Special Issue "Nutrition and Mitochondrial Function: Role in Health and Disease"

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

Deadline for manuscript submissions: closed (30 October 2021).

Special Issue Editors

Prof. Dr. Alessandra Valerio
E-Mail Website
Guest Editor
Department of Molecular and Translational Medicine, University of Brescia, Brescia, 25123, Italy
Interests: mitochondrial bioenergetics; nutraceuticals; lifestyle medicine; obesity; ageing
Prof. Dr. Enzo Nisoli
E-Mail Website
Guest Editor
Department of Medical Biotechnology & Translational Medicine, University of Milan, Milan 20129, Italy
Interests: nitric oxide and mitochondrial biogenesis; amino acids and metabolic health; role of cytokines in the pathogenesis of obesity and related disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are at the core of normal cellular and organismal metabolic processes. Mitochondrial dysfunction impacts the pathophysiology of primary mitochondrial diseases as well as of many acquired or age-related metabolic disorders, including obesity, diabetes, cardiovascular and neurological disorders, and cancer, among others.

We welcome the submission of manuscripts, either describing original research or reviewing scientific literature. Manuscripts should focus on well-defined topics not conclusively established in the literature, such as (but not limited to):

  • Fasting-mimicking diets and mitochondrial health;
  • Dietary supplements effects on mitochondrial or organismal metabolism;
  • Molecular and mechanistic insights on nutrient restriction or supplementation;
  • Dietary restriction and supplements in childhood, adulthood, and elderly;
  • Food supplements in mitochondrial diseases;
  • Health value of nutrients active on nutrient sensors;
  • Nutrition and gut microbiome interaction;
  • Intervention studies in humans.

Papers covering unsolved aspects of nutrition and mitochondrial metabolism are encouraged, e.g., intermittent fasting regimens, dietary supplements in older adults and critical patients, controversy on glucose homeostasis and amino acid supplements, beneficial and detrimental effects of antioxidants.

Prof. Dr. Alessandra Valerio
Prof. Dr. Enzo Nisoli
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 papers will be 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 monthly 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 2400 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

  • Dietary supplements
  • Protein and amino acid supplementation
  • Antioxidants
  • Mitochondrial biogenesis
  • Mitochondrial bioenergetics
  • Fasting-mimicking diet
  • Metabolic disorders
  • Energy metabolism imbalance
  • Aging
  • Sarcopenia
  • Critical illness
  • Mitochondrial diseases

Published Papers (2 papers)

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Research

Article
L-Arginine Reduces Nitro-Oxidative Stress in Cultured Cells with Mitochondrial Deficiency
Nutrients 2021, 13(2), 534; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13020534 - 06 Feb 2021
Viewed by 1081
Abstract
L-Arginine (L-ARG) supplementation has been suggested as a therapeutic option in several diseases, including Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like syndrome (MELAS), arguably the most common mitochondrial disease. It is suggested that L-ARG, a nitric oxide (NO) precursor, can restore NO levels in [...] Read more.
L-Arginine (L-ARG) supplementation has been suggested as a therapeutic option in several diseases, including Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like syndrome (MELAS), arguably the most common mitochondrial disease. It is suggested that L-ARG, a nitric oxide (NO) precursor, can restore NO levels in blood vessels, improving cerebral blood flow. However, NO also participates in mitochondrial processes, such as mitochondrial biogenesis, the regulation of the respiratory chain, and oxidative stress. This study investigated the effects of L-ARG on mitochondrial function, nitric oxide synthesis, and nitro-oxidative stress in cell lines harboring the MELAS mitochondrial DNA (mtDNA) mutation (m.3243A>G). We evaluated mitochondrial enzyme activity, mitochondrial mass, NO concentration, and nitro-oxidative stress. Our results showed that m.3243A>G cells had increased NO levels and protein nitration at basal conditions. Treatment with L-ARG did not affect the mitochondrial function and mass but reduced the intracellular NO concentration and nitrated proteins in m.3243A>G cells. The same treatment led to opposite effects in control cells. In conclusion, we showed that the main effect of L-ARG was on protein nitration. Lowering protein nitration is probably involved in the mechanism related to L-ARG supplementation benefits in MELAS patients. Full article
(This article belongs to the Special Issue Nutrition and Mitochondrial Function: Role in Health and Disease)
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Article
Preserved Skeletal Muscle Mitochondrial Function, Redox State, Inflammation and Mass in Obese Mice with Chronic Heart Failure
Nutrients 2020, 12(11), 3393; https://0-doi-org.brum.beds.ac.uk/10.3390/nu12113393 - 04 Nov 2020
Cited by 2 | Viewed by 1004
Abstract
Background: Skeletal muscle (SM) mitochondrial dysfunction, oxidative stress, inflammation and muscle mass loss may worsen prognosis in chronic heart failure (CHF). Diet-induced obesity may also cause SM mitochondrial dysfunction as well as oxidative stress and inflammation, but obesity per se may be [...] Read more.
Background: Skeletal muscle (SM) mitochondrial dysfunction, oxidative stress, inflammation and muscle mass loss may worsen prognosis in chronic heart failure (CHF). Diet-induced obesity may also cause SM mitochondrial dysfunction as well as oxidative stress and inflammation, but obesity per se may be paradoxically associated with high SM mass and mitochondrial adenosine triphosphate (ATP) production, as well as with enhanced survival in CHF. Methods: We investigated interactions between myocardial infarction(MI)-induced CHF and diet-induced obesity (12-wk 60% vs. standard 10% fat) in modulating gastrocnemius muscle (GM) mitochondrial ATP and tissue superoxide generation, oxidized glutathione (GSSG), cytokines and insulin signalling activation in 10-wk-old mice in the following groups: lean sham-operated, lean CHF (LCHF), obese CHF (ObCHF; all n = 8). The metabolic impact of obesity per se was investigated by pair-feeding ObCHF to standard diet with stabilized excess body weight until sacrifice at wk 8 post-MI. Results: Compared to sham, LCHF had low GM mass, paralleled by low mitochondrial ATP production and high mitochondrial reative oxygen species (ROS) production, pro-oxidative redox state, pro-inflammatory cytokine changes and low insulin signaling (p < 0.05). In contrast, excess body weight in pair-fed ObCHF was associated with high GM mass, preserved mitochondrial ATP and mitochondrial ROS production, unaltered redox state, tissue cytokines and insulin signaling (p = non significant vs. Sham, p < 0.05 vs. LCHF) despite higher superoxide generation from non-mitochondrial sources. Conclusions: CHF disrupts skeletal muscle mitochondrial function in lean rodents with low ATP and high mitochondrial ROS production, associated with tissue pro-inflammatory cytokine profile, low insulin signaling and muscle mass loss. Following CHF onset, obesity per se is associated with high skeletal muscle mass and preserved tissue ATP production, mitochondrial ROS production, redox state, cytokines and insulin signaling. These paradoxical and potentially favorable obesity-associated metabolic patterns could contribute to reported obesity-induced survival advantage in CHF. Full article
(This article belongs to the Special Issue Nutrition and Mitochondrial Function: Role in Health and Disease)
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