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.

营养不良的饮食与脂肪组织扩张以及中枢和外周低度炎症有关。从这个意义上讲，中枢神经系统中的小胶质细胞被激活并释放促炎性细胞因子，该因子上调诱导型一氧化氮合酶（iNOS），从而促进一氧化氮（NO）的产生。已经提出过量的NO来促进人类和啮齿动物的焦虑状态。我们评估了在前额叶皮层（PFC）和海马（HIP）中通过NO的新颖性抑制喂养测试（NFST）促进了小鼠食用高含量的含碳水化合物饮食（HC）是否引起焦虑样行为。我们还证实了HC饮食是否能诱导小胶质细胞激活，这些区域中细胞因子和瘦素水平的改变。雄性BALB / c小鼠接受标准饮食或HC饮食3天或12周。长期食用HC饮食（而非急性饮食）在NSF测试中引起了类似焦虑的作用，并在PFC和HIP中引起了亚硝酸盐含量的增加。优先的iNOS抑制剂氨基胍（50 mg / kg，ip。），减弱了这种影响。此外，长期食用HC饮食后，HIP和PFC中的小胶质细胞被激活。最后，慢性HC喂养的小鼠中iNOS在PFC中的表达以及HIP中的TNF，IL6和瘦素水平较高。综上所述，我们的数据强化了这样的观念，即含有高精碳水化合物的饮食主要在长期食用后会促进类似焦虑的行为。该机制至少部分涉及在负责焦虑控制的脑区域中神经炎症过程的增强。