Tissue-specific differences in mitochondrial DNA content in type 2 diabetes

Ching Jung Hsieh, Shao Wen Weng, Chia Wei Liou, Tsu Kung Lin, Jin Bor Chen, Mao Meng Tiao, Yun Ting Hung, I. Ya Chen, Wen Te Huang, Pei Wen Wang*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

28 Scopus citations


Background: To investigate whether the effect of hyperglycemia on mitochondrial DNA (mtDNA) content is tissue-specific. Method: We compared the mtDNA contents in leg muscle, blood vessel, and peripheral leucocytes in seventeen patients with type 2 diabetes (T2DM) with those of seven controls. We measured 8-hydroxydeoxyguanosine (8-OHdG) expression in the muscles and thiobarbituric acid reactive substance (TBARS) in sera to evaluate oxidative stress. Immunohistochemical detection of peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC1-α), mitochondrial transcription factor A (Tfam), and apoptosis were performed in the muscle tissue. Results: The mtDNA copy number was highest in muscle tissue, followed by blood vessel tissue, and lowest in leucocytes in both the diabetic and control subjects. The diabetic patients had less mtDNA content in the muscle than the controls (2.86 ± 0.33 vs. 3.20 ± 0.14, P = 0.025), but more mtDNA content in the leucocytes (2.25 ± 0.26 vs. 1.98 ± 0.06, P = 0.04). In both groups, there was a positive correlation between muscle tissue mtDNA content and the expression of 8-OHdG. Patients with T2DM had significantly increased 8-OHdG and TUNEL labeling index and non-significant increases in the expression of PGC1-α and Tfam. Conclusion: Oxidative stress stimulates mitochondrial biogenesis but induces a greater degree of apoptosis in diabetic patients, resulting in a decrease in muscle tissue mtDNA content.

Original languageEnglish
Pages (from-to)106-110
Number of pages5
JournalDiabetes Research and Clinical Practice
Issue number1
StatePublished - 04 2011


  • Diabetes mellitus
  • Mitochondrial DNA
  • Oxidative stress


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