Mitochondrial Dynamics in the Regulation of Nutrient Utilization and Energy Expenditure
Open accessAbstract
Mitochondrial fusion, fission, and mitophagy form an essential axis of mitochondrial quality control. However, quality control might not be the only task carried out by mitochondrial dynamics. Recent studies link mitochondrial dynamics to the balance between energy demand and nutrient supply, suggesting changes in mitochondrial architecture as a mechanism for bioenergetic adaptation to metabolic demands. By favoring either connected or fragmented architectures, mitochondrial dynamics regulates bioenergetic efficiency and energy expenditure. Placement of bioenergetic adaptation and quality control as competing tasks of mitochondrial dynamics might provide a new mechanism, linking excess nutrient environment to progressive mitochondrial dysfunction, common to age-related diseases.
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Mitochondrial mass is dynamic, and individual organelles can fuse with or shed from the network to meet the metabolic requirements of the cell.
“The mitochondrial mass is dynamic; individual organelles can fuse or shed from the network to address the metabolic requirements of the cell97–99”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [97]
Mitochondrial architectural changes might offer a new molecular mechanism to connect nutrient availability to bioenergetic adaptations.
“Thus, mitochondrial architectural changes might offer a new molecular mechanism to connect nutrient availability to bioenergetic adaptations (Liesa & Shirihai, 2013).”
From Mitochondrial response to nutrient availability and its role in metabolic disease (2014) · cites this paper as Liesa & Shirihai, 2013
Under nutrient scarcity, mitochondrial fusion is typically observed.
“Under these circumstances, mitochondrial fusion is typically observed (Liesa & Shirihai, 2013) (Fig 2A).”
From Mitochondrial response to nutrient availability and its role in metabolic disease (2014) · cites this paper as Liesa & Shirihai, 2013
Mitochondrial fission is induced within minutes after lipid overload in INS-1 cells.
“Along with this fusion deficiency, mitochondrial fission is induced within minutes after a lipid overload in INS-1 cells (Molina et al, 2009; Liesa & Shirihai, 2013) (Fig 3A).”
From Mitochondrial response to nutrient availability and its role in metabolic disease (2014) · cites this paper as Liesa & Shirihai, 2013
Mitochondrial fission events promoted mitochondrial uncoupled respiration.
“These mitochondrial fission events promoted mitochondrial uncoupled respiration (Liesa & Shirihai, 2013; Wikstrom et al, 2014).”
From Mitochondrial response to nutrient availability and its role in metabolic disease (2014) · cites this paper as Liesa & Shirihai, 2013
Mitochondrial uncoupling upon lipid loading may be a way to dissipate energy and prevent detrimental lipid deposition in the cell.
“Irrespective of the mechanism, mitochondrial uncoupling upon lipid loading may be a way to dissipate energy and prevent detrimental lipid deposition in the cell (Liesa & Shirihai, 2013).”
From Mitochondrial response to nutrient availability and its role in metabolic disease (2014) · cites this paper as Liesa & Shirihai, 2013
Lipid overloading promotes fast and transient changes in mitochondrial architecture.
“Lipid overloading promotes fast and transient changes in mitochondrial architecture.”
From Mitochondrial response to nutrient availability and its role in metabolic disease (2014) · cites this paper as Liesa & Shirihai, 2013
Mitochondrial fusion is positively associated with increased energy efficiency and ATP production, while a shift towards fission results in a drop in mitochondrial efficiency and a concomitant increase in ROS production.
“Particularly, mitochondrial fusion is positively associated with increased energy efficiency and ATP production, while a shift towards mitochondrial fission results in a drop in mitochondrial efficiency and a concomitant increase in ROS production (Liesa and Shirihai, 2013; Wai and Langer, 2016; Lin et al., 2018).”
From Mitochondrial (Dys)function and Insulin Resistance: From Pathophysiological Molecular Mechanisms to the Impact of Diet (2019) · cites this paper as Liesa and Shirihai, 2013
Absolute or relative energy deficits, underlain by a drop in ATP levels or an increase in ATP demand, trigger mitochondrial fusion.
“Particularly, absolute or relative energy deficits, underlain by a drop in ATP levels or an increase in ATP demand, trigger mitochondrial fusion (Liesa and Shirihai, 2013; Hesselink et al., 2016)”
From Mitochondrial (Dys)function and Insulin Resistance: From Pathophysiological Molecular Mechanisms to the Impact of Diet (2019) · cites this paper as Liesa and Shirihai, 2013
Fusion and fission cycles are governed by cellular metabolic perturbations and metabolic demand and respond to fluctuations in the energy status of the cell depending on cell type.
“which in turn are governed by cellular metabolic perturbations and metabolic demand (Wai and Langer, 2016) and respond to fluctuation in the energy status of the cell (Liesa and Shirihai, 2013) depending on the cell type.”
From Mitochondrial (Dys)function and Insulin Resistance: From Pathophysiological Molecular Mechanisms to the Impact of Diet (2019) · cites this paper as Liesa and Shirihai, 2013
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Effect of Roux-en-Y gastric bypass on liver mitochondrial dynamics in a rat model of obesity
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“Emerging research underscores the signi fi cance of mitochondrial architectural dynamics in adapting to varying metabolic requirements (Liesa and Shirihai, 2013).”
Cahill, T. J., Leo, V., Kelly, M., Stockenhuber, A., Kennedy, N. W., Bao, L., Cereghetti, G. M., Harper, A. R., Czibik, G., Liao, C., et al. (2016) · Journal of Biological Chemistry · doi:10.1074/jbc.a115.665695 · Cited by 14 · see citing works
“For example, mitochondrial elongation under conditions of nutrient deprivation protects against mitophagic degradation and preserves ATP synthesis (7, 8) Failure of cellular control over mitochondria triggers inflammation by Toll-like receptors or the inflammasome, leading to heart failure (9, 10).”
BackgroundPotes, Y., Díaz-Luis, A., Bermejo-Millo, J. C., Pérez-Martínez, Z., de Luxán-Delgado, B., Rubio-González, A., Menéndez-Valle, I., Gutiérrez-Rodríguez, J., Solano, J. J., Caballero, B., et al. (2023) · Antioxidants · doi:10.3390/antiox12111962 · Cited by 8 · see citing works
- Authors
- Liesa, M., & Shirihai, O. S.
- Affiliations
- Boston University (US)
- Corresponding author
- Shirihai, Orian S.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2013-04
- Volume
- 17
- Issue
- 4
- Pages
- 491-506
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC5967396
- OpenAlex
- W2019455536
- Cited by
- 1,341
- References
- 115
- Citations by year
- 2026: 71 · 2025: 110 · 2024: 135 · 2023: 115 · 2022: 107 · 2021: 143 · 2020: 142 · 2019: 100 · 2018: 117 · 2017: 82 · 2016: 79 · 2015: 70 · 2014: 52 · 2013: 17
- FWCI
- 6.84
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL071629)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK035914, P30DK046200, R01 DK35914, R01 DK56690, R01DK074778, R01DK056690)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- mitochondrial dynamics, mitochondrial fusion, mitochondrial fission, mitophagy, mitochondrial quality control, nutrient utilization, energy expenditure, mitochondrial architecture, mitochondrial dysfunction, age-related diseases
- MeSH terms
- Adenosine Triphosphate, Aging, Animals, Adipose Tissue, Brown, Diabetes Mellitus, Type 2, Energy Metabolism, Humans, Mitochondria, Obesity, Muscle, Skeletal, Insulin-Secreting Cells, Mitochondrial Dynamics
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