Cited by 365Adipose Tissue and MetabolismMitochondrial Function and PathologyMetabolism, Diabetes, and Cancer

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Mitochondria are impaired in the adipocytes of type 2 diabetic mice.

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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.·2006·Diabetologia

DOI 10.1007/s00125-006-0170-2

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Abstract

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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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.
ORCID: Choo, H.-J.
Kim, J.-H.
Lee, C. S.
Yoon, G.
Choi, K.-M.
Ko, Y.-G.
Venue: Diabetologia
Publisher: Springer Science and Business Media LLC
Published: 2006-02-25
Volume: 49
Issue: 4
Pages: 784-791
ISSN: 0012-186X (ISSN-L)
1432-0428
DOI: 10.1007/s00125-006-0170-2
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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Mitochondria are impaired in the adipocytes of type 2 diabetic mice.

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