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The journal of nutrition, health & aging

Erschienen in:

12.11.2016

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

verfasst von: Kazutoshi Nishijima, T. Ohno, A. Amano, Y. Kishimoto, Y. Kondo, A. Ishigami, S. Tanaka

Erschienen in: The journal of nutrition, health & aging | Ausgabe 5/2017

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Abstract

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.

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Titel: Bone degeneration and its recovery in SMP30/GNL-knockout mice
verfasst von: Kazutoshi Nishijima
T. Ohno
A. Amano
Y. Kishimoto
Y. Kondo
A. Ishigami
S. Tanaka
Publikationsdatum: 12.11.2016
Verlag: Springer Paris
Erschienen in: The journal of nutrition, health & aging / Ausgabe 5/2017
Print ISSN: 1279-7707
Elektronische ISSN: 1760-4788
DOI: https://doi.org/10.1007/s12603-016-0841-8

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

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