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Nutrient Interaction, Metabolic Adaptation and Healthy Aging

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Geriatric Nutrition".

Deadline for manuscript submissions: closed (25 January 2026) | Viewed by 1901

Special Issue Editors


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Guest Editor
National Institute for Nutrition and Health, Chinese Center for Disease Control and Prevention, Beijing 100050, China
Interests: animal experiments on the pathogenesis of diseases (e.g., nutrients, interactions, metabolic reprogramming, mechanisms)

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Guest Editor
School of Public Health, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China
Interests: population epidemiology and cohort studies (e.g., nutritional epidemiology, metabolic dysfunction-associated steatotic liver disease, type 2 diabetes, cardiovascular disease)
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Special Issue Information

Dear Colleagues,

Aging is a complex and multifactorial process that is determined by many factors, including genetic background, metabolic regulation, and external environmental factors. Unhealthy aging is a major risk factor for the development of many diseases, prominently including neurodegenerative disease, cancer, diabetes, and cardiovascular disease. In the central nervous system, microglia can quickly adapt to varying nutrient availability, transitioning from glycolysis to other metabolic pathways such as glutaminolysis under acute stress. Under neuroinflammatory conditions, metabolic reprogramming occurs primarily through a shift from oxidative glycolysis to aerobic glycolysis, essential for proper cytokine release. In tumorigenesis, beyond the metabolic reprogramming of the glucose metabolism, the important role of other amino acids, such as serine, glycine, and methionine, gradually becomes clear. Diabetic neuropathy is often a formidable challenge in the clinical management of diabetes, markedly diminishing the patient's quality of life, and is now liked to toxic sphingolipids caused by metabolic reprogramming due to serine deficiency. Other nutrients, such as elenium and vitamin K, have recently become to be considered as key regulators of ferroptosis—which is a newly identified novel form of regulated, non-apoptotic cell death caused by iron-overload-dependent phospholipid peroxidation—and then influences cell aging, tumorigenesis, and cell death.

We welcome original in vitro, animal, and human studies, as well as reviews of the scholarship around aging. Submissions that address the mechanisms of genetic and epigenetic adaptation and metabolic programming among metabolic pathways, the interactions of nutrients during healthy aging, as well as nutrient imbalance under disease conditions and nutrient rebalancing for disease prevention and treatment are strongly encouraged.

In this Special Issue, we focus on high-quality studies on the interactions and rebalancing of nutrients that benefit healthy aging.

Dr. Zhenwu Huang
Dr. Shunming Zhang
Guest Editors

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Keywords

  • nutrients
  • healthy aging
  • genetic and epigenetic mechanisms
  • metabolic reprogramming
  • interaction
  • intervention

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Published Papers (3 papers)

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Research

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14 pages, 821 KB  
Article
Plasma Phospholipid Biomarkers Related to the Risk of Cognitive Decline in the Elderly: Results from a Cohort Study
by Ting-Ting Liu, Jia-Wei Xie, Xin Long, Xin-Can Yu, Shan-Shan Jia, Qing-Qing Man, Jing Li, Pu-Jun Quan, Ke-Chang Shan, Jian Zhang, Shuang Song and Dan Liu
Nutrients 2026, 18(2), 185; https://doi.org/10.3390/nu18020185 - 6 Jan 2026
Viewed by 385
Abstract
Phospholipids provide both structural and functional varieties for neuro cells, and their dysregulation in brain has been related to pathogenesis of cognitive impairment. The reflection of these phospholipid alterations in the blood might serve as biomarkers for the early recognition of cognitive decline [...] Read more.
Phospholipids provide both structural and functional varieties for neuro cells, and their dysregulation in brain has been related to pathogenesis of cognitive impairment. The reflection of these phospholipid alterations in the blood might serve as biomarkers for the early recognition of cognitive decline risk preceding clinical symptoms and provide potential targets for intervention. In this cohort study, detailed phospholipid molecular profiles including 229 species were quantified. A total of 209 participants aged 60–80 years (including 138 women and 73 men) were followed for one year, during which 32 participants developed significant cognitive decline, defined as a decrease of three or more points in the Montreal Cognitive Assessment score. A biomarker panel of eight phospholipid molecular species related to cognitive decline was identified by Least Absolute Shrinkage and Selection Operator (LASSO) logistic regression between cases and non-cases. Among these, four biomarkers, including PE(O-40:5), LPC(18:3), PI(38:2) and PA(39:4), were further proved to be significantly associated with the risk of cognitive decline through a logistic regression model, indicating that the degradation of phospholipids and the accumulation of ether phospholipid and PI might participate in the process of cognitive decline in early stage. By adding the eight phospholipid biomarkers to a reference model that included demographics, lifestyle, hypertension, fasting blood glucose and blood lipid parameters, the AUC value of the predictive model improved from 0.743 to 0.866, which provided a possible auxiliary screening tool for the early detection of cognitive impairment in the elderly. Full article
(This article belongs to the Special Issue Nutrient Interaction, Metabolic Adaptation and Healthy Aging)
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17 pages, 3096 KB  
Article
Activation of Sirtuin3 by 6,4′-Dihydroxy-7-methoxyflavanone Against Myoblasts Senescence by Attenuating D-Galactose-Induced Oxidative Stress and Inflammation
by Bingsi Li, Yuxuan Gu, Libing Zhou, Rui Chen, Yiwei Liu, Zexuan Wan, Ziyi Liang, Yukang Wang, Renlei Ji and Zhian Liu
Nutrients 2025, 17(20), 3298; https://doi.org/10.3390/nu17203298 - 20 Oct 2025
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Abstract
Background/Objective: Cellular senescence is increasingly recognized as a key mechanism underlying sarcopenia, an age-related muscle disorder with no effective therapeutic. 6,4′-Dihydroxy-7-methoxyflavanone (DMF), a flavonoid isolated from Dalbergia odorifera T. Chen, has shown anti-senescence potential. This study aimed to investigate the protective effects of [...] Read more.
Background/Objective: Cellular senescence is increasingly recognized as a key mechanism underlying sarcopenia, an age-related muscle disorder with no effective therapeutic. 6,4′-Dihydroxy-7-methoxyflavanone (DMF), a flavonoid isolated from Dalbergia odorifera T. Chen, has shown anti-senescence potential. This study aimed to investigate the protective effects of DMF against myoblasts senescence and elucidate the underlying molecular mechanisms. Method: A cellular model of senescence was established in C2C12 myoblasts using D-galactose (D-gal). The effects of DMF pretreatment were evaluated by assessing senescence phenotypes, myogenic differentiation, and mitochondrial function. The role of Sirtuin3 (SIRT3) was confirmed using siRNA-mediated knockdown. Results: DMF Pre-treatment effectively attenuated D-gal-induced senescence, as indicated by restored proliferation, reduced senescence-associated β-galactosidase activity, decreased DNA damage, and the downregulation of p53, p21Cip1/WAF1 and p16INK4a. Furthermore, DMF rescued myogenic differentiation capacity, enhancing the expression of Myoblast determination protein 1, Myogenin, Myosin heavy chain and Muscle-specific regulatory factor 4, and promoting myotube formation. Mechanistically, DMF was identified as a SIRT3 activator. It enhanced SIRT3 expression and activity, leading to the deacetylation and activation of the mitochondrial antioxidant enzyme superoxide dismutase 2. This consequently reduced mitochondrial reactive oxygen species, improved mitochondrial membrane potential and ATP production, and suppressed the NF-κB pathway by inhibiting IκBα phosphorylation and p65 acetylation/nuclear translocation. Crucially, all the beneficial effects of DMF—including oxidative stress reduction, mitochondrial functional recovery, anti-inflammatory action, and ultimately, the attenuation of senescence and improvement of myogenesis—were abolished upon SIRT3 knockdown. Conclusions: Our findings demonstrate that DMF alleviates myoblasts senescence and promotes myogenic differentiation by activating the SIRT3-SOD2 pathway, thereby reducing oxidative stress and NF-κB-driven inflammation responses. DMF emerges as a promising therapeutic candidate for sarcopenia. Full article
(This article belongs to the Special Issue Nutrient Interaction, Metabolic Adaptation and Healthy Aging)
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Review

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24 pages, 2860 KB  
Review
Integrating Sensory Perception and Wearable Monitoring to Promote Healthy Aging: A New Frontier in Nutritional Personalization
by Alessandro Tonacci, Francesca Gorini, Francesco Sansone and Francesca Venturi
Nutrients 2026, 18(2), 214; https://doi.org/10.3390/nu18020214 - 9 Jan 2026
Viewed by 274
Abstract
Aging involves progressive changes in sensory perception, appetite regulation, and metabolic flexibility, which together affect dietary intake, nutrient adequacy, and health-related outcomes. Meanwhile, current wearable technologies allow continuous, minimally invasive monitoring of physiological and behavioral markers relevant to metabolic health, such as physical [...] Read more.
Aging involves progressive changes in sensory perception, appetite regulation, and metabolic flexibility, which together affect dietary intake, nutrient adequacy, and health-related outcomes. Meanwhile, current wearable technologies allow continuous, minimally invasive monitoring of physiological and behavioral markers relevant to metabolic health, such as physical activity, sleep, heart rate variability, glycemic patterns, and so forth. However, digital nutrition approaches have largely focused on physiological signals while underutilizing the sensory dimensions of eating—taste, smell, texture, and hedonic response—that strongly drive dietary intake and adherence. This narrative review synthesizes evidence on the following: (1) age-related sensory changes and their nutritional consequences, (2) metabolic adaptation and markers of resilience in older adults, and (3) current and emerging wearable technologies applicable to nutritional personalization. Following this, we propose an integrative framework linking subjective (implicit) sensory perception and objective (explicit) wearable-derived physiological responses into adaptive feedback loops to support personalized dietary strategies for healthy aging. In this light, we discuss practical applications, technological and methodological challenges, ethical considerations, and research priorities to validate and implement sensory–physiological integrated models. Merging together sensory science and wearable monitoring has the potential to enhance adherence, preserve nutritional status, and bolster metabolic resilience in aging populations, moving nutrition from one-size-fits-all prescriptions toward dynamic, person-centered, sensory-aware interventions. Full article
(This article belongs to the Special Issue Nutrient Interaction, Metabolic Adaptation and Healthy Aging)
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