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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...

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Detalles Bibliográficos
Autores principales: Yang, Liang, Shen, Junfeng, Liu, Chunhua, Kuang, Zhonghua, Tang, Yong, Qian, Zhengjiang, Guan, Min, Yang, Yongfeng, Zhan, Yang, Li, Nan, Li, Xiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2023
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
Descripción
Sumario: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.