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Short Reports

Mitochondrial Aldehyde Dehydrogenase in Diabetes Associated With Mitochondrial tRNALeu(UUR) Mutation at Position 3243

  1. Yoshihiko Suzuki, MD,
  2. Taro Muramatsu, MD,
  3. Matsuo Taniyama, MD,
  4. Yoshihito Atsumi, MD,
  5. Makoto Suematsu, MD,
  6. Ryuji Kawaguchi, PHD,
  7. Susumu Higuchi, MD,
  8. Takayuki Asahina, MD,
  9. Chisato Murata, MD,
  10. Michiko Handa, MD and
  11. Kempei Matsuoka, MD
  1. Saiseikai Central Hospital Tokyo
  2. Third Department of Internal Medicine, Showa University Tokyo
  3. Department of Biochemistry, Keio University Tokyo
  4. SRL Inc, Center for Molecular Biology and Cytogenetics Tokyo
  5. National Institute of Alcoholism, Kurihama National Hospital Kanagawa, Japan
  6. Kawasaki City Ida Hospital Kanagawa, Japan
  1. Address correspondence and reprint requests to Yoshihiko Suzuki, MD, Saiseikai Central Hospital, 1-4-17, Mita, Minato-ku, Tokyo 108, Japan. E-mail: drsuzuki{at}ba2.so-net.or.jp
Diabetes Care 1996 Dec; 19(12): 1423-1425. https://doi.org/10.2337/diacare.19.12.1423
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Abstract

OBJECTIVE To ascertain why alcohol is prone to manifest unpleasant effects in diabetes associated with mitochondrial tRNALeu(UUR) mutation at position 3243 (DM-Mt3243), we investigated the genotype of aldehyde dehydrogenase (ALDH) 2 and alcohol dehydrogenase 2 (ADH2) in DM-Mt3243.

RESEARCH DESIGN AND METHODS Nineteen unrelated patients with DM-Mt3243 were included in the study (12 men and 7 women). They were recruited from ∼700 diabetic patients at three different institutes, without prior information of alcohol habit. ALDH2, ADH2, and 3243 mutation were genotyped by polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) methods. There were 461 unrelated Japanese individuals and 170 non-3243 mutant NIDDM patients enrolled as control subjects.

RESULTS In the DM-Mt3243 group, 15 (79%) patients had inactive ALDH2 and 18 (95%) had atypical ADH2. The frequency of the inactive ALDH2 genotype was higher than that in the normal control subjects (P < 0.002) and that in the NIDDM control subjects (P < 0.003). However, the frequencies of ADH2 genotype in the DM-Mt3243 group, the normal control subjects, and the NIDDM control subjects were not different.

CONCLUSIONS Inactive ALDH2 genotype was frequently observed in DM-Mt3243. It suggests that DM-Mt3243 is associated with ALDH2 inactivity. We speculate the trait of acetaldehyde accumulation on ALDH2 inactivity may favor mitochondrial DNA abnormalities, thereby worsening ATP production and impairing insulin secretion. In addition, the interaction of ALDH1 and ALDH2 may alter the retinoid metabolism in the pancreas, thereby influencing insulin secretion and precipitating diabetes. Thus, this association of ALDH2 genotype with DM-Mt3243 provides insight into the etiology of diabetes in the mitochondrial diseases.

  • Received January 31, 1996.
  • Revision received July 19, 1996.
  • Accepted July 19, 1996.
  • Copyright © 1996 by the American Diabetes Association

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December 1996, 19(12)
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Mitochondrial Aldehyde Dehydrogenase in Diabetes Associated With Mitochondrial tRNALeu(UUR) Mutation at Position 3243
Yoshihiko Suzuki, Taro Muramatsu, Matsuo Taniyama, Yoshihito Atsumi, Makoto Suematsu, Ryuji Kawaguchi, Susumu Higuchi, Takayuki Asahina, Chisato Murata, Michiko Handa, Kempei Matsuoka
Diabetes Care Dec 1996, 19 (12) 1423-1425; DOI: 10.2337/diacare.19.12.1423

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Mitochondrial Aldehyde Dehydrogenase in Diabetes Associated With Mitochondrial tRNALeu(UUR) Mutation at Position 3243
Yoshihiko Suzuki, Taro Muramatsu, Matsuo Taniyama, Yoshihito Atsumi, Makoto Suematsu, Ryuji Kawaguchi, Susumu Higuchi, Takayuki Asahina, Chisato Murata, Michiko Handa, Kempei Matsuoka
Diabetes Care Dec 1996, 19 (12) 1423-1425; DOI: 10.2337/diacare.19.12.1423
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