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These changes enhanced nicotinamide adenine dinucleotide availability, limited ceramide accumulation, and improved energy homeostasis, which are molecular adaptations that correlated with delayed motor decline. Credit: Neuroscience News<\/p>\nSummary: A new study demonstrates that long-term oral nicotine administration reprograms aging-related metabolism and slows motor decline in mice. By targeting the sphingolipid-energy axis, nicotine improved energy homeostasis, preserved gut microbial diversity, and supported neuromuscular resilience.<\/p>\n
Treated mice displayed a biologically younger phenotype based on integrated behavioral and metabolic analysis. The findings suggest nicotine\u2019s molecular pathways may inspire the design of non-addictive compounds to promote healthy aging, though long-term safety in humans remains unresolved.<\/p>\n
Key Facts<\/p>\n
Metabolic Reprogramming: Nicotine altered glycolipid and sphingolipid pathways, improving energy balance.Motor Protection: Mice on nicotine showed delayed age-related motor decline and a biologically younger profile.Therapeutic Potential: Results may guide the development of safer, non-addictive cholinergic modulators for aging interventions.<\/p>\n
Source: SIAT<\/p>\n
Aging is a systemic process marked by energy imbalance and organ-specific metabolic decline, with motor deterioration emerging as a key component of frailty.\u00a0As the global population ages, challenges remain in healthy aging.<\/p>\n
Nicotine is the principal bioactive compound in tobacco. Smoking accelerates metabolic and cardiovascular disease. However, epidemiological studies suggest that\u00a0smokers have\u00a0lower risks of certain neurodegenerative disorders such as Parkinson\u2019s disease. It is unclear that whether nicotine itself can influence aging trajectories.<\/p>\n
These changes enhanced nicotinamide adenine dinucleotide availability, limited ceramide accumulation, and improved energy homeostasis, which are molecular adaptations that correlated with delayed motor decline. Credit: Neuroscience News<\/p>\n
In a study published in\u00a0Advanced Science, a team led by Prof. LIU Xin\u2019an and Prof. CHEN Zuxin at the Shenzhen Institutes of Advanced Technology of the Chinese Academy of Sciences, along with collaborators, for the first time demonstrated that life-long oral nicotine administration reprograms aging-related systemic metabolism via the sphingolipid-energy metabolic axis, and attenuates age-associated motor decline in mice.<\/p>\n
A 22\u2011month longitudinal experiment was conducted to examine the effects of life\u2011long oral nicotine exposure in mice. Moderate or high doses of highly purified nicotine were added to drinking water to mimic plasma concentrations in human smokers but without combustion byproducts.<\/p>\n
Nicotine\u2019s systemic effects on aging were mapped through high\u2011precision three-dimensional (3D) behavioral tracking, multi\u2011organ metabolomics, gut microbiota sequencing, and cell\u2011based assays.<\/p>\n
Researchers discovered that nicotine reprograms aging\u2011associated metabolism in a dose\u2011dependent manner, particularly through glycolipid and sphingolipid pathways.<\/p>\n
These changes enhanced nicotinamide adenine dinucleotide availability, limited ceramide accumulation, and improved energy homeostasis, which are molecular adaptations that correlated with delayed motor decline.<\/p>\n
Longitudinal gut microbiota analysis revealed preserved microbial diversity and the enrichment of sphingolipid\u2011related metabolites linked to sarcopenia prevention. By integrating behavioral and metabolic profiles, researchers developed a \u201cBehavior\u2011Metabolome Age\u201d score, and confirmed that nicotine\u2011treated mice displayed a biologically younger phenotype.<\/p>\n
This study provides the first systemic mapping of nicotine\u2011driven metabolic remodeling during natural aging, and identifies a gut-sphingolipid-energy axis underlying motor function resilience.<\/p>\n
It makes a life\u2011long, dose\u2011dependent assessment of nicotine\u2019s systemic impact, integrates AI-based 3D behavioral and multi\u2011omics data to quantify biological aging, and provides insight into sphingolipid\u2011mediated neuromuscular protection.<\/p>\n
Researchers note that while oral nicotine in this controlled paradigm avoids combustion\u2011related toxicants and may pose lower systemic risks than conventional tobacco products, its long\u2011term safety and complex biological effects warrant careful evaluation.<\/p>\n
The study\u00a0provides a mechanistic framework to evaluate long\u2011term nicotine exposure and inspires the development of \u201cnon\u2011addictive cholinergic metabolic modulators\u201d aimed at sustaining mobility and metabolic health in aging populations.<\/p>\n
Building on years of expertise in metabolism, neurobiology, and inhalable materials, the research team will continue making systematic, forward\u2011looking research to uncover the scientific basis and potential value of nicotine as well as novel aerosolized compounds in aging intervention and metabolic health.<\/p>\n
About this aging, nicotine, and motor decline research news<\/p>\n
Author: Qun LU<\/a>
Source: SIAT<\/a>
Contact: Qun LU \u2013 SIAT
Image: The image is credited to Neuroscience News<\/p>\n