Chronic High Fat Diet Induced Weight Gain, Hyperglycaemia and Cognitive Impairment in Albino Mice

I. Abi, SO Adeniyi, E. Abi, Muhammad K Imam
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引用次数: 2

Abstract

With the global rise in consumption of western diet, obesity is becoming a pandemic. High fat and high calorie diet (though more palatable) have been associated with a range of metabolic disorders. Oxidative stress and insulin resistance have a link to the dietary etiology of diabetes and obesity; on the other hand, neuroinflammation and abnormal brain insulin signaling is said to cause cognitive decline when high fat diet (HFD) is consumed. In this study, mice were fed a home-made HFD with a total energy content of 5340kcal/kg. The overall energy contribution of saturated and unsaturated fat was about 70%. Animals were divided into Group I and II of 5 mice each. Group I (control group) were fed normal chow and water ad libidum. Group II (test group) were fed HFD and water ad libidum. HFD significantly (p<0.05) increased the body weight of the test group (40 ±7.7) as compared to control (30 ± 2.9). Blood glucose levels in the test group was also significantly higher (111.6 ± 5.2) compared to the control (77.6 ± 8.7). Morris water maze escape latency in the test group was not significantly different (68 ± 26.3) compared to the control (72 ± 20.9). Similarly, the time spent in target quadrant in the test group was not significantly different (20.8 ± 10.9) compared to the control (15.8 ± 5.6). In the Y-maze the control group had a significantly higher (29.6 ± 3.5) percentage alternations compared to the test group (21 ± 13.1). It is obvious that the chronic administration of HFD in mice altered the body's metabolic processes as evident in the significant weight gain, hyperglycemia and cognitive deficit. These can be attributed to the oxidative damage, insulin dysregulation and pro-inflammatory potentials of HFD.
慢性高脂饮食诱导白化病小鼠体重增加、高血糖和认知障碍
随着西方饮食在全球消费的增加,肥胖正在成为一种流行病。高脂肪和高热量饮食(虽然更美味)与一系列代谢紊乱有关。氧化应激和胰岛素抵抗与糖尿病和肥胖的饮食病因有关;另一方面,据说当食用高脂肪饮食(HFD)时,神经炎症和异常的脑胰岛素信号会导致认知能力下降。在本研究中,小鼠喂食总能量为5340kcal/kg的自制HFD。饱和脂肪和不饱和脂肪的总能量贡献约为70%。动物分为ⅰ组和ⅱ组,每组5只。第一组(对照组)饲喂正常食物和饮水。第二组(试验组)饲喂高脂饲料和性欲水。试验组体重(40±7.7)显著高于对照组(30±2.9)(p<0.05)。实验组的血糖水平(111.6±5.2)也明显高于对照组(77.6±8.7)。实验组Morris水迷宫逃避潜伏期(68±26.3)与对照组(72±20.9)差异无统计学意义(p < 0.05)。同样,实验组在目标象限的停留时间(20.8±10.9)与对照组(15.8±5.6)无显著差异(p < 0.05)。在y型迷宫中,对照组(29.6±3.5)个百分比的改变明显高于试验组(21±13.1)个百分比。很明显,小鼠长期服用HFD改变了身体的代谢过程,如显著的体重增加、高血糖和认知障碍。这些可归因于HFD的氧化损伤、胰岛素失调和促炎潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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