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Metabolic Features and Nutritional Interventions in Chronic Diseases—2nd Edition

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

Deadline for manuscript submissions: 15 December 2025 | Viewed by 392

Special Issue Editors

Department of Nutrition and Health, China Agricultural University, Beijing 100083, China
Interests: metabolic diseases; cancer; aging; molecular nutrition; mitochondrial metabolism; mitochondrial metal ions; mtDNA mutation/editing; ROS; ferroptosis
Special Issues, Collections and Topics in MDPI journals
Beijing Advanced Innovation Center for Food Nutrition and Human Health, Department of Nutrition and Health, China Agricultural University, Beijing 100083, China
Interests: iron metabolism; oxidative stress; intervention strategies; ferroptosis; meta-analysis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolic dysfunction is a hallmark feature of a spectrum of chronic diseases, comprising aging, cancer, and diseases affecting the cardiovascular system, digestive system, and endocrine system. The phenotypes associated with metabolic dysfunction vary depending on disease type and stage. In turn, altered metabolism drives disease progression and incidence. Nutritional interventions, utilizing bioactive compounds or tailored dietary regimens, have emerged as effective strategies to modulate metabolic dysfunctions, thereby mitigating disease progression and improving outcomes. For instance, tailored nutritional intervention in cancers with altered metabolism determines improved therapeutic responses. Additionally, counteracting muscle loss and osteoporosis are clinical goals that can provide nutritional support to an aging population. Mechanistically, nutritional interventions modulate metabolism through mitochondrial homeostasis, metabolic pathway reprogramming, immuno-regulation, and epigenome regulation to impact disease progression and outcome.

This Special Issue aims to provide an interdisciplinary platform covering the following topics:

  1. Characterizing metabolic features and/or nutritional requirements in certain types of chronic disease;
  2. Defining the effects and mechanism of a specific nutrient or nutritional intervention to target metabolism and disease;
  3. Developing new nutritional strategies that improve disease outcomes by altering metabolism.

We invite the submission of well-designed research articles, reviews, and meta-analyses addressing the above issues.

Dr. Yongting Luo
Dr. Junjie Luo
Dr. Peng An
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

  • metabolic features
  • metabolic reprogramming
  • nutritional intervention
  • bioactive nutrients
  • dietary regimen
  • chronic disease
  • metabolic disease
  • cardiovascular disease
  • aging
  • cancer

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Published Papers (1 paper)

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Research

16 pages, 2816 KiB  
Article
Zinc-Enriched Bifidobacterium longum subsp. longum CCFM1195 Alleviates Cutibacterium acnes-Induced Skin Lesions in Mice by Mitigating Inflammatory Responses and Oxidative Stress
by Xiangyue Gu, Botao Wang, Tianmeng Zhang, Qiuxiang Zhang, Bingyong Mao, Xin Tang, Jianxin Zhao and Shumao Cui
Nutrients 2025, 17(11), 1803; https://doi.org/10.3390/nu17111803 - 26 May 2025
Viewed by 334
Abstract
Background: Acne vulgaris, a prevalent inflammatory skin disorder, stems from factors like Cutibacterium acnes overgrowth, inflammation dysregulation, and immune dysfunction. Clinically, acne severity inversely correlates with serum zinc (Zn) levels, and oral Zn supplementation shows efficacy. Lactic acid bacteria are capable of converting [...] Read more.
Background: Acne vulgaris, a prevalent inflammatory skin disorder, stems from factors like Cutibacterium acnes overgrowth, inflammation dysregulation, and immune dysfunction. Clinically, acne severity inversely correlates with serum zinc (Zn) levels, and oral Zn supplementation shows efficacy. Lactic acid bacteria are capable of converting inorganic Zn into organic forms via biological transformation, potentially generating Zn-enriched bacteria as superior Zn delivery vehicles. Methods: In this study, a Zn-deficient acne mouse model was established through dietary Zn restriction combined with intradermal C. acnes injection. The therapeutic effects of orally administered Zn-containing supplements, including Zn-enriched Bifidobacterium longum subsp. longum CCFM1195 (Zn-CCFM1195), were systematically evaluated through multiple parameters: histopathological evaluation of skin lesions, cutaneous inflammatory and oxidative stress markers, serum Zn concentration, and gene expression levels of pathway-associated proteins. Results: Induction of C. acnes led to decreased serum Zn levels (14.98 μmol/L in Control vs. 9.71 μmol/L in Model) and skin metallothionein content, causing Zn imbalance. Zn deficiency caused increased levels of lesion elevation (9.23 in Model vs. 10.53 in Zn-deficient Model), IL-17A, TNF-α, and MMP9 in skin, thereby exacerbating the inflammatory response in C. acnes-induced mice. Zn supplementation alleviated inflammatory responses and oxidative stress in Zn-deficient acne-like mice. Notably, inactivated Zn-CCFM1195 exhibited superior efficacy to ZnSO4, significantly reducing lesion diameter and decreasing cutaneous levels of IL-1β, IL-17A, and MDA while enhancing GSH-Px activity. Similarly, viable Zn-CCFM1195 treatment significantly decreased IL-17A and enhanced GSH-Px activity compared with ZnSO4 treatment. Furthermore, Zn supplementation downregulated the expression of TLR2, IκBα, and IKKβ, which may exert its anti-acne effect by regulating related pathways. Conclusions: Zn deficiency exacerbates skin inflammation, whereas Zn supplementation, particularly with Zn-CCFM1195, alleviates acne vulgaris through anti-inflammatory and antioxidant effects. Full article
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