Vitamin E as an Antiosteoporotic Agent via Receptor Activator of Nuclear Factor Kappa-B Ligand Signaling Disruption: Current Evidence and Other Potential Research Areas

Osteoporosis is a growing healthcare burden that affects the quality of life in the aging population. Vitamin E is a potential prophylactic agent that can impede the progression of osteoporosis. Various in vivo studies demonstrated the antiosteoporotic potential of vitamin E, but evidence on its mol...

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Bibliographic Details
Published in:Evidence-based complementary and alternative medicine 2012-01, Vol.2012 (2012), p.1-9
Main Authors: Chin, Kok-Yong, Soelaiman, Ima Nirwana
Format: Article
Language:English
Subjects:
Aging
Bone cancer
Bone growth
Bone turnover
Chemical compounds
Coenzyme A
Cytokines
Disease
Estrogens
Fractures
Inflammation
Isoforms
Kinases
Ligands
Long bone
Long term health care
Menopause
Metabolites
Molecular chains
Nutrition research
Osteoclastogenesis
Osteoclasts
Osteogenesis
Osteoporosis
Physiology
Proteins
Quality of life
Review
Signal transduction
TRANCE protein
Vitamin E
Womens health
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Summary:Osteoporosis is a growing healthcare burden that affects the quality of life in the aging population. Vitamin E is a potential prophylactic agent that can impede the progression of osteoporosis. Various in vivo studies demonstrated the antiosteoporotic potential of vitamin E, but evidence on its molecular mechanism of action is limited. A few in vitro studies showed that various forms of vitamin E can affect the receptor activator of nuclear factor kappa-B ligand (RANKL) signaling and their molecular targets, thus preventing the formation of osteoclasts in the early stage of osteoclastogenesis. Various studies have also shown that the effects of the different isoforms of vitamin E differ. The effects of single isoforms and combinations of isoforms on bone metabolism are also different. Vitamin E may affect bone metabolism by disruption of free radical-mediated RANKL signaling, by its oestrogen-like effects, by its effects on the molecular mechanism of bone formation, by the anti-inflammatory effects of its long-chain metabolites on bone cells, and by the inhibition of 3-hydroxyl-3-methyglutaryl coenzyme A (HMG-CoA). In conclusion, the vitamin E isoforms have enormous potential to be used as prophylactic and therapeutic agents in preventing osteoporosis, but further studies should be conducted to elucidate their mechanisms of action.
ISSN:1741-427X
1741-4288
DOI:10.1155/2012/747020