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Nicotine rebalances NAD(+) homeostasis and improves aging-related symptoms in male mice by enhancing NAMPT activity
Imbalances in NAD(+) homeostasis have been linked to aging and various diseases. Nicotine, a metabolite of the NAD(+) metabolic pathway, has been found to possess anti-inflammatory and neuroprotective properties, yet the underlying molecular mechanisms remained unknown. Here we find that, independen...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9935903/ https://www.ncbi.nlm.nih.gov/pubmed/36797299 http://dx.doi.org/10.1038/s41467-023-36543-8 |
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author | Yang, Liang Shen, Junfeng Liu, Chunhua Kuang, Zhonghua Tang, Yong Qian, Zhengjiang Guan, Min Yang, Yongfeng Zhan, Yang Li, Nan Li, Xiang |
author_facet | Yang, Liang Shen, Junfeng Liu, Chunhua Kuang, Zhonghua Tang, Yong Qian, Zhengjiang Guan, Min Yang, Yongfeng Zhan, Yang Li, Nan Li, Xiang |
author_sort | Yang, Liang |
collection | PubMed |
description | Imbalances in NAD(+) homeostasis have been linked to aging and various diseases. Nicotine, a metabolite of the NAD(+) metabolic pathway, has been found to possess anti-inflammatory and neuroprotective properties, yet the underlying molecular mechanisms remained unknown. Here we find that, independent of nicotinic acetylcholine receptors, low-dose nicotine can restore the age-related decline of NAMPT activity through SIRT1 binding and subsequent deacetylation of NAMPT, thus increasing NAD(+) synthesis. (18)F-FDG PET imaging revealed that nicotine is also capable of efficiently inhibiting glucose hypermetabolism in aging male mice. Additionally, nicotine ameliorated cellular energy metabolism disorders and deferred age-related deterioration and cognitive decline by stimulating neurogenesis, inhibiting neuroinflammation, and protecting organs from oxidative stress and telomere shortening. Collectively, these findings provide evidence for a mechanism by which low-dose nicotine can activate NAD(+) salvage pathways and improve age-related symptoms. |
format | Online Article Text |
id | pubmed-9935903 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-99359032023-02-18 Nicotine rebalances NAD(+) homeostasis and improves aging-related symptoms in male mice by enhancing NAMPT activity Yang, Liang Shen, Junfeng Liu, Chunhua Kuang, Zhonghua Tang, Yong Qian, Zhengjiang Guan, Min Yang, Yongfeng Zhan, Yang Li, Nan Li, Xiang Nat Commun Article Imbalances in NAD(+) homeostasis have been linked to aging and various diseases. Nicotine, a metabolite of the NAD(+) metabolic pathway, has been found to possess anti-inflammatory and neuroprotective properties, yet the underlying molecular mechanisms remained unknown. Here we find that, independent of nicotinic acetylcholine receptors, low-dose nicotine can restore the age-related decline of NAMPT activity through SIRT1 binding and subsequent deacetylation of NAMPT, thus increasing NAD(+) synthesis. (18)F-FDG PET imaging revealed that nicotine is also capable of efficiently inhibiting glucose hypermetabolism in aging male mice. Additionally, nicotine ameliorated cellular energy metabolism disorders and deferred age-related deterioration and cognitive decline by stimulating neurogenesis, inhibiting neuroinflammation, and protecting organs from oxidative stress and telomere shortening. Collectively, these findings provide evidence for a mechanism by which low-dose nicotine can activate NAD(+) salvage pathways and improve age-related symptoms. Nature Publishing Group UK 2023-02-17 /pmc/articles/PMC9935903/ /pubmed/36797299 http://dx.doi.org/10.1038/s41467-023-36543-8 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Yang, Liang Shen, Junfeng Liu, Chunhua Kuang, Zhonghua Tang, Yong Qian, Zhengjiang Guan, Min Yang, Yongfeng Zhan, Yang Li, Nan Li, Xiang Nicotine rebalances NAD(+) homeostasis and improves aging-related symptoms in male mice by enhancing NAMPT activity |
title | Nicotine rebalances NAD(+) homeostasis and improves aging-related symptoms in male mice by enhancing NAMPT activity |
title_full | Nicotine rebalances NAD(+) homeostasis and improves aging-related symptoms in male mice by enhancing NAMPT activity |
title_fullStr | Nicotine rebalances NAD(+) homeostasis and improves aging-related symptoms in male mice by enhancing NAMPT activity |
title_full_unstemmed | Nicotine rebalances NAD(+) homeostasis and improves aging-related symptoms in male mice by enhancing NAMPT activity |
title_short | Nicotine rebalances NAD(+) homeostasis and improves aging-related symptoms in male mice by enhancing NAMPT activity |
title_sort | nicotine rebalances nad(+) homeostasis and improves aging-related symptoms in male mice by enhancing nampt activity |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9935903/ https://www.ncbi.nlm.nih.gov/pubmed/36797299 http://dx.doi.org/10.1038/s41467-023-36543-8 |
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