• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

烟酰胺稳态:一种对外源生物至关重要的途径,是发育和退行性疾病的关键。

Nicotinamide homeostasis: a xenobiotic pathway that is key to development and degenerative diseases.

作者信息

Williams A C, Ramsden D B

机构信息

Division of Neuroscience, University of Birmingham, Edgbaston, Birminham B15 2 TT, UK.

出版信息

Med Hypotheses. 2005;65(2):353-62. doi: 10.1016/j.mehy.2005.01.042.

DOI:10.1016/j.mehy.2005.01.042
PMID:15922112
Abstract

Monkeys and man are very closely related genetically. Yet intellectually there are big differences and they suffer from a broad range of different diseases. For example, monkeys do not get Parkinson's or Alzheimer's disease. The former is surprising given that both get parkinsonism from MPTP poisoning and the latter initially less surprising as the cortex predominantly affected in Alzheimer's never developed as fully in the monkey. Man is an omnivore whilst other primates are predominantly herbivores. The one primate who was almost wholly carnivorous was Neanderthal man who became extinct. Red meat has a high content of Nicotinamide, Choline, and methyl donors. The enzyme NNMT converts nicotinamide to N-methyl-nicotinamide using SAM as the methyl donor. It is not present to any degree in herbivores. It has recently been shown to be present in human brain and up regulated in Parkinson's disease. Omnivores presumably need it for nicotinamide homeostasis but the production of N-methyl-nicotinamide will also be beneficial as it will reduce the export of Choline from neurones. Both will aid brain growth and development. However, as N-methyl-nicotinamide resembles MPTP it could cause parkinsonism later in life for man but not monkeys as they would be predicted not to have as much NNMT. Humans with a diet low in Nicotinamide,Choline or methyl donors early in life and low enzyme activity may be prone to Alzheimer's as their brain and therefore its reserves may never have developed as fully. The possession of NNMT plus a diet rich in Nicotinamide, Choline and methyl providers may explain many of the advantages but also the disadvantages of the human condition. One prediction is that a diet rich in these micronutrients whilst young will improve brain development and reduce the risk of Alzheimer's but that a lower dose later in life will reduce the risk of Parkinsonism. A second prediction is that it will become clear that dietary factors including vitamins are signalers and at the head of vital biochemical pathways. A time point will be reached when errors emerge that could not be deleted by evolutionary pressures. Finding and rectifying them will be the key to preventing many common diseases.

摘要

猴子和人类在基因上密切相关。然而,在智力方面存在很大差异,并且它们患多种不同疾病。例如,猴子不会患帕金森病或阿尔茨海默病。鉴于两者都会因MPTP中毒而出现帕金森综合征,前者令人惊讶;而后者最初不那么令人惊讶,因为在阿尔茨海默病中主要受影响的大脑皮层在猴子中从未充分发育。人类是杂食动物,而其他灵长类动物主要是食草动物。几乎完全食肉的一种灵长类动物是已灭绝的尼安德特人。红肉富含烟酰胺、胆碱和甲基供体。NNMT酶利用SAM作为甲基供体将烟酰胺转化为N-甲基烟酰胺。它在食草动物中不存在。最近发现它存在于人类大脑中,并且在帕金森病中上调。杂食动物可能需要它来维持烟酰胺稳态,但N-甲基烟酰胺的产生也将是有益的,因为它将减少胆碱从神经元的输出。两者都将有助于大脑的生长和发育。然而,由于N-甲基烟酰胺类似于MPTP,它可能在人类后期导致帕金森综合征,但对猴子不会,因为预计它们没有那么多NNMT。早年饮食中烟酰胺、胆碱或甲基供体含量低且酶活性低的人可能易患阿尔茨海默病,因为他们的大脑以及因此其储备可能从未充分发育。拥有NNMT加上富含烟酰胺、胆碱和甲基供体的饮食可以解释人类状况的许多优点和缺点。一个预测是,年轻时富含这些微量营养素的饮食将改善大脑发育并降低患阿尔茨海默病的风险,但在生命后期较低剂量将降低患帕金森综合征的风险。第二个预测是,将清楚地表明包括维生素在内的饮食因素是信号分子,并且处于重要生化途径的首位。将会达到一个时间点,那时会出现无法被进化压力消除的错误。发现并纠正它们将是预防许多常见疾病的关键。

相似文献

1
Nicotinamide homeostasis: a xenobiotic pathway that is key to development and degenerative diseases.烟酰胺稳态:一种对外源生物至关重要的途径,是发育和退行性疾病的关键。
Med Hypotheses. 2005;65(2):353-62. doi: 10.1016/j.mehy.2005.01.042.
2
Parkinson's disease: the first common neurological disease due to auto-intoxication?帕金森病:首例由自身中毒引起的常见神经疾病?
QJM. 2005 Mar;98(3):215-26. doi: 10.1093/qjmed/hci027.
3
Autotoxicity, methylation and a road to the prevention of Parkinson's disease.自身毒性、甲基化与帕金森病的预防之路
J Clin Neurosci. 2005 Jan;12(1):6-11. doi: 10.1016/j.jocn.2004.10.002.
4
Broad neuroprotective profile of nicotinamide in different mouse models of MPTP-induced parkinsonism.烟酰胺在MPTP诱导的帕金森病不同小鼠模型中的广泛神经保护作用
Eur J Neurosci. 2008 Aug;28(3):610-7. doi: 10.1111/j.1460-9568.2008.06356.x.
5
High doses of nicotinamide prevent oxidative mitochondrial dysfunction in a cellular model and improve motor deficit in a Drosophila model of Parkinson's disease.高剂量烟酰胺可预防细胞模型中的氧化线粒体功能障碍,并改善帕金森病果蝇模型中的运动缺陷。
J Neurosci Res. 2008 Jul;86(9):2083-90. doi: 10.1002/jnr.21650.
6
Alzheimer's neuroborreliosis with trans-synaptic spread of infection and neurofibrillary tangles derived from intraneuronal spirochetes.伴有感染跨突触传播及源自神经元内螺旋体的神经纤维缠结的阿尔茨海默神经莱姆病
Med Hypotheses. 2007;68(4):822-5. doi: 10.1016/j.mehy.2006.08.043. Epub 2006 Oct 20.
7
Nicotinamide: a double edged sword.烟酰胺:一把双刃剑。
Parkinsonism Relat Disord. 2005 Nov;11(7):413-20. doi: 10.1016/j.parkreldis.2005.05.011. Epub 2005 Sep 23.
8
Neuroinflammation in Alzheimer's disease and Parkinson's disease: are microglia pathogenic in either disorder?阿尔茨海默病和帕金森病中的神经炎症:小胶质细胞在这两种疾病中都具有致病性吗?
Int Rev Neurobiol. 2007;82:235-46. doi: 10.1016/S0074-7742(07)82012-5.
9
Mitochondria, metabolic disturbances, oxidative stress and the kynurenine system, with focus on neurodegenerative disorders.线粒体、代谢紊乱、氧化应激与犬尿氨酸系统,重点关注神经退行性疾病
J Neurol Sci. 2007 Jun 15;257(1-2):221-39. doi: 10.1016/j.jns.2007.01.033. Epub 2007 Apr 25.
10
Risk is in the air: an intranasal MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) rat model of Parkinson's disease.风险就在空气中:帕金森病的鼻腔内注射MPTP(1-甲基-4-苯基-1,2,3,6-四氢吡啶)大鼠模型。
Ann N Y Acad Sci. 2009 Jul;1170:629-36. doi: 10.1111/j.1749-6632.2009.03885.x.

引用本文的文献

1
Multi-Omics Analysis Reveals Aberrant Gut-Metabolome-Immune Network in Schizophrenia.多组学分析揭示精神分裂症中肠道代谢组-免疫网络的异常
Front Immunol. 2022 Mar 3;13:812293. doi: 10.3389/fimmu.2022.812293. eCollection 2022.
2
Nicotinamide restricts neural precursor proliferation to enhance catecholaminergic neuronal subtype differentiation from mouse embryonic stem cells.烟酰胺限制神经前体细胞增殖,以增强小鼠胚胎干细胞中儿茶酚胺能神经元亚型的分化。
PLoS One. 2020 Sep 14;15(9):e0233477. doi: 10.1371/journal.pone.0233477. eCollection 2020.
3
The 4 D's of Pellagra and Progress.
糙皮病的“4D”与进展
Int J Tryptophan Res. 2020 Apr 16;13:1178646920910159. doi: 10.1177/1178646920910159. eCollection 2020.
4
The Influence of Nicotinamide on Health and Disease in the Central Nervous System.烟酰胺对中枢神经系统健康与疾病的影响。
Int J Tryptophan Res. 2018 May 21;11:1178646918776658. doi: 10.1177/1178646918776658. eCollection 2018.
5
Meat Intake and the Dose of Vitamin B - Nicotinamide: Cause of the Causes of Disease Transitions, Health Divides, and Health Futures?肉类摄入量与维生素B-烟酰胺剂量:疾病转变、健康差距及健康未来的成因之成因?
Int J Tryptophan Res. 2017 May 3;10:1178646917704662. doi: 10.1177/1178646917704662. eCollection 2017.
6
Activation of the nicotinamide N-methyltransferase (NNMT)-1-methylnicotinamide (MNA) pathway in pulmonary hypertension.肺动脉高压中烟酰胺N-甲基转移酶(NNMT)-1-甲基烟酰胺(MNA)途径的激活。
Respir Res. 2016 Aug 31;17(1):108. doi: 10.1186/s12931-016-0423-7.
7
Down-regulation of nicotinamide N-methyltransferase induces apoptosis in human breast cancer cells via the mitochondria-mediated pathway.烟酰胺N-甲基转移酶的下调通过线粒体介导的途径诱导人乳腺癌细胞凋亡。
PLoS One. 2014 Feb 18;9(2):e89202. doi: 10.1371/journal.pone.0089202. eCollection 2014.
8
Nicotinamide, NAD(P)(H), and Methyl-Group Homeostasis Evolved and Became a Determinant of Ageing Diseases: Hypotheses and Lessons from Pellagra.烟酰胺、NAD(P)(H)与甲基基团稳态的演变及其成为衰老相关疾病的决定因素:来自糙皮病的假说与启示
Curr Gerontol Geriatr Res. 2012;2012:302875. doi: 10.1155/2012/302875. Epub 2012 Mar 21.
9
Effects of N1-methylnicotinamide on oxidative and glycooxidative stress markers in rats with streptozotocin-induced diabetes mellitus.N1-甲基烟酰胺对链脲佐菌素诱导的糖尿病大鼠氧化和糖基化应激标志物的影响。
Redox Rep. 2012;17(1):1-7. doi: 10.1179/1351000211Y.0000000016.
10
Dietary and genetic compromise in folate availability reduces acetylcholine, cognitive performance and increases aggression: critical role of S-adenosyl methionine.叶酸可利用性方面的饮食和基因缺陷会减少乙酰胆碱、降低认知能力并增加攻击性:S-腺苷甲硫氨酸的关键作用。
J Nutr Health Aging. 2008 Apr;12(4):252-61. doi: 10.1007/BF02982630.