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Nutrients
Special Issues
Healthy Aging through Nutrition and Exercise
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Healthy Aging through Nutrition and Exercise

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

Deadline for manuscript submissions: closed (25 April 2024) | Viewed by 1729

Special Issue Editors

Dr. Isabel Iguacel

E-Mail Website
Guest Editor
Faculty of Health Sciences, University of Zaragoza, 50009 Zaragoza, Spain
Interests: public health; epidemiology; social vulnerabilities; disparities; diet
Dr. David Navarrete Villanueva

E-Mail Website
Co-Guest Editor
Faculty of Health Sciences, University of Zaragoza, 50009 Zaragoza, Spain
Interests: healthy ageing; frailty; health disparities; physical exercise
Dr. Ana Moradell Fernández

E-Mail Website
Co-Guest Editor
GENuD Research Group, University of Zaragoza, 50009 Zaragoza, Spain
Interests: healthy ageing; nutrition; body composition

Special Issue Information

Dear Colleagues,

Research on the effects of diet and physical activity on the aging process is crucial to enhancing the quality of life for the elderly, addressing the challenges posed by an aging population, and mitigating the burden on healthcare systems. Aging is often accompanied by a decline in physical function, increased susceptibility to chronic diseases, and a decrease in overall well-being. Studies show that adopting a balanced diet rich in essential nutrients and engaging in regular exercise can help older adults maintain their mobility, cognitive function, and emotional health, contributing to an improved quality of life. However, this area continues to have some knowledge gaps. Each individual's aging process is unique, influenced by genetics, environment, and lifestyle. Investigating the personalized effects of nutrition and exercise can lead to tailored recommendations that optimize healthspan (the period of life spent in good health) based on an individual's specific needs and circumstances.

Moreover, by promoting healthy aging, research can potentially reduce the financial burden on healthcare systems by preventing or delaying the onset of chronic diseases and their related healthcare expenses.

Thus, this Special Issue aims to develop scientific advancements in the knowledge of the complex interactions between nutrition, exercise, genetics, and aging. This knowledge can drive the development of innovative interventions, pharmaceuticals, and technologies aimed at extending healthy lifespans.

Dr. Isabel Iguacel
Dr. David Navarrete Villanueva
Dr. Ana Moradell Fernández
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • fitness
  • body composition
  • physical activity
  • physical exercise
  • frailty

Published Papers (1 paper)

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Research

19 pages, 4463 KiB  
Article
Vitamin D3 Exerts Beneficial Effects on C2C12 Myotubes through Activation of the Vitamin D Receptor (VDR)/Sirtuins (SIRT)1/3 Axis
by Nurul Fatihah Talib, Zunshu Zhu and Kyoung-Soo Kim
Nutrients 2023, 15(22), 4714; https://doi.org/10.3390/nu15224714 - 07 Nov 2023
Viewed by 1442
Abstract
The onset of sarcopenia is associated with a decline in vitamin D receptor (VDR) expression, wherein reduced VDR levels contribute to muscle atrophy, while heightened expression promotes muscle hypertrophy. Like VDR, the age-related decline in protein deacetylase sirtuin (SIRT) expression is linked to [...] Read more.
The onset of sarcopenia is associated with a decline in vitamin D receptor (VDR) expression, wherein reduced VDR levels contribute to muscle atrophy, while heightened expression promotes muscle hypertrophy. Like VDR, the age-related decline in protein deacetylase sirtuin (SIRT) expression is linked to the development of sarcopenia and age-related muscle dysfunction. This study aimed to investigate whether the VDR agonist 1,25-dihydroxyvitamin D3 (1,25VD3) exerts beneficial effects on muscles through interactions with sirtuins and, if so, the underlying molecular mechanisms. Treatment of 1,25VD3 in differentiating C2C12 myotubes substantially elevated VDR, SIRT1, and SIRT3 expression, enhancing their differentiation. Furthermore, 1,25VD3 significantly enhanced the expression of key myogenic markers, including myosin heavy chain (MyHC) proteins, MyoD, and MyoG, and increased the phosphorylation of AMPK and AKT. Conversely, VDR knockdown resulted in myotube atrophy and reduced SIRT1 and SIRT3 levels. In a muscle-wasting model triggered by IFN-γ/TNF-α in C2C12 myotubes, diminished VDR, SIRT1, and SIRT3 levels led to skeletal muscle atrophy and apoptosis. 1,25VD3 downregulated the increased expression of muscle atrophy-associated proteins, including FoxO3a, MAFbx, and MuRF1 in an IFN-γ/TNF-α induced atrophy model. Importantly, IFN-γ/TNF-α significantly reduced the mtDNA copy number in the C2C12 myotube, whereas the presence of 1,25VD3 effectively prevented this decrease. These results support that 1,25VD3 could serve as a potential preventive or therapeutic agent against age-related muscle atrophy by enhancing the VDR/SIRT1/SIRT3 axis. Full article
(This article belongs to the Special Issue Healthy Aging through Nutrition and Exercise)
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