The DOI matches its Crossref record; 106 of the 106 references it cites were found in a registry or an index.
Role of mitochondrial dynamics proteins in the pathophysiology of obesity and type 2 diabetes
Abstract
Mitochondrial dysfunction has been reported in skeletal muscle of obese subjects and of type 2 diabetic patients. Reduced mitochondrial mass and defective activity have been proposed to explain this dysfunction. Alterations in mitochondrial function may be crucial to explain the metabolic changes and insulin resistance that characterize both obesity and type 2 diabetes. Consequently, the identification of the primary mechanisms involved is of great relevance. Mitochondrial dynamics refers to the movement of mitochondria along the cytoskeleton and also to the regulation of mitochondrial morphology and distribution, which depend on fusion and fission events. In recent years, some of the proteins that participate in mitochondrial fusion and fission have been identified in mammalian cells. Recent evidence indicates that proteins participating in these processes are also involved in metabolism. The mitochondrial fusion protein mitofusin 2 stimulates respiration, substrate oxidation and the expression of subunits that participate in respiratory complexes in cultured cells. In this regard, skeletal muscle of obese subjects and of type 2 diabetic patients shows reduced mitofusin 2 expression. Therefore, alterations in the activity of the proteins involved in mitochondrial dynamics, and particularly mitofusin 2, may participate in the reduced mitochondrial function present in skeletal muscle in obesity and in type 2 diabetes.
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“Mice with skeletal muscle-specific deletion of Mfn2 exhibit impaired mitochondrial morphology, localization, and calcium uptake, ultimately resulting in decreased muscle cross-sectional area and strength.”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [46]
In the citing paper
“Skeletal muscle exhibits a high abundance of MFN2, and disruption of this protein have been related to disruption in mitochondrial membrane potential and cellular oxygen consumption [46].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [46]
In the citing paper
“reduced PGC1α expression in obese and diabetic muscle repressed MFN2 level [46], emphasizing the role of PGC1α as regulators of mitochondrial morphology and insulin sensitivity.”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [46]
In the citing paper
“The transcriptional activity of Mfn2 gene was shown to be stimulated by PGC1α, as overexpression of PGC1α enhanced Mfn2 mRNA and protein levels in cultured muscle cells and”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [46]
In the citing paper
“Further, alterations in mitochondrial dynamics and in particular in Mfn2, have been associated with a reduced mitochondrial function in skeletal muscle in obesity and T2DM (Zorzano et al., 2009) and recently aberrant mitochondrial fission has been also associated with insulin resistance in mouse skeletal muscle (Jheng et al., 2012).”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Zorzano et al., 2009
In the citing paper
“alterations in mitochondrial dynamics and in particular in Mfn2, have been associated with a reduced mitochondrial function in skeletal muscle in obesity and T2DM (Zorzano et al., 2009)”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Zorzano et al., 2009
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“particular in Mfn2, have been associated with a reduced mitochondrial function in skeletal muscle in obesity and T2DM (Zorzano et al., 2009) and recently aberrant mitochondrial fission has been also associated with insulin resistance in mouse skeletal muscle (Jheng et al.”
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Metadata
- Authors
- Zorzano, A., Liesa, M., & Palacín, M.
- Affiliations
- Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas (ES)
- ORCID
- Liesa, Marc
- Venue
- The International Journal of Biochemistry & Cell Biology
- Publisher
- Elsevier BV
- Published
- 2009-10
- Volume
- 41
- Issue
- 10
- Pages
- 1846-1854
- ISSN
- 1357-2725 (ISSN-L)
- OpenAlex
- W2056253513
- Cited by
- 209
- References
- 105
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 11 · 2023: 16 · 2022: 13 · 2021: 16 · 2020: 20 · 2019: 13 · 2018: 10 · 2017: 12 · 2016: 12 · 2015: 10 · 2014: 20 · 2013: 17 · 2012: 15
- FWCI
- 0.79
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The International Journal of Biochemistry & Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Generalitat de Catalunya
- Instituto de Salud Carlos III
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial dynamics, mitofusin 2, mitochondrial fusion, mitochondrial fission, mitochondrial dysfunction, skeletal muscle, obesity, type 2 diabetes, insulin resistance, mitochondrial respiration, substrate oxidation
- MeSH terms
- Animals, Diabetes Mellitus, Type 2, Humans, Insulin Resistance, Mitochondria, Obesity, Mitochondrial Proteins
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