外源性游离 Nε-(羧甲基)赖氨酸对糖尿病相关认知功能障碍、神经炎症和代谢紊乱的影响

IF 5.6 1区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY
{"title":"外源性游离 Nε-(羧甲基)赖氨酸对糖尿病相关认知功能障碍、神经炎症和代谢紊乱的影响","authors":"","doi":"10.26599/FSHW.2022.9250240","DOIUrl":null,"url":null,"abstract":"<div><div>Diabetes-associated cognitive dysfunction has already been attracted considerable attention. Advanced glycation end products (AGEs) from daily diets are thought to be a vital contributor to the development of this diseases. However, the effect of one of the best-characterized exogenous AGEs <em>N</em><sup>ε</sup>-(carboxymethyl)lysine (CML) on cognitive function is not fully reported. In the present study, diabetical Goto-Kakizaki (GK) rats were treated with free CML for 8-weeks. It was found that oral consumption of exogenous CML significantly aggravated diabetes-associated cognitive dysfunction in behavioral test. In details, exogenous CML increased levels of oxidative stress, promoted the activation of glial cells in the brain, up-regulated the release of inflammatory cytokines interleukin-6, inhibited the protein expression of the brain-derived neurotrophic factor and thus led to neuroinflammation. Furthermore, exogenous CML promoted the amyloidogenesis in the brain of GK rats, and inhibited the expression of GLUT4. Additionally, several tricarboxylic acid cycle and glutamate-glutamine/<em>γ</em>-aminobutyric acid cycle intermediates including pyruvate, succinic acid, glutamine, glutamate were significantly changed in brain of GK rats treated with exogenous free CML. In conclusion, exogenous free CML is a potentially noxious compounds led to aggravated diabetes-associated cognitive dysfunction which could be possibly explained by its effects on neuroinflammation, energy and neurotransmitter amino acid homeostasis.</div></div>","PeriodicalId":12406,"journal":{"name":"Food Science and Human Wellness","volume":"13 5","pages":"Pages 2970-2981"},"PeriodicalIF":5.6000,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Effect of exogenous free Nε-(carboxymethyl)lysine on diabetes-associated cognitive dysfunction: neuroinflammation, and metabolic disorders\",\"authors\":\"\",\"doi\":\"10.26599/FSHW.2022.9250240\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Diabetes-associated cognitive dysfunction has already been attracted considerable attention. Advanced glycation end products (AGEs) from daily diets are thought to be a vital contributor to the development of this diseases. However, the effect of one of the best-characterized exogenous AGEs <em>N</em><sup>ε</sup>-(carboxymethyl)lysine (CML) on cognitive function is not fully reported. In the present study, diabetical Goto-Kakizaki (GK) rats were treated with free CML for 8-weeks. It was found that oral consumption of exogenous CML significantly aggravated diabetes-associated cognitive dysfunction in behavioral test. In details, exogenous CML increased levels of oxidative stress, promoted the activation of glial cells in the brain, up-regulated the release of inflammatory cytokines interleukin-6, inhibited the protein expression of the brain-derived neurotrophic factor and thus led to neuroinflammation. Furthermore, exogenous CML promoted the amyloidogenesis in the brain of GK rats, and inhibited the expression of GLUT4. Additionally, several tricarboxylic acid cycle and glutamate-glutamine/<em>γ</em>-aminobutyric acid cycle intermediates including pyruvate, succinic acid, glutamine, glutamate were significantly changed in brain of GK rats treated with exogenous free CML. In conclusion, exogenous free CML is a potentially noxious compounds led to aggravated diabetes-associated cognitive dysfunction which could be possibly explained by its effects on neuroinflammation, energy and neurotransmitter amino acid homeostasis.</div></div>\",\"PeriodicalId\":12406,\"journal\":{\"name\":\"Food Science and Human Wellness\",\"volume\":\"13 5\",\"pages\":\"Pages 2970-2981\"},\"PeriodicalIF\":5.6000,\"publicationDate\":\"2024-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Food Science and Human Wellness\",\"FirstCategoryId\":\"97\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2213453024002179\",\"RegionNum\":1,\"RegionCategory\":\"农林科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"FOOD SCIENCE & TECHNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Food Science and Human Wellness","FirstCategoryId":"97","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2213453024002179","RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"FOOD SCIENCE & TECHNOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

与糖尿病相关的认知功能障碍已经引起了广泛关注。日常饮食中的高级糖化终产物(AGEs)被认为是导致这种疾病发生的重要因素。然而,关于外源性 AGEs Nε-(羧甲基)赖氨酸(CML)对认知功能的影响,目前还没有充分的报道。在本研究中,糖尿病后藤柿崎(GK)大鼠接受了为期 8 周的游离 CML 治疗。结果发现,在行为测试中,口服外源性 CML 会明显加重糖尿病相关的认知功能障碍。具体而言,外源性 CML 增加了氧化应激水平,促进了脑胶质细胞的活化,上调了炎症细胞因子白细胞介素-6 的释放,抑制了脑源性神经营养因子的蛋白表达,从而导致神经炎症。此外,外源性 CML 会促进 GK 大鼠脑内淀粉样蛋白的生成,并抑制 GLUT4 的表达。此外,用外源性游离 CML 处理的 GK 大鼠脑中的一些三羧酸循环和谷氨酸-谷氨酰胺/γ-氨基丁酸循环中间产物(包括丙酮酸、琥珀酸、谷氨酰胺、谷氨酸)发生了显著变化。总之,外源性游离 CML 是一种可能导致糖尿病相关认知功能障碍加重的有毒化合物,这可能是由于它对神经炎症、能量和神经递质氨基酸平衡的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Effect of exogenous free Nε-(carboxymethyl)lysine on diabetes-associated cognitive dysfunction: neuroinflammation, and metabolic disorders

Effect of exogenous free Nε-(carboxymethyl)lysine on diabetes-associated cognitive dysfunction: neuroinflammation, and metabolic disorders
Diabetes-associated cognitive dysfunction has already been attracted considerable attention. Advanced glycation end products (AGEs) from daily diets are thought to be a vital contributor to the development of this diseases. However, the effect of one of the best-characterized exogenous AGEs Nε-(carboxymethyl)lysine (CML) on cognitive function is not fully reported. In the present study, diabetical Goto-Kakizaki (GK) rats were treated with free CML for 8-weeks. It was found that oral consumption of exogenous CML significantly aggravated diabetes-associated cognitive dysfunction in behavioral test. In details, exogenous CML increased levels of oxidative stress, promoted the activation of glial cells in the brain, up-regulated the release of inflammatory cytokines interleukin-6, inhibited the protein expression of the brain-derived neurotrophic factor and thus led to neuroinflammation. Furthermore, exogenous CML promoted the amyloidogenesis in the brain of GK rats, and inhibited the expression of GLUT4. Additionally, several tricarboxylic acid cycle and glutamate-glutamine/γ-aminobutyric acid cycle intermediates including pyruvate, succinic acid, glutamine, glutamate were significantly changed in brain of GK rats treated with exogenous free CML. In conclusion, exogenous free CML is a potentially noxious compounds led to aggravated diabetes-associated cognitive dysfunction which could be possibly explained by its effects on neuroinflammation, energy and neurotransmitter amino acid homeostasis.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Food Science and Human Wellness
Food Science and Human Wellness Agricultural and Biological Sciences-Food Science
CiteScore
8.30
自引率
5.70%
发文量
80
审稿时长
28 days
期刊介绍: Food Science and Human Wellness is an international peer-reviewed journal that provides a forum for the dissemination of the latest scientific results in food science, nutriology, immunology and cross-field research. Articles must present information that is novel, has high impact and interest, and is of high scientific quality. By their effort, it has been developed to promote the public awareness on diet, advocate healthy diet, reduce the harm caused by unreasonable dietary habit, and directs healthy food development for food industrial producers.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信