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首页> 外文期刊>Journal of chemical neuroanatomy >Swimming reduces fatty acids-associated hypothalamic damage in mice
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Swimming reduces fatty acids-associated hypothalamic damage in mice

机译：游泳减少了小鼠中的脂肪酸相关的下丘脑损伤

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摘要

The arcuate and the paraventricular and lateral hypothalamic nuclei, related to hunger and satiety control, are generally compromised by excess fatty acids. In this situation, fatty acids cause inflammation via TLR4 (toll like receptor 4) and the nuclei become less responsive to the hormones leptin and insulin, contributing to the development of obesity. In this work, these nuclei were analyzed in animals fed with high-fat diet and submitted to swimming without and with load for two months. For this, frontal sections of the hypothalamus were immunolabelled with GFAP (glial fibrillary acidic protein), synaptophysin, IL-6 (interleukin 6) and TLR4. Also, proteins extracted from the hypothalamus were analyzed using Western blotting (GFAP and synaptophysin), fluorometric analysis for caspases 3 and 7, and CBA (cytometric bead array) for Th1, Th2, and Th17 profiles. The high-fat diet significantly caused overweight and, in the hypothalamus, decreased synapses and increased astrocytic reactivity. The swimming with load, especially 80 % of the maximum load, reduced those consequences. The high-fat diet increased TLR4 in the arcuate nucleus and the swimming exercise with 80 % of the maximum load showed a tendency of reducing this expression. Swimming did not significantly influence the inflammatory or anti-inflammatory cytokines in the hypothalamus or in plasma. The high-fat diet in sedentary animals increased the expression of caspases 3 and 7 and swimming practice reduced this increment to levels compatible with animals fed on a normal diet. The set of results conclude that the impact of swimming on the damage caused in the hypothalamus by a high-fat diet is positive. The different aspects analyzed in here point to better cellular viability and conservation of the synapses in the hypothalamic nuclei of overweight animals that practiced swimming with a load.
机译：与饥饿和饱腹感染有关的弧形和旁注和侧丘脑核，通常由过量的脂肪酸损害。在这种情况下，脂肪酸通过TLR4（像受体4）的炎症引起炎症，并且核对激素瘦蛋白和胰岛素的核心变得不那么响应，有助于肥胖的发展。在这项工作中，用高脂饮食喂养的动物分析了这些细胞核，并提交游泳而没有和负载两个月。为此，下丘脑的正面部分用GFAP（胶质纤维酸性酸性蛋白），突波敏素，IL-6（白细胞介素6）和TLR4免疫标签。此外，使用蛋白质印迹（GFAP和Sypaptophysin），用于Caspases 3和7的荧光分析，CBA（细胞计序珠阵列），分析从下丘脑中提取的蛋白质，用于Th1，Th2和Th17型材。高脂饮食显着引起超重，在下丘脑中，减少突触和增加的星形织造酵母反应性。用负荷游泳，尤其是最大负荷的80％，减少了这些后果。高脂饮食在弓形核中增加TLR4，并且游泳运动，80％的最大负荷显示出降低该表达的趋势。游泳没有显着影响下丘脑或血浆中的炎症或抗炎细胞因子。久入动物的高脂饮食增加了木质酶的表达3和7，游泳实践将这种增量降低到与喂养正常饮食中的动物相容的水平。这组结果得出结论是，游泳对丘脑损伤的影响，高脂饮食是阳性的。在此分析的不同方面指向更好的细胞存活率和保护超重动物的突触突触的突触，这些核心的超重动物用负荷游泳。

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