Mitochondria are impaired in the adipocytes of type 2 diabetic mice

H. J. Choo, J. H. Kim, O. B. Kwon, C. S. Lee, J. Y. Mun, S. S. Han, Y. S. Yoon, G. Yoon, K. M. Choi, Y. G. Ko

Research output: Contribution to journalArticlepeer-review

286 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)784-791
Number of pages8
Issue number4
Publication statusPublished - 2006 Apr

Bibliographical note

Funding Information:
Acknowledgement This work was supported by a grant to Y. Ko from the Korea Research Foundation (KRF-2002-070-C00074). The authors have declared that no conflict of interest exists.


  • Adipocyte
  • Diabetes
  • Mitochondria
  • Rosiglitazone

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism


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