{"title":"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","authors":"I. Abi, SO Adeniyi, E. Abi, Muhammad K Imam","doi":"10.46912/jbrcp.193","DOIUrl":null,"url":null,"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.","PeriodicalId":301476,"journal":{"name":"Journal of BioMedical Research and Clinical Practice","volume":"128 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2020-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"Chronic High Fat Diet Induced Weight Gain, Hyperglycaemia and Cognitive Impairment in Albino Mice\",\"authors\":\"I. Abi, SO Adeniyi, E. Abi, Muhammad K Imam\",\"doi\":\"10.46912/jbrcp.193\",\"DOIUrl\":null,\"url\":null,\"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.\",\"PeriodicalId\":301476,\"journal\":{\"name\":\"Journal of BioMedical Research and Clinical Practice\",\"volume\":\"128 1\",\"pages\":\"0\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-12-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of BioMedical Research and Clinical Practice\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.46912/jbrcp.193\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of BioMedical Research and Clinical Practice","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.46912/jbrcp.193","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Chronic High Fat Diet Induced Weight Gain, Hyperglycaemia and Cognitive Impairment in Albino Mice
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.