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Dietary conjugated linoleic acid and n-3 polyunsaturated fatty acids in inflammatory bowel disease.

机译:饮食性共轭亚油酸和n-3多不饱和脂肪酸在炎症性肠病中的作用。

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PURPOSE OF REVIEW: Inflammatory bowel disease (IBD) is a debilitating and widespread immune-mediated illness of unknown etiology. Current treatments are modestly successful and with significant side-effects. The purpose of this review is to summarize the current understanding of mechanisms of action underlying the anti-inflammatory actions of conjugated linoleic acid (CLA) and n-3 polyunsaturated fatty acids (PUFAs) in IBD. RECENT FINDINGS: Nutrition-based interventions that target peroxisome proliferator-activated receptors (PPARs) such as dietary CLA and n-3 PUFA have demonstrated anti-inflammatory efficacy in animal models of IBD. Clinical data on n-3 PUFA in IBD remains generally unimpressive, although results of a recent human study demonstrate that IBD remission can be maintained by maintaining the n-3: n-6 ratio more than 0.65 via n-3 PUFA intervention. In mice, CLA prevented inflammation-driven colorectal cancer by activating PPAR gamma and modulating regulatory T cells and macrophages. CLA is the subject of an ongoing clinical study in Crohn's disease patients. SUMMARY: Compelling evidence demonstrates that n-3 PUFA and CLA prevent or ameliorate IBD in animal models. However, this basic knowledge has not been translated into novel nutrition-based clinical interventions. For both compounds there is an urgent need for placebo-controlled, large-scale, multicenter clinical trials.
机译:审查目的:炎症性肠病(IBD)是一种病因不明的衰弱性广泛的免疫介导疾病。目前的治疗方法取得了一定程度的成功,并具有明显的副作用。这篇综述的目的是总结目前对IBD中共轭亚油酸(CLA)和n-3多不饱和脂肪酸(PUFAs)抗炎作用的作用机理的理解。最近的发现:以过氧化物酶体增殖物激活受体(PPAR)为基础的基于营养的干预措施,如饮食CLA和n-3 PUFA已证明在IBD动物模型中具有抗炎功效。尽管最近的一项人类研究结果表明,通过n-3 PUFA干预将n-3:n-6的比例维持在0.65以上,可以维持IBD缓解,但IBD中n-3 PUFA的临床数据通常不会令人印象深刻。在小鼠中,CLA通过激活PPARγ和调节调节性T细胞和巨噬细胞来预防炎症驱动的大肠癌。 CLA是正在进行的针对克罗恩病患者的临床研究的主题。摘要:有力的证据表明,n-3 PUFA和CLA可以预防或改善动物模型中的IBD。但是,这种基本知识尚未转化为基于营养的新型临床干预措施。对于这两种化合物,迫切需要安慰剂对照的大规模多中心临床试验。

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