Calcified Tissue International

, Volume 66, Issue 3, pp 190–194

Association of Methylenetetrahydrofolate Reductase (MTHFR) Polymorphism with Bone Mineral Density in Postmenopausal Japanese Women

Authors

  • M.  Miyao
    • Department of Geriatric Medicine, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
  • H.  Morita
    • Department of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
  • T.  Hosoi
    • Endocrinology Section, Tokyo Metropolitan Geriatric Hospital, Tokyo, Japan
  • H.  Kurihara
    • Department of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
  • S.  Inoue
    • Department of Geriatric Medicine, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
  • S.  Hoshino
    • Department of Geriatric Medicine, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
  • M.  Shiraki
    • Research Institute and Practice for Involutional Diseases, Nagano, Japan
  • Y.  Yazaki
    • Department of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
  • Y.  Ouchi
    • Department of Geriatric Medicine, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan

DOI: 10.1007/s002230010038

Cite this article as:
Miyao, M., Morita, H., Hosoi, T. et al. Calcif Tissue Int (2000) 66: 190. doi:10.1007/s002230010038

Abstract.

The pathogenesis of osteoporosis is controlled by genetic and environmental factors. Considering the high prevalence of osteoporosis in homocystinuria, abnormal homocysteine metabolism would contribute to the pathogenesis of osteoporosis. It is known that the polymorphism of methylenetetrahydrofolate reductase (MTHFR), the enzyme catalyzing the reduction of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, correlates with hyperhomocysteinemia. In this study, we examined the association of this polymorphism with bone mineral density (BMD). BMD was measured by dual-energy X-ray absorptiometry (DXA) in 307 postmenopausal women. MTHFR A/V polymorphism was analyzed using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). We compared BMD, clinical characteristics, and bone metabolic markers among MTHFR groups (AA, AV, VV). The groups did not differ in terms of baseline data. The values of lumbar spine BMD and total body BMD were as follows: lumbar spine: AA, 0.91 ± 0.18, AV, 0.88 ± 0.16, VV, 0.84 ± 0.14 g/cm2; total body: AA, 0.97 ± 0.11, AV, 0.96 ± 0.11, VV, 0.93 ± 0.09 g/cm2. In the VV genotype, lumbar spine BMD values were significantly lower than those of the women with the AA genotype (P= 0.016) and total body BMD was significantly lower than those of the women with AA genotype (P= 0.03) and AV genotype (P= 0.04). This is the first report that suggests that the VV genotype of MTHFR is one of the genetic risk factors for low BMD.

Key words: Osteoporosis — Bone mineral density — Genetic risk factor — Methylenetetrahydrofolate reductase — Homocysteine.

Copyright information

© 2000 Springer-Verlag New York Inc.