Recent evidence suggests that young rodents submitted to high fructose (FRU) diet develop metabolic, and cognitive dysfunctions. However, it remains unclear whether these detrimental effects of FRU intake can also be observed in middle-aged mice. Nine months-old C57BL/6 female mice were fed with water (Control) or 10% FRU in drinking water during 12 weeks. After that, metabolic, and neurochemical alterations were evaluated, focusing on neurotransmitters, and antioxidant defenses. Behavioral parameters related to motor activity, memory, anxiety, and depression were also evaluated. Mice consuming FRU diet displayed increased water, and caloric intake, resulting in weight gain, which was partially compensated due to decreased food pellet intake. FRU fed animals displayed increased plasma glucose, and cholesterol levels, which was not observed in overnight-fasted animals. Superoxide dismutase (SOD), and catalase (CAT) activities were markedly decreased in the prefrontal cortex of animals receiving FRU diet, while glutathione peroxidase (GPx) slightly increased. Liver (lower GPx), striatum (higher SOD and lower CAT), and hippocampus (no changes) were less impacted. No changes were observed in glutathione reductase, and thioredoxin reductase activities, two ancillary enzymes for peroxide detoxification. FRU intake did not alter serotonin, dopamine, and norepinephrine levels in the hippocampus, prefrontal cortex, and striatum. No significant alterations were observed in working, and short-term spatial memory; and in anxiety- and depressive-like behaviors in animals treated with FRU. Increased locomotor activity was observed in FRU-fed middle-aged mice, as evaluated in the open field, elevated plus-maze, Y maze, and object location tasks. Overall, these results demonstrate that high FRU consumption can disturb antioxidant defenses, and increase locomotor activity in middle-aged mice, open the opportunity for further studies to address the underlying mechanisms related to these findings.

最近的证据表明，服食高果糖（FRU）饮食的年轻啮齿动物会发生代谢和认知功能障碍。但是，尚不清楚在中年小鼠中是否也能观察到FRU摄入的这些有害作用。在12周内给9个月大的C57BL / 6雌性小鼠喂水（对照组）或饮用水中10％FRU。之后，评估了代谢和神经化学变化，重点是神经递质和抗氧化防御。还评估了与运动活动，记忆，焦虑和抑郁有关的行为参数。食用FRU饮食的小鼠的水分和热量摄入增加，导致体重增加，这是由于食物颗粒摄入减少而部分弥补的。FRU喂养的动物血浆葡萄糖和胆固醇水平升高，在过夜禁食的动物中未观察到。在接受FRU饮食的动物的前额叶皮层中，超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性明显降低，而谷胱甘肽过氧化物酶（GPx）则略有增加。肝脏（GPx较低），纹状体（SOD较高和CAT较低）和海马（无变化）受到的影响较小。谷胱甘肽还原酶和硫氧还蛋白还原酶活性（用于过氧化物解毒的两种辅助酶）活性未见变化。FRU摄入量不会改变海马，前额叶皮层和纹状体中的血清素，多巴胺和去甲肾上腺素水平。在工作和短期空间记忆中未观察到明显的改变；以及用FRU治疗的动物的焦虑和抑郁样行为。在FRU喂养的中年小鼠中观察到运动能力增强，如在野外评估，高架迷宫，Y迷宫和对象定位任务。总体而言，这些结果表明，高FRU摄入量可能会干扰抗氧化剂防御能力，并增加中年小鼠的自发活动，为进一步研究以解决与这些发现相关的潜在机制提供了机会。