...
【24h】

Metabolic syndrome: A brain disease

机译:代谢综合征:一种脑疾病

获取原文
获取原文并翻译 | 示例
           

摘要

Recent research indicates an association between brain dysfunction and the pathogenesis of metabolic syndrome. To investigate this, we created a Medline search (up to December 2011) of articles in PubMed. The results indicated that refined carbohydrates, saturated and total fat, high levels of ω-6 fatty acids, and low levels of ω-3 fatty acids and other long chain polyunsaturated fatty acids (PUFA), all in conjunction with sedentary behaviour and mental stress can predispose to inflammation. Increased sympathetic activity, with increased secretion of catecholamine, cortisol, and serotonin can cause oxidative stress, which may damage the arcuate nucleus as well as the hypothalamus and macrophages, and the liver may release pro-inflammatory cytokines. These, in conjunction with an underlying deficiency in long chain PUFA, may damage the arcuate nucleus as well as neuropeptide-Y and pro-opiomelanocortin neurons and insulin receptors in the brain, especially during fetal life, infancy, and childhood, resulting in their dysfunction. Of the fatty acids in the brain, 30%-50% are long chain PUFA, which are incorporated in the cell membrane phospholipids. Hence, ω-3 fatty acids, which are also known to enhance parasympathetic activity and increase the secretion of anti-inflammatory cytokines interleukin (IL)-4 and IL-10 as well as acetylcholine in the hippocampus, may be protective. Therefore, treatment with ω-3 fatty acids may be applied for the prevention of metabolic syndrome.
机译:最近的研究表明脑功能障碍与代谢综合征的发病机制之间存在关联。为了对此进行调查,我们创建了Medline搜索(截至2011年12月)中PubMed中的文章。结果表明,精制碳水化合物,饱和脂肪和总脂肪,高水平的ω-6脂肪酸,低水平的ω-3脂肪酸和其他长链多不饱和脂肪酸(PUFA)均与久坐行为和精神压力相关容易诱发炎症。交感活动增加,儿茶酚胺,皮质醇和5-羟色胺的分泌增加会引起氧化应激,这可能会损害弓形核以及下丘脑和巨噬细胞,并且肝脏可能会释放促炎性细胞因子。这些与长链PUFA的潜在缺陷相结合,可能会损害弓形核以及大脑中的神经肽-Y和前opiomelanocortin神经元和胰岛素受体,尤其是在胎儿的生命,婴儿期和儿童期,导致其功能障碍。脑中的脂肪酸中,有30%-50%是长链PUFA,掺入细胞膜磷脂中。因此,ω-3脂肪酸(也可增强副交感神经活性并增加海马中抗炎细胞因子白介素(IL)-4和IL-10以及乙酰胆碱的分泌)可能是保护性的。因此,用ω-3脂肪酸治疗可用于预防代谢综合征。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号