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Vitamin E decreases bone mass by stimulating osteoclast fusion
Koji Fujita1, Makiko Iwasaki, Hiroki Ochi
1Department of Orthopedic Surgery, Tokyo Medical and Dental University, Tokyo, Japan.
Nature Medicine
|March 6, 2012
Summary
Vitamin E deficiency in mice leads to high bone mass by reducing bone resorption. Supplementing vitamin E in mice and rats decreased bone mass, revealing vitamin E
Area of Science:
- Bone Biology
- Nutritional Science
- Cell Biology
Background:
- Bone homeostasis relies on balanced osteoblast and osteoclast activity.
- Vitamin D is crucial for skeletal integrity, but vitamin E's role is unclear.
- Osteoclasts, key to bone resorption, form via mononuclear cell fusion.
Purpose of the Study:
- To investigate the role of vitamin E in bone remodeling.
- To determine the mechanism by which vitamin E affects bone resorption.
- To assess the impact of vitamin E levels on bone mass.
Main Methods:
- Utilized genetically modified mice lacking alpha-tocopherol transfer protein (Ttpa(-/-)) to model vitamin E deficiency.
- Performed cell-based assays to examine alpha-tocopherol's effect on osteoclast fusion.
- Analyzed gene expression and protein interactions related to osteoclast fusion.
- Administered alpha-tocopherol-supplemented diets to wild-type mice and rats.
Main Results:
- Ttpa(-/-) mice exhibited high bone mass due to decreased bone resorption.
- Alpha-tocopherol directly stimulated osteoclast fusion by upregulating dendritic-cell-specific transmembrane protein (DC-STAMP) expression via p38 and MITF pathways.
- The bone phenotype in Ttpa(-/-) mice was reversed by a DC-STAMP transgene.
- Dietary alpha-tocopherol supplementation led to bone loss in wild-type mice and rats.
Conclusions:
- Serum vitamin E levels are a key determinant of bone mass.
- Vitamin E regulates bone mass primarily by modulating osteoclast fusion, independent of its antioxidant properties.
- This study elucidates a novel mechanism linking vitamin E to bone metabolism.
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