ArticleAmerican journal of physiology. Endocrinology and metabolism2013
Mitochondrial uncoupling in skeletal muscle by UCP1 augments energy expenditure and glutathione content while mitigating ROS production.
Article in American journal of physiology. Endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 48 citations in OpenAlex.
- STX4 Is Indispensable for Mitochondrial Homeostasis in Skeletal Muscle.Journal of cachexia, sarcopenia and muscle · 2025Article
- Ventromedial hypothalamic nucleus subset stimulates tissue thermogenesis via preoptic area outputs.Molecular metabolism · 2024Article
- Beneficial Effects of Low-Grade Mitochondrial Stress on Metabolic Diseases and Aging.Yonsei medical journal · 2024Review
- Exercise-Induced Adipose Tissue Thermogenesis and Browning: How to Explain the Conflicting Findings?International journal of molecular sciences · 2022Review
- Hepatocyte Mitochondrial Dynamics and Bioenergetics in Obesity-Related Non-Alcoholic Fatty Liver Disease.Current obesity reports · 2022Review
- Protective Role of Mitochondrial Uncoupling Proteins against Age-Related Oxidative Stress in Type 2 Diabetes Mellitus.Antioxidants (Basel, Switzerland) · 2022Review
- Skeletal Muscle Uncoupling Proteins in Mice Models of Obesity.Metabolites · 2022Review
- Mitochondrial Uncoupling Proteins (UCPs) as Key Modulators of ROS Homeostasis: A Crosstalk between Diabesity and Male Infertility?Antioxidants (Basel, Switzerland) · 2021Review
- The Role of Mitochondrial Adaptation and Metabolic Flexibility in the Pathophysiology of Obesity and Insulin Resistance: an Updated Overview.Current obesity reports · 2021Review
- Management of Oxidative Stress: Crosstalk Between Brown/Beige Adipose Tissues and Skeletal Muscles.Frontiers in physiology · 2021Review
- Restoration of Sarcoplasmic Reticulum CaInternational journal of molecular sciences · 2020Article
- IDH2 Deficiency Is Critical in Myogenesis and Fatty Acid Metabolism in Mice Skeletal Muscle.International journal of molecular sciences · 2020Article
- Predictive and reactive changes in antioxidant defence system in a heterothermic rodent.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2020Article
- Development and thyroid hormone dependence of skeletal muscle mitochondrial function towards birth.The Journal of physiology · 2020Article
- Regulation of Nrf2 by Mitochondrial Reactive Oxygen Species in Physiology and Pathology.Biomolecules · 2020Review
- Uncoupling protein 1 inhibits mitochondrial reactive oxygen species generation and alleviates acute kidney injury.EBioMedicine · 2019Article
- Partial involvement of Nrf2 in skeletal muscle mitohormesis as an adaptive response to mitochondrial uncoupling.Scientific reports · 2018Article
- Mitochondrial dysfunction and insulin resistance: an update.Endocrine connections · 2015Review
- Neuronal UCP1 expression suggests a mechanism for local thermogenesis during hibernation.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Dietary fat overload reprograms brown fat mitochondria.Frontiers in physiology · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Enhancement of proton leaks in muscle tissue represents a potential target for obesity treatment. In this study, we examined the bioenergetic and physiological implications of increased proton leak in skeletal muscle. To induce muscle-specific increases in proton leak, we used mice that selectively express uncoupling protein-1 (UCP1) in skeletal muscle tissue. UCP1 expression in muscle mitochondria was ∼13% of levels in brown adipose tissue (BAT) mitochondria and caused increased GDP-sensitive proton leak. This was associated with an increase in whole body energy expenditure and a decrease in white adipose tissue content. Muscle UCP1 activity had divergent effects on mitochondrial ROS emission and glutathione levels compared with BAT. UCP1 in muscle increased total mitochondrial glutathione levels ∼7.6 fold. Intriguingly, unlike in BAT mitochondria, leak through UCP1 in muscle controlled mitochondrial ROS emission. Inhibition of UCP1 with GDP in muscle mitochondria increased ROS emission ∼2.8-fold relative to WT muscle mitochondria. GDP had no impact on ROS emission from BAT mitochondria from either genotype. Collectively, these findings indicate that selective induction of UCP1-mediated proton leak in muscle can increase whole body energy expenditure and decrease adiposity. Moreover, ectopic UCP1 expression in skeletal muscle can control mitochondrial ROS emission, while it apparently plays no such role in its endogenous tissue, brown fat.
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