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Molecular and Cellular Exercise Physiology in Metabolism 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (20 January 2024) | Viewed by 8754

Special Issue Editor

Department of Molecular Medicine, College of Medicine, Gachon University, Incheon 21565, Republic of Korea
Interests: exercise; mitochondria; metabolism; metabolic disease; aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues

Exercise is one of the major strategies to protect and improve metabolic disease induced by a sedentary lifestyle, abnormal diet, and aging. People perform various exercise types, leading to numerous molecular and cellular alterations. These changes enhance cellular metabolism and functions in tissues including skeletal muscle, liver, heart, adipose tissue, brain, and others. Exercise also enhances the interplay between cells, tissues, organs, and systems. Numerous molecules are involved in the interaction, and their crosstalk can facilitate metabolic rate and function to support energy in contracting muscle. In addition, regular exercise training leads to molecular and cellular adaptations, which can help to protect and improve health against various diseases. Understanding molecular and cellular mechanisms that are induced by various exercise types can provide more advanced treatment to improve sports performance or health. In addition, the exercise-induced molecular pathway can be targeted to prevent and treat metabolic disease patients who are unable to perform exercise training regularly. We are interested in metabolic molecules, such as PPARβ/δ, PGC-1α, AMPK, and any other molecules that are linked to metabolic function. We are also interested in not only mitochondrial function that is induced by a specific molecule with exercise but also certain metabolites, anti-inflammatory peptides, and RNA species, termed as exerkines, that are released in response to exercise and which could promote healthy systemic energy homeostasis via signaling and interplay between cells, tissues, and organs.

Thus, this Special Issue entitled ‘Molecular and Cellular Exercise Physiology in Metabolism’ will discuss the recent advances in metabolic molecular mechanisms that are induced by exercise to understand exercise physiology and treat a health problem. Topics related to both original and reviewed articles are welcome.

Dr. Jin-Ho Koh
Guest Editor

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Keywords

  • exercise
  • physiology
  • metabolism
  • molecular mechanisms
  • mitochondria
  • exerkine
  • metabolic disease
  • health
  • aging

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Related Special Issue

Published Papers (3 papers)

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Review

18 pages, 1205 KiB  
Review
Mitochondria-Associated Membranes as Key Regulators in Cellular Homeostasis and the Potential Impact of Exercise on Insulin Resistance
by Xi Li, Yangjun Yang, Xiaoyu Shi, Zhe Zhang and Shuzhe Ding
Int. J. Mol. Sci. 2024, 25(6), 3196; https://doi.org/10.3390/ijms25063196 - 11 Mar 2024
Cited by 1 | Viewed by 1592
Abstract
The communication between mitochondria and the endoplasmic reticulum (ER) is facilitated by a dynamic membrane structure formed by protein complexes known as mitochondria-associated membranes (MAMs). The structural and functional integrity of MAMs is crucial for insulin signal transduction, relying heavily on their regulation [...] Read more.
The communication between mitochondria and the endoplasmic reticulum (ER) is facilitated by a dynamic membrane structure formed by protein complexes known as mitochondria-associated membranes (MAMs). The structural and functional integrity of MAMs is crucial for insulin signal transduction, relying heavily on their regulation of intracellular calcium homeostasis, lipid homeostasis, mitochondrial quality control, and endoplasmic reticulum stress (ERS). This article reviews recent research findings, suggesting that exercise may promote the remodeling of MAMs structure and function by modulating the expression of molecules associated with their structure and function. This, in turn, restores cellular homeostasis and ultimately contributes to the amelioration of insulin resistance (IR). These insights provide additional possibilities for the study and treatment of insulin resistance-related metabolic disorders such as obesity, diabetes, fatty liver, and atherosclerosis. Full article
(This article belongs to the Special Issue Molecular and Cellular Exercise Physiology in Metabolism 2.0)
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17 pages, 2094 KiB  
Review
Research Progress on Lipophagy-Mediated Exercise Intervention in Non-Alcoholic Fatty Liver Disease
by Xi Li, Yangjun Yang, Yi Sun and Shuzhe Ding
Int. J. Mol. Sci. 2024, 25(6), 3153; https://doi.org/10.3390/ijms25063153 - 9 Mar 2024
Cited by 3 | Viewed by 1431
Abstract
Lipophagy is a cellular pathway targeting the lysosomal degradation of lipid droplets, playing a role in promoting lipid turnover and renewal. Abnormal lipophagy processes can lead to the occurrence and development of non-alcoholic fatty liver disease (NAFLD), characterized by the deposition of lipid [...] Read more.
Lipophagy is a cellular pathway targeting the lysosomal degradation of lipid droplets, playing a role in promoting lipid turnover and renewal. Abnormal lipophagy processes can lead to the occurrence and development of non-alcoholic fatty liver disease (NAFLD), characterized by the deposition of lipid droplets (LDs) in the liver. The importance of exercise training in preventing and improving NAFLD has been well-established, but the exact mechanisms remain unclear. Recent research findings suggest that lipophagy may serve as a crucial hub for liver lipid turnover under exercise conditions. Exercise may alleviate hepatic lipid accumulation and mitigate inflammatory responses and fibrosis through lipophagy, thereby improving the onset and progression of NAFLD. Full article
(This article belongs to the Special Issue Molecular and Cellular Exercise Physiology in Metabolism 2.0)
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21 pages, 2164 KiB  
Review
Exercise-Induced Adipose Tissue Thermogenesis and Browning: How to Explain the Conflicting Findings?
by Yupeng Zhu, Zhengtang Qi and Shuzhe Ding
Int. J. Mol. Sci. 2022, 23(21), 13142; https://doi.org/10.3390/ijms232113142 - 28 Oct 2022
Cited by 10 | Viewed by 4994
Abstract
Brown adipose tissue (BAT) has been widely studied in targeting against metabolic diseases such as obesity, type 2 diabetes and insulin resistance due to its role in nutrient metabolism and energy regulation. Whether exercise promotes adipose tissue thermogenesis and browning remains controversial. The [...] Read more.
Brown adipose tissue (BAT) has been widely studied in targeting against metabolic diseases such as obesity, type 2 diabetes and insulin resistance due to its role in nutrient metabolism and energy regulation. Whether exercise promotes adipose tissue thermogenesis and browning remains controversial. The results from human and rodent studies contradict each other. In our opinion, fat thermogenesis or browning promoted by exercise should not be a biomarker of health benefits, but an adaptation under the stress between body temperature regulation and energy supply and expenditure of multiple organs. In this review, we discuss some factors that may contribute to conflicting experimental results, such as different thermoneutral zones, gender, training experience and the heterogeneity of fat depots. In addition, we explain that a redox state in cells potentially causes thermogenesis heterogeneity and different oxidation states of UCP1, which has led to the discrepancies noted in previous studies. We describe a network by which exercise orchestrates the browning and thermogenesis of adipose tissue with total energy expenditure through multiple organs (muscle, brain, liver and adipose tissue) and multiple pathways (nerve, endocrine and metabolic products), providing a possible interpretation for the conflicting findings. Full article
(This article belongs to the Special Issue Molecular and Cellular Exercise Physiology in Metabolism 2.0)
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