Epidemiological studies showed that a high-fat diet threatened human health seriously. It can induce various diseases, such as obesity, metabolic disturbance and cognitive dysfunction which also related to insulin signaling. In the present study, Aβ1-42 induced AD model mice and normal mice were given a standard diet and high-fat diet, respectively. Meanwhile, Okra polysaccharides were used to treat AD mice to explore the possible mechanism between Alzheimer's disease and insulin signals. Weight and blood glucose of mice were measured weekly. Through the Morris water maze and the novel object recognition test, the Okra polysaccharides could improve the cognitive impairment of the AD mice. In addition, we also performed the serum chemistry analysis of mice, studied the histopathological changes in the hippocampal CA1 region by HE staining and detected the expressions of AKT, PI3K, ERK1/2, and GSK3β in the hippocampus by western blot. These results suggested that a high-fat diet can aggravate the metabolic disorder in AD mice and Okra polysaccharides can significantly reverse the metabolic disorder induced by high-fat diet and cognitive function injury in AD mice.

中文翻译：

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黄秋葵多糖可以逆转高脂饮食和认知功能损伤引起的Aβ1-42小鼠代谢紊乱。

流行病学研究表明，高脂饮食严重威胁着人类健康。它可以诱发多种疾病，例如肥胖，代谢紊乱和认知功能障碍，这些疾病也与胰岛素信号传导有关。在本研究中，Aβ1-42诱导的AD模型小鼠和正常小鼠分别接受标准饮食和高脂饮食。同时，使用秋葵多糖治疗AD小鼠，以探讨阿尔茨海默氏病与胰岛素信号之间的可能机制。每周测量小鼠的体重和血糖。通过莫里斯水迷宫和新颖的物体识别测试，秋葵多糖可以改善AD小鼠的认知障碍。此外，我们还对小鼠进行了血清化学分析，通过HE染色研究海马CA1区的组织病理学变化，并通过蛋白质印迹法检测海马中AKT，PI3K，ERK1 / 2和GSK3β的表达。这些结果表明，高脂饮食可以加重AD小鼠的代谢紊乱，而秋葵多糖可以显着逆转高脂饮食和AD小鼠认知功能损伤引起的代谢紊乱。