Bone degeneration and its recovery in SMP30/GNL-knockout mice

Kazutoshi Nishijima*, T. Ohno, A. Amano, Y. Kishimoto, Y. Kondo, A. Ishigami, S. Tanaka

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)


Senescence marker protein-30 (SMP30) decreases androgen-independently with aging and is a lactone-hydrolyzing enzyme gluconolactonase (GNL) that is involved in vitamin C biosynthesis. In the present study, bone properties of SMP30/GNL knockout (KO) mice with deficiency in vitamin C synthesis were investigated to reveal the effects of SMP30/GNL and exogenous vitamin C supplementation on bone formation. Mineral content (BMC) and mineral density (BMD) of the mandible and femur of SMP30/GNL KO and wild-type mice at 2 and 3 months of age with or without vitamin C supplementation were measured by dual-energy X-ray absorptiometry. Body and bone weight of both age groups decreased and became significantly lower than those of wild-type mice. The bones of SMP30/GNL KO mice were rough and porous, with BMC and BMD significantly below wild-type. Oral supplementation with vitamin C eliminated differences in body weight, bone weight, BMC, and BMD between SMP30/GNL KO and wild-type mice at each age. These results indicate that bone degeneration in SMP30/GNL KO mice was caused by lack of vitamin C, and that this mouse strain is an appropriate model for bone metabolism in humans, which have no ability to synthesize vitamin C.

Original languageEnglish
Pages (from-to)573-578
Number of pages6
JournalJournal of Nutrition, Health and Aging
Issue number5
Publication statusPublished - 2017 May 1
Externally publishedYes


  • Vitamin C
  • animal model
  • bone mineral density
  • bone mineral ratio
  • femur
  • mandible

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Nutrition and Dietetics
  • Geriatrics and Gerontology


Dive into the research topics of 'Bone degeneration and its recovery in SMP30/GNL-knockout mice'. Together they form a unique fingerprint.

Cite this