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Research Article Free access | 10.1172/JCI117790

Increased expression of mitochondrial-encoded genes in skeletal muscle of humans with diabetes mellitus.

D A Antonetti, C Reynet, and C R Kahn

Research Division, Joslin Diabetes Center, Boston, Massachusetts 02215.

Find articles by Antonetti, D. in: PubMed | Google Scholar

Research Division, Joslin Diabetes Center, Boston, Massachusetts 02215.

Find articles by Reynet, C. in: PubMed | Google Scholar

Research Division, Joslin Diabetes Center, Boston, Massachusetts 02215.

Find articles by Kahn, C. in: PubMed | Google Scholar

Published March 1, 1995 - More info

Published in Volume 95, Issue 3 on March 1, 1995
J Clin Invest. 1995;95(3):1383–1388. https://doi.org/10.1172/JCI117790.
© 1995 The American Society for Clinical Investigation
Published March 1, 1995 - Version history
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Abstract

Screening subtraction libraries from normal and type II diabetic human skeletal muscle, we identified four different mitochondrially encoded genes which were increased in expression in diabetes. The genes were cytochrome oxidase I, cytochrome oxidase III, NADH dehydrogenase IV, and 12s rRNA, all of which are located on the heavy strand of the mitochondrial genome. There was a 1.5- to 2.2-fold increase in the expression of these mRNA molecules relative to total RNA in both type I and type II diabetes as assessed by Northern blot analyses. Since there was approximately 50% decrease in mitochondrial DNA copy number as estimated by Southern blot analyses, mitochondrial gene expression increased approximately 2.5-fold when expressed relative to mitochondrial DNA copy number. For cytochrome oxidase I similar changes in mitochondrial gene expression were observed in muscle of nonobese diabetic and ob/ob mice, models of type I and type II diabetes, respectively. By contrast there was no change or a slight decrease in expression of cytochrome oxidase 7a, a nuclear-encoded subunit of cytochrome oxidase, and the expression of mitochondrial transcription factor 1 in human skeletal muscle did not change with type I or type II diabetes. The increased mitochondrial gene expression may contribute to the increase in mitochondrial respiration observed in uncontrolled diabetes.

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