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.

中文翻译：

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游泳可减少小鼠脂肪酸相关的下丘脑损伤

与饥饿和饱腹感控制相关的弓状核、室旁核和侧下丘脑核通常受到过量脂肪酸的损害。在这种情况下，脂肪酸通过 TLR4（toll 样受体 4）引起炎症，细胞核对激素瘦素和胰岛素的反应降低，从而导致肥胖的发展。在这项工作中，这些细胞核在高脂肪饮食喂养的动物中进行了分析，并在两个月的无负荷和有负荷的游泳中进行了分析。为此，下丘脑的额叶部分用 GFAP（胶质纤维酸性蛋白）、突触素、IL-6（白介素 6）和 TLR4 进行了免疫标记。此外，使用蛋白质印迹法（GFAP 和突触素）、半胱天冬酶 3 和 7 的荧光分析以及 Th1、Th2、CBA（细胞计数珠阵列）分析从下丘脑提取的蛋白质。和 Th17 配置文件。高脂肪饮食显着导致超重，并且在下丘脑，突触减少，星形胶质细胞反应性增加。负重游泳，尤其是最大负重的 80%，减少了这些后果。高脂饮食使弓状核中的 TLR4 增加，最大负荷 80% 的游泳运动显示出降低该表达的趋势。游泳对下丘脑或血浆中的炎症或抗炎细胞因子没有显着影响。久坐动物的高脂肪饮食增加了半胱天冬酶 3 和 7 的表达，游泳练习将这种增加降低到与正常饮食喂养的动物相容的水平。这组结果得出的结论是，游泳对高脂肪饮食对下丘脑造成的损害的影响是积极的。