High-refined carbohydrate diet consumption induces neuroinflammation and anxiety-like behavior in mice.

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.

Exercise attenuates alveolar bone loss and anxiety-like behaviour in rats with periodontitis.

AIM: To evaluate the effects of physical training on inflammatory and behavioural parameters of Wistar rats with periodontal disease (PD). MATERIALS AND METHODS: Twenty four animals were distributed in a 2 × 2 factorial design (with and without exercise, with and without PD). Trained animals swimmed one hour daily during 8 weeks. PD was induced by ligature 14 days before the end of experiment, and in the last week, all animals were submitted to the Marble Burying Test. Histomorphometric analyses of the mandibles and expression of cytokines were conducted by Western blotting. We also evaluated the morphometry of hippocampal astrocytes using anti-glial fibrillary acidic protein antibody. RESULTS: Physical training attenuated bone loss and epithelial attachment loss levels of rats with PD. Trained animals with PD presented lower TNF-α expression in periodontal tissues while IL-10 was increased. TNF-α/IL-10 ratio was lower in trained animals with PD compared to those with induced periodontitis. PD increased anxiety-like behaviour, and physical training attenuated this parameter. Exercise increased the ramifications of hippocampal astrocytes in rats without PD. CONCLUSIONS: Exercise decreased anxiety behaviour, inflammatory proteins expression and bone loss in rats with PD.