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NAD+ 前体与肠道炎症:涉及肠道微生物组的治疗新视角。

NAD+ Precursors and Intestinal Inflammation: Therapeutic Insights Involving Gut Microbiota.

机构信息

Institut d'Investigació Biomèdica Sant Pau (IIB Sant Pau), 08041 Barcelona, Spain.

Grupo de Obesidad y Metabolismo, Instituto Murciano de Investigación Biosanitaria (IMIB), 30120 Murcia, Spain.

出版信息

Nutrients. 2023 Jun 30;15(13):2992. doi: 10.3390/nu15132992.

DOI:10.3390/nu15132992
PMID:37447318
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10346866/
Abstract

The oxidized form of nicotinamide adenine dinucleotide (NAD+) is a critical metabolite for living cells. NAD+ may act either as a cofactor for many cellular reactions as well as a coenzyme for different NAD+-consuming enzymes involved in the physiological homeostasis of different organs and systems. In mammals, NAD+ is synthesized from either tryptophan or other vitamin B3 intermediates that act as NAD+ precursors. Recent research suggests that NAD+ precursors play a crucial role in maintaining the integrity of the gut barrier. Indeed, its deficiency has been associated with enhanced gut inflammation and leakage, and dysbiosis. Conversely, NAD+-increasing therapies may confer protection against intestinal inflammation in experimental conditions and human patients, with accumulating evidence indicating that such favorable effects could be, at least in part, mediated by concomitant changes in the composition of intestinal microbiota. However, the mechanisms by which NAD+-based treatments affect the microbiota are still poorly understood. In this context, we have focused specifically on the impact of NAD+ deficiency on intestinal inflammation and dysbiosis in animal and human models. We have further explored the relationship between NAD+ and improved host intestinal metabolism and immunity and the composition of microbiota in vivo. Overall, this comprehensive review aims to provide a new perspective on the effect of NAD+-increasing strategies on host intestinal physiology.

摘要

烟酰胺腺嘌呤二核苷酸(NAD+)的氧化形式是活细胞的关键代谢物。NAD+可以作为许多细胞反应的辅助因子,也可以作为参与不同器官和系统生理稳态的不同 NAD+消耗酶的辅酶。在哺乳动物中,NAD+可以由色氨酸或其他维生素 B3 中间体合成,这些中间体作为 NAD+的前体。最近的研究表明,NAD+前体在维持肠道屏障的完整性方面起着至关重要的作用。事实上,其缺乏与增强的肠道炎症和渗漏以及微生物失调有关。相反,在实验条件和人类患者中,增加 NAD+的治疗可能提供对肠道炎症的保护,越来越多的证据表明,这种有利的影响至少部分可以通过肠道微生物组组成的伴随变化来介导。然而,基于 NAD+的治疗方法影响微生物组的机制仍知之甚少。在这种情况下,我们特别关注 NAD+缺乏对动物和人类模型中肠道炎症和微生物失调的影响。我们进一步探讨了 NAD+与改善宿主肠道代谢和免疫以及体内微生物组组成之间的关系。总的来说,这篇综合综述旨在为 NAD+增加策略对宿主肠道生理学的影响提供新的视角。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b86/10346866/1c8a821427d4/nutrients-15-02992-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b86/10346866/f9fbe1b98cea/nutrients-15-02992-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b86/10346866/1c8a821427d4/nutrients-15-02992-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b86/10346866/f9fbe1b98cea/nutrients-15-02992-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b86/10346866/1c8a821427d4/nutrients-15-02992-g002.jpg

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Transpl Immunol. 2023 Jun;78:101835. doi: 10.1016/j.trim.2023.101835. Epub 2023 Apr 7.
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Oral supplementation of nicotinamide riboside alters intestinal microbial composition in rats and mice, but not humans.
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Nicotinamide Mononucleotide Restores NAD Levels to Alleviate LPS-Induced Inflammation via the TLR4/NF-κB/MAPK Signaling Pathway in Mice Granulosa Cells.烟酰胺单核苷酸通过小鼠颗粒细胞中的TLR4/NF-κB/MAPK信号通路恢复NAD水平以减轻脂多糖诱导的炎症。
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