H.-J. Choo1, J.-H. Kim1, O.-B. Kwon1, C. S. Lee1, J. Y. Mun1, S. S. Han1, Y.-S. Yoon2, G. Yoon2, K.-M. Choi3 and Y.-G. Ko1,*
(1)Graduate School of Life Sciences and Biotechnology, Korea University, 1, 5-ka, Anam-dong, Sungbuk-gu, Seoul, 136-701, South Korea
(2)College of Medicine, Ajou University, Suwon, Kyunggi-Do, South Korea
(3)Guro Hospital, College of Medicine, Korea University, Seoul, South Korea
*Correspondence. Y.-G. Ko
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.
Electronic Supplementary Material
Supplementary material is available for this article at http://dx.doi.org/10.1007/s00125-006-0170-2
Keywords: Adipocyte, Diabetes, Mitochondria, Rosiglitazone