糖尿病とミトコンドリア機能  [in Japanese] Mitochondrial Function and Diabetes  [in Japanese]

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Author(s)

    • 尾形 真規子 Ogata Makiko
    • 東京女子医科大学医学部内科学(第三) Department of Medicine III, Tokyo Women's Medical University School of Medicine

Abstract

(医学部内科学(第三)教室岩本安彦教授退任記念特別号)

Diabetes Mellitus is characterized as hyperglycemia, which is caused by insulin secretion deficit and insulin resistance. The significance of mitochondrial function in diabetes had thought to be a secondary factor for target organ dysfunction in patients with diabetes because of the vulnerability of mitochondrial genes by hyperglycemic condition. After finding that mitochondrial gene mutation induces diabetes; mitochondrial myopathy, encepharopathy, lactic acidosis and stroke-like episodes (MELAS), mitochondrial dysfunction have thought to be the principal cause of diabetes. Recently, it has become evident that mitochondrial function plays an important role for cell survival and maintenance of insulin secretion function using rodent and cultured cells. There is plurality of evidence for insulin resistance, although glucose uptake in liver need mitochondrial pathway. Interestingly, hyperinsulinemia in high lipid fed rats as a model of metabolic syndrome has also been reported to be related to mitochondrial function. Hepatocyte nuclear factor(HNF) 1 whose gene is reported to cause MODY3, affects mitochondrial membrane function in cells. Furthermore, we reported that Q268XHNF4 mutaion causes MODY1 and affects the mitochondrial pH reaction by glucose. The HNF4 gene is also reported to affect the susceptibility gene for type2 diabetes. Based on this, it can be concluded that diabetes can be said to some degree that it is a mitochondrial disease.

Journal

  • Journal of Tokyo Women's Medical College

    Journal of Tokyo Women's Medical College 81(臨時増刊(岩本安彦教授退任記念特別)), E85-E88, 2011-03-31

    Tokyo Women's Medical University

Codes

  • NII Article ID (NAID)
    110008441449
  • NII NACSIS-CAT ID (NCID)
    AN00161368
  • Text Lang
    JPN
  • Article Type
    journal article
  • ISSN
    0040-9022
  • Data Source
    NII-ELS  IR 
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