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首页> 外文期刊>The Journal of Nutritional Biochemistry >High-refined carbohydrate diet consumption induces neuroinflammation and anxiety-like behavior in mice
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High-refined carbohydrate diet consumption induces neuroinflammation and anxiety-like behavior in mice

机译:高精制的碳水化合物饮食消耗诱导小鼠的神经炎症和焦虑的行为

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Consumption of poor nutrients diets is associated with fat tissue expansion and with a central and peripheral low-grade inflammation. In this sense, the microglial cells in the central nervous system are activated and release pro-inflammatory cytokines that up-regulate the inducible nitric oxide synthase (iNOS), promoting Nitric Oxide (NO) production. The excess of NO has been proposed to facilitate anxious states in humans and rodents. We evaluated whether consumption of a high-refined carbohydrate-containing diet (HC) in mice induced anxiety-like behavior in the Novelty Suppressed Feeding Test (NFST) trough facilitation of NO, in the prefrontal cortex (PFC) and hippocampus (HIP). We also verified if HC diet induces activation of microglial cells, alterations in cytokine and leptin levels in such regions. Male BALB/c mice received a standard diet or a HC diet for 3 days or 12 weeks. The chronic consumption of HC diet, but not acute, induced an anxiogenic-like effect in the NSF test and an increase in the nitrite levels in the PFC and HIP. The preferential iNOS inhibitor, aminoguanidine (50 mg/kg, i.p.), attenuated such effects. Moreover, microglial cells in the HIP and PFC were activated after chronic consumption of HC diet. Finally, the expression of iNOS in the PFC and TNF, IL6 and leptin levels in HIP were higher in chronically HC fed mice. Taken together, our data reinforce the notion that diets containing high-refined carbohydrate facilitate anxiety-like behavior, mainly after a long period of consumption. The mechanisms involve, at least in part, the augmentation of neuroinflammatory processes in brain areas responsible for anxiety control. (C) 2019 Elsevier Inc. All rights reserved.
机译:消耗较差的营养饮食与脂肪组织膨胀和中央和外周低级炎症有关。从这个意义上讲,中枢神经系统中的微胶质细胞是激活的,并释放促炎细胞因子,该细胞因子上调诱导型一氧化氮合酶(InOS),促进一氧化氮(NO)产生。已经提出过多的否则促进人类和啮齿动物的焦虑状态。我们评估了小鼠中含有高精度的碳水化合物的饮食(HC)的食用诱导的焦虑状行为在新颖的抑制喂养试验(NFST)促进的促进促进的舒适性,在前额叶皮质(PFC)和海马(臀部)中。如果HC饮食诱导激活微胶质细胞,则在这些区域中的细胞因子和瘦素水平的改变。雄性BALB / C小鼠在3天或12周接受标准饮食或HC饮食。 HC饮食的慢性消耗,但不急性,诱导NSF试验中的焦虑效果,并增加了PFC和臀部的亚硝酸盐水平。优选的InOS抑制剂,氨基胍(50mg / kg,I.p.),减弱了这些效果。此外,在HC饮食的慢性消耗后激活髋关节和PFC中的小胶质细胞。最后,在阶下的髋菌和TNF,IL6和肝脏水平中表达在髋氏蛋白的浓度饲料小鼠中较高。我们的数据加强了含有高精制碳水化合物的饮食的观念,促进了焦虑的行为,主要是经过长期的消费。至少部分地涉及,负责焦虑控制的脑区中神经炎性过程的增强。 (c)2019 Elsevier Inc.保留所有权利。

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