The DOI matches its Crossref record; 100 of the 100 references it cites were found in a registry or an index.
Mitochondrial dysfunction in obesity
Open accessAbstract
PURPOSE OF REVIEW: The review highlights recent findings regarding the functions of mitochondria in adipocytes, providing an understanding of their central roles in regulating substrate metabolism, energy expenditure, disposal of reactive oxygen species (ROS), and in the pathophysiology of obesity and insulin resistance, as well as roles in the mechanisms that affect adipogenesis and mature adipocyte function. RECENT FINDINGS: Nutrient excess leads to mitochondrial dysfunction, which in turn leads to obesity-related pathologies, in part due to the harmful effects of ROS. The recent recognition of 'ectopic' brown adipose in humans suggests that this tissue may play an underappreciated role in the control of energy expenditure. Transcription factors, PGC-1alpha and PRDM16, which regulate brown adipogenesis, and members of the TGF-beta superfamily that modulate this process may be important new targets for antiobesity drugs. SUMMARY: Mitochondria play central roles in ATP production, energy expenditure, and disposal of ROS. Excessive energy substrates lead to mitochondrial dysfunction with consequential effects on lipid and glucose metabolism. Adipocytes help to maintain the appropriate balance between energy storage and expenditure and maintaining this balance requires normal mitochondrial function. Many adipokines, including members of the TGF-beta superfamily, and transcriptional coactivators, PGC-1alpha and PRDM16, are important regulators of this process.
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Cites
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Identification and Importance of Brown Adipose Tissue in Adult Humans
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Functional Brown Adipose Tissue in Healthy Adults
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Reactive oxygen species have a causal role in multiple forms of insulin resistance
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“Similarly, TNF-alpha-mediated ROS accumulation leads to insulin resistance in 3T3L1 pre-adipocytes [21].”
BackgroundPRDM16 controls a brown fat/skeletal muscle switch
Seale, P., Bjork, B., Yang, W., Kajimura, S., Chin, S., Kuang, S., Scimè, A., Devarakonda, S., Conroe, H. M., Erdjument-Bromage, H., et al. (2008) · Nature · doi:10.1038/nature07182 · Cited by 2,347 · cited 1×
“Also, PRDM16 interacts with C-terminal binding proteins, CtBP1 and Ct-BP2, to repress white adipocyte genes [47], and reducing PRDM16 in brown adipocytes blocks mitochondrial gene expression and increases myogenic markers [48].”
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Cited by
Mitochondrial dysfunction in obesity
de Mello, A. H., Costa, A. B., Engel, J. D. G., & Rezin, G. T. (2018) · Life Sciences · doi:10.1016/j.lfs.2017.11.019 · Cited by 508
Correa-de-Araujo, R., Addison, O., Miljkovic, I., Goodpaster, B. H., Bergman, B. C., Clark, R. V., Elena, J. W., Esser, K. A., Ferrucci, L., Harris-Love, M. O., et al. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2020.00963 · Cited by 468
Singh, A., D’Amico, D., Andreux, P. A., Fouassier, A. M., Blanco-Bose, W., Evans, M., Aebischer, P., Auwerx, J., & Rinsch, C. (2022) · Cell Reports Medicine · doi:10.1016/j.xcrm.2022.100633 · Cited by 256
Pipatpiboon, N., Pratchayasakul, W., Chattipakorn, N., & Chattipakorn, S. C. (2012) · Endocrinology · doi:10.1210/en.2011-1502 · Cited by 198
Role of Mitochondrial Dysfunction in Hypertension and Obesity
Lahera, V., de las Heras, N., López-Farré, A., Manucha, W., & Ferder, L. (2017) · Current Hypertension Reports · doi:10.1007/s11906-017-0710-9 · Cited by 176
Metadata
- Authors
- Bournat, J. C., & Brown, C. W.
- Venue
- Current Opinion in Endocrinology, Diabetes and Obesity
- Published
- 2010-10
- Volume
- 17
- Issue
- 5
- Pages
- 446-452
- ISSN
- 1752-296X (ISSN-L)
- OpenAlex
- W2313583633
- Cited by
- 470
- References
- 100
- FWCI
- 9.70
- Type
- journal article
- Language
- en
- Open access
- green
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
