Mito-mice∆ and mitochondrial DNA mutator mice as models of human osteoporosis caused not by aging but by hyperparathyroidism

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著者

    • MITO Takayuki
    • Faculty of Life and Environmental Sciences, University of Tsukuba|Japan Society for the Promotion of Science (JSPS)
    • TANI Haruna
    • Graduate School of Life and Environmental Sciences, University of Tsukuba
    • SUZUKI Michiko
    • Graduate School of Life and Environmental Sciences, University of Tsukuba
    • ISHIKAWA Kaori
    • Faculty of Life and Environmental Sciences, University of Tsukuba|Graduate School of Life and Environmental Sciences, University of Tsukuba
    • NAKADA Kazuto
    • Faculty of Life and Environmental Sciences, University of Tsukuba|Graduate School of Life and Environmental Sciences, University of Tsukuba

抄録

<p>Mitochondrial DNA (mtDNA) mutator mice showing accelerated accumulation of mtDNA with somatic mutations are potentially useful models of human aging, whereas mito-miceΔ showing accelerated accumulation of mtDNA with a deletion mutation (ΔmtDNA) are potentially useful models of mitochondrial diseases but not human aging, even though both models express an age-associated decrease in mitochondrial respiration. Because osteoporosis is the only premature aging phenotype observed in mtDNA mutator mice with the C57BL/6J nuclear genetic background, our previous study precisely examined its expression spectra and reported that both mtDNA mutator mice and mito-miceΔ, but not aged mice, developed decreased cortical bone thickness. Moreover, decreased cortical bone thickness is usually not seen in aged humans but is commonly seen in the patients with hyperparathyroidism caused by oversecretion of parathyroid hormone (PTH). In the present study, we showed higher concentrations of blood PTH in mtDNA mutator mice and mito-miceΔ than in aged mice. We also found that both models developed decreased mitochondrial respiration in the duodenum or renal tubules, which would lead to hypocalcemia, oversecretion of PTH, and ultimately osteoporosis. Thus, mtDNA mutator mice and mito-miceΔ may be useful models of human osteoporosis caused not by aging but by hyperparathyroidism.</p>

収録刊行物

  • 実験動物彙報

    実験動物彙報, 2018

    公益社団法人 日本実験動物学会

各種コード

  • NII論文ID(NAID)
    130007393867
  • 本文言語コード
    ENG
  • ISSN
    1341-1357
  • データ提供元
    J-STAGE 
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