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Mitochondria are impaired in the adipocytes of type 2 diabetic mice.
Open accessAbstract
Aims/hypothesis The aim of this study was to confirm a link between mitochondrial dysfunction and type 2 diabetes.Materials and methods Cellular levels of mitochondrial proteins, cellular mitochondrial DNA content, and mitochondrial function and morphology were assessed by MitoTracker staining and electron microscopy, in white adipose tissue of 12-week-old male wild-type, obese (ob/ob), and diabetic (db/db) mice.Results Levels of mitochondrial proteins were found to be very similar in the livers and muscles of all the mice studied. However, levels were greatly decreased in the adipocytes of db/db mice, but not in those of the wild-type and ob/ob mice. Levels of mitochondrial DNA were also found to be considerably reduced in the adipocytes of db/db mice. MitoTracker staining and under electron microscopy revealed that the number of mitochondria was reduced in adipocytes of db/db mice. Respiration and fatty acid oxidation studies indicated mitochondrial dysfunction in adipocytes of db/db mice. Interestingly, there was an increase in mitochondria and mitochondrial protein production in adipocytes of db/db mice treated with rosiglitazone, an agent that enhances insulin sensitivity.Conclusions/interpretation Taken together, these data indicate that mitochondrial loss in adipose tissue is correlated with the development of type 2 diabetes.
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“Mitochondrial function, as indicated by respiration and fatty acid oxidation, were reported to be decreased in db/db mice, a leptin receptor–deficient obese model of type 2 diabetes (61).”
From Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010) · cites this paper as [61]
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“White adipocyte mitochondrial content is decreased in both rodent and human obesity (177, 188 -191) and correlates with insulin resistance that accompanies obesity.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [188]
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Metadata
- Authors
- Choo, H.-J., Kim, J.-H., Kwon, O.-B., Lee, C. S., Mun, J. Y., Han, S. S., Yoon, Y.-S., Yoon, G., Choi, K.-M., & Ko, Y.-G.
- Affiliations
- Korea University (KR)
- Ajou University (KR)
- Corresponding author
- Ko, Y.-G.
- Venue
- Diabetologia
- Published
- 2006-02-25
- Volume
- 49
- Issue
- 4
- Pages
- 784-791
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W2051674591
- Cited by
- 365
- References
- 27
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 17 · 2023: 16 · 2022: 13 · 2021: 14 · 2020: 25 · 2019: 17 · 2018: 14 · 2017: 18 · 2016: 23 · 2015: 20 · 2014: 24 · 2013: 26 · 2012: 19
- FWCI
- 14.36
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- AJOU Open Repository (Ajou University) (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- mitochondrial dysfunction, type 2 diabetes, adipocytes, white adipose tissue, mitochondrial DNA, mitochondrial respiration, fatty acid oxidation, rosiglitazone, insulin sensitivity, db/db mice, ob/ob mice, mitochondrial loss
- MeSH terms
- Rosiglitazone, Animals, Diabetes Mellitus, Type 2, DNA, Mitochondrial, Female, Male, Microscopy, Electron, Mitochondria, Adipocytes, Mitochondrial Proteins, Thiazolidinediones, Mice, Rats
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