪酸。最近的研究表明，通过遗传删除或抑制硬脂酰辅酶A去饱和酶1可以看到SFA的积累会促进炎症，TLR4超敏反应和加速动脉粥样硬化。因此，硬脂酰辅酶A去饱和酶1可能通过防止内源性SFA衍生的TLR4激动剂的过度积累而在抑制炎症中发挥意想不到的作用。同时，几个独立的实验室已经证明，TLR4对于饮食SFA在啮齿动物模型中诱导肥胖，胰岛素抵抗和血管炎症是必需的。摘要：代谢综合征和动脉粥样硬化性心血管疾病长期以来一直与饮食中SFA的摄入和炎症有关。本文讨论了有关SFA和下游代谢产物如何增强炎症驱动的代谢性疾病的最新机制。

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