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Mitochondrial gene mutation in islet-cell-antibody-positive patients who were initially non-insulin-dependent diabetics.

Abstract
Autoimmunity is thought to lead to islet-cell-antibody (ICA) formation in diabetes mellitus. However, we found a mitochondrial gene mutation at nucleotide pair 3243 in 3 of 27 Japanese ICA-positive, initially non-insulin-dependent diabetic patients. All 3 progressed to insulin-dependency within 13-31 months, whereas 5 of the other 24 are non-insulin-dependent after 54-90 months. ICA, at least in these 3 patients, may follow gradual beta-cell destruction due to mitochondrial gene mutation, although the possibility of beta-cells with the mutation being susceptible to autoimmune destruction cannot be excluded.
AuthorsY Oka, H Katagiri, Y Yazaki, T Murase, T Kobayashi
JournalLancet (London, England) (Lancet) Vol. 342 Issue 8870 Pg. 527-8 (Aug 28 1993) ISSN: 0140-6736 [Print] England
PMID8102670 (Publication Type: Journal Article)
Chemical References
  • Autoantibodies
  • DNA, Mitochondrial
Topics
  • Adolescent
  • Adult
  • Aged
  • Autoantibodies (biosynthesis)
  • DNA, Mitochondrial (genetics)
  • Diabetes Mellitus, Type 1 (genetics, immunology)
  • Diabetes Mellitus, Type 2 (genetics, immunology)
  • Female
  • Humans
  • Islets of Langerhans (immunology)
  • Male
  • Middle Aged
  • Point Mutation
  • Prospective Studies

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