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Mitochondrial DNA Mutations and Diabetes: Another Step toward Individualized Medicine

Nathan Fischel-Ghodsian, MD
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Dr. Fischel-Ghodsian: Cedars-Sinai Medical Center; Los Angeles, CA 90048

Acknowledgment: The author thanks Drs. Leslie Raffel, Ricardo Perfetti, and Jerome Rotter for their comments on the editorial.

Grant Support: By the National Institutes of Health/National Institute on Deafness and Other Communication Disorders (RO1DC01402 and RO1DC04092).

Requests for Single Reprints: Nathan Fischel-Ghodsian, MD, Department of Pediatrics, Suite 1165WT, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048.

Ann Intern Med. 2001;134(9_Part_1):777-779. doi:10.7326/0003-4819-134-9_Part_1-200105010-00014
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Twenty years ago, the mitochondrial chromosome was completely sequenced and the functions of all its genes were identified (1). Those genes code for 13 polypeptides, which are part of the more than 60 polypeptides that form the oxidative phosphorylation and adenosine triphosphate synthetase protein complexes in the inner membrane of the mitochondria. In addition, the mitochondrial chromosome codes for two ribosomal RNAs and 22 transfer RNAs, which participate in the translation of the 13 polypeptides on the mitochondrial ribosomes. Each cell contains hundreds of these chromosomes, and they are transmitted only through the ovum, leading to a maternal inheritance pattern. Inherited and acquired mutations in the mitochondrial chromosome have been implicated in a wide range of human diseases, including neuromuscular disorders, cardiomyopathies, skin lesions, aplastic anemia, Parkinson disease, and aging in general.





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