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Diet, Exercise, and the Metabolic Syndrome: Enrollment of Mitochondrial Machinery

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

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 17269

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Special Issue Editors

Dr. Elena Silvestri

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Guest Editor

Department of Science and Technologies, University of Sannio, 82100 Benevento, Italy
Interests: metabolism; body adiposity; insulin sensitivity; thyroid hormone; mitochondria
Special Issues, Collections and Topics in MDPI journals

Dr. Antonia Giacco

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Guest Editor

Department of Science and Technology, University of Sannio, Via De Sanctis snc, I-82100 Benevento, Italy
Interests: exercise; diet; diabetes; thyroid hormones; skeletal muscle; mitichondria; obesity; metabolism; NAFLD

Special Issue Information

Dear Colleagues,

The aim of this Special Issue on “Diet, Exercise, and the Metabolic Syndrome: Enrollment of Mitochondrial Machinery” is to collect new information on the biochemical and molecular links between metabolic disturbances, mitochondrial structural/functional changes, and lifestyle interventions which remain not completely understood today and urgently need further investigation.

Mitochondria are the powerhouses of the cell and play a key role in maintaining homeostasis by finely regulating the balance between energy storage and energy expenditure. The physiological and flexible adaptation of mitochondria to either caloric excess or caloric restriction, and in times of either low or high energy demand, such as during exercise, requires the intricate modulation of mitochondrial biogenesis, bioenergetics, and dynamics, which in turn determine ATP production, intracellular Ca2+ regulation, reactive oxygen species production and scavenging, and regulation of apoptotic cell death. Systemically, in districts such as liver, adipose tissues, skeletal muscle, and the brain, within a complex intra- and inter-organ communication, the network of mitochondria and their closely interacting metabolic enzymes (e.g., AMPK, mTOR, sirtuins) and transcription factors (e.g., PGC1α, TFAM) orchestrate nutrient sensing, uptake, transport, storage, and usage.

Genetic as well as environmental factor-dependent dysfunction of such a system has been reported to result in detrimental effects on lipid metabolism, insulin sensitivity, oxidative capacity, and thermogenesis, all known pathological causes of increased risk to develop the escalating condition of metabolic syndrome and type 2 diabetes mellitus.

Thus, this Special Issue will focus on whether and how healthy diet and exercise are useful approaches to prevent and/or counteract metabolic diseases with emphasis on the impacts of dietary composition, feeding frequency, exercise training, and bioactive compounds, on the mitochondrial compartment in metabolically active tissues. We outline the importance of the expected contributions in furnishing new perspectives for translational interventions in specific targeting of metabolic diseases.

Prof. Dr. Elena Silvestri
Dr. Antonia Giacco
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

obesity
NAFLD
insulin resistance
endurance/resistance training
caloric restriction
fasting
Mediterranean diet
oxidative stress
autophagy
hormones
appetite regulation

Published Papers (5 papers)

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Editorial

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6 pages, 232 KiB

Open AccessEditorial

Diet, Exercise, and the Metabolic Syndrome: Enrollment of the Mitochondrial Machinery

by Elena Silvestri and Antonia Giacco

Nutrients 2022, 14(21), 4519; https://doi.org/10.3390/nu14214519 - 27 Oct 2022

Cited by 3 | Viewed by 1486

Abstract

Metabolic syndrome (MS), a cluster of metabolic risk factors, ranging from abdominal obesity, dyslipidaemia, hypertension, type 2 diabetes and non-alcoholic fatty liver disease [...] Full article

(This article belongs to the Special Issue Diet, Exercise, and the Metabolic Syndrome: Enrollment of Mitochondrial Machinery)

Research

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15 pages, 2394 KiB

Open AccessArticle

Resistance Exercise Training Improves Metabolic and Inflammatory Control in Adipose and Muscle Tissues in Mice Fed a High-Fat Diet

by Pauline S. Effting, Anand Thirupathi, Alexandre P. Müller, Bárbara C. Pereira, Diane M. Sepa-Kishi, Luis F. B. Marqueze, Franciane T. F. Vasconcellos, Renata T. Nesi, Talita C. B. Pereira, Luiza W. Kist, Maurício R. Bogo, Rolando B. Ceddia and Ricardo A. Pinho

Nutrients 2022, 14(11), 2179; https://doi.org/10.3390/nu14112179 - 24 May 2022

Cited by 7 | Viewed by 2493

Abstract

This study investigates whether ladder climbing (LC), as a model of resistance exercise, can reverse whole-body and skeletal muscle deleterious metabolic and inflammatory effects of high-fat (HF) diet-induced obesity in mice. To accomplish this, Swiss mice were fed for 17 weeks either standard chow (SC) or an HF diet and then randomly assigned to remain sedentary or to undergo 8 weeks of LC training with progressive increases in resistance weight. Prior to beginning the exercise intervention, HF-fed animals displayed a 47% increase in body weight (BW) and impaired ability to clear blood glucose during an insulin tolerance test (ITT) when compared to SC animals. However, 8 weeks of LC significantly reduced BW, adipocyte size, as well as glycemia under fasting and during the ITT in HF-fed rats. LC also increased the phosphorylation of Akt_Ser473 and AMPK_Thr172 and reduced tumor necrosis factor-alpha (TNF-α) and interleukin 1 beta (IL1-β) contents in the quadriceps muscles of HF-fed mice. Additionally, LC reduced the gene expression of inflammatory markers and attenuated HF-diet-induced NADPH oxidase subunit gp91phox in skeletal muscles. LC training was effective in reducing adiposity and the content of inflammatory mediators in skeletal muscle and improved whole-body glycemic control in mice fed an HF diet. Full article

(This article belongs to the Special Issue Diet, Exercise, and the Metabolic Syndrome: Enrollment of Mitochondrial Machinery)

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17 pages, 2496 KiB

Open AccessArticle

Mild Endurance Exercise during Fasting Increases Gastrocnemius Muscle and Prefrontal Cortex Thyroid Hormone Levels through Differential BHB and BCAA-Mediated BDNF-mTOR Signaling in Rats

by Antonia Giacco, Federica Cioffi, Arianna Cuomo, Roberta Simiele, Rosalba Senese, Elena Silvestri, Angela Amoresano, Carolina Fontanarosa, Giuseppe Petito, Maria Moreno, Antonia Lanni, Assunta Lombardi and Pieter de Lange

Nutrients 2022, 14(6), 1166; https://doi.org/10.3390/nu14061166 - 10 Mar 2022

Cited by 5 | Viewed by 3965

Abstract

Mild endurance exercise has been shown to compensate for declined muscle quality and may positively affect the brain under conditions of energy restriction. Whether this involves brain-derived neurotrophic factor (BDNF) and mammalian target of rapamycin (mTOR) activation in relation to central and peripheral tissue levels of associated factors such as beta hydroxy butyrate (BHB), branched-chain amino acids (BCAA) and thyroid hormone (T3) has not been studied. Thus, a subset of male Wistar rats housed at thermoneutrality that were fed or fasted was submitted to 30-min-mild treadmill exercise bouts (five in total, twice daily, 15 m/min, 0° inclination) over a period of 66 h. Prefrontal cortex and gastrocnemius muscle BHB, BCAA, and thyroid hormone were measured by LC-MS/MS analysis and were related to BDNF and mammalian target of rapamycin (mTOR) signaling. In gastrocnemius muscle, mild endurance exercise during fasting maintained the fasting-induced elevated BHB levels and BDNF-CREB activity and unlocked the downstream Akt-mTORC1 pathway associated with increased tissue BCAA. Consequently, deiodinase 3 mRNA levels decreased whereas increased phosphorylation of the mTORC2 target FOXO1 was associated with increased deiodinase 2 mRNA levels, accounting for the increased T3 tissue levels. These events were related to increased expression of CREB and T3 target genes beneficial for muscle quality previously observed in this condition. In rat L6 myoblasts, BHB directly induced BDNF transcription and maturation. Mild endurance exercise during fasting did not increase prefrontal cortex BHB levels nor was BDNF activated, whereas increased leucine levels were associated with Akt-independent increased phosphorylation of the mTORC1 target P70S6K. The associated increased T3 levels modulated the expression of known T3-target genes involved in brain tissue maintenance. Our observation that mild endurance exercise modulates BDNF, mTOR and T3 during fasting provides molecular clues to explain the observed beneficial effects of mild endurance exercise in settings of energy restriction. Full article

(This article belongs to the Special Issue Diet, Exercise, and the Metabolic Syndrome: Enrollment of Mitochondrial Machinery)

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18 pages, 3175 KiB

Open AccessArticle

Elovl2-Ablation Leads to Mitochondrial Membrane Fatty Acid Remodeling and Reduced Efficiency in Mouse Liver Mitochondria

by Alexia Gómez Rodríguez, Emanuela Talamonti, Alba Naudi, Anastasia V. Kalinovich, Anna M. Pauter, Gustavo Barja, Tore Bengtsson, Anders Jacobsson, Reinald Pamplona and Irina G. Shabalina

Nutrients 2022, 14(3), 559; https://doi.org/10.3390/nu14030559 - 27 Jan 2022

Cited by 6 | Viewed by 4012

Abstract

The fatty acid elongase elongation of very long-chain fatty acids protein 2 (ELOVL2) controls the elongation of polyunsaturated fatty acids (PUFA) producing precursors for omega-3, docosahexaenoic acid (DHA), and omega-6, docosapentaenoic acid (DPAn-6) in vivo. Expectedly, Elovl2-ablation drastically reduced the DHA and DPAn-6 in liver mitochondrial membranes. Unexpectedly, however, total PUFAs levels decreased further than could be explained by Elovl2 ablation. The lipid peroxidation process was not involved in PUFAs reduction since malondialdehyde-lysine (MDAL) and other oxidative stress biomarkers were not enhanced. The content of mitochondrial respiratory chain proteins remained unchanged. Still, membrane remodeling was associated with the high voltage-dependent anion channel (VDAC) and adenine nucleotide translocase 2 (ANT2), a possible reflection of the increased demand on phospholipid transport to the mitochondria. Mitochondrial function was impaired despite preserved content of the respiratory chain proteins and the absence of oxidative damage. Oligomycin-insensitive oxygen consumption increased, and coefficients of respiratory control were reduced by 50%. The mitochondria became very sensitive to fatty acid-induced uncoupling and permeabilization, where ANT2 is involved. Mitochondrial volume and number of peroxisomes increased as revealed by transmission electron microscopy. In conclusion, the results imply that endogenous DHA production is vital for the normal function of mouse liver mitochondria and could be relevant not only for mice but also for human metabolism. Full article

(This article belongs to the Special Issue Diet, Exercise, and the Metabolic Syndrome: Enrollment of Mitochondrial Machinery)

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Review

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19 pages, 1165 KiB

Open AccessReview

Nutrients, Physical Activity, and Mitochondrial Dysfunction in the Setting of Metabolic Syndrome

by Gabriela de Oliveira Lemos, Raquel Susana Torrinhas and Dan Linetzky Waitzberg

Nutrients 2023, 15(5), 1217; https://doi.org/10.3390/nu15051217 - 28 Feb 2023

Cited by 9 | Viewed by 4250

Abstract

Metabolic syndrome (MetS) is a cluster of metabolic risk factors for diabetes, coronary heart disease, non-alcoholic fatty liver disease, and some tumors. It includes insulin resistance, visceral adiposity, hypertension, and dyslipidemia. MetS is primarily linked to lipotoxicity, with ectopic fat deposition from fat storage exhaustion, more than obesity per se. Excessive intake of long-chain saturated fatty acid and sugar closely relates to lipotoxicity and MetS through several pathways, including toll-like receptor 4 activation, peroxisome proliferator-activated receptor-gamma regulation (PPARγ), sphingolipids remodeling, and protein kinase C activation. These mechanisms prompt mitochondrial dysfunction, which plays a key role in disrupting the metabolism of fatty acids and proteins and in developing insulin resistance. By contrast, the intake of monounsaturated, polyunsaturated, and medium-chain saturated (low-dose) fatty acids, as well as plant-based proteins and whey protein, favors an improvement in sphingolipid composition and metabolic profile. Along with dietary modification, regular exercises including aerobic, resistance, or combined training can target sphingolipid metabolism and improve mitochondrial function and MetS components. This review aimed to summarize the main dietary and biochemical aspects related to the physiopathology of MetS and its implications for mitochondrial machinery while discussing the potential role of diet and exercise in counteracting this complex clustering of metabolic dysfunctions. Full article

(This article belongs to the Special Issue Diet, Exercise, and the Metabolic Syndrome: Enrollment of Mitochondrial Machinery)

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