Vitamin E homologues α- and γ-tocopherol are not associated with bone turnover markers or bone mineral density in peri-menopausal and post-menopausal women

Yang, Tiffany; Duthie, Garry G.; Aucott, Lorna; Macdonald, Helen

doi:10.1007/s00198-015-3470-x

Cited by 23 publications

(17 citation statements)

References 46 publications

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“…The relationship between vitamin E (particularly αTF), inflammation, and bone health has been investigated in a large cohort study of older women consisting of two visits (first visit: 1997–1999, age: 55 ± 2.2 years, n = 3883; second visit: 2007–2011, age: 66 ± 2.2 years, n = 2130). In this study, Yang et al (2016) found a positive association between serum αTF and BMD at the femoral neck, but a negative association between serum αTF and inflammation, evidenced by higher concentrations of IL-6 and high-sensitivity C-reactive protein (hs-CRP), among participants not taking vitamin E supplements [73].…”

Section: Molecular Actions Of Vitamin E On Bonementioning

confidence: 90%

The Molecular Mechanism of Vitamin E as a Bone-Protecting Agent: A Review on Current Evidence

Wong

Mohamad

Ibrahim

et al. 2019

IJMS

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Bone remodelling is a tightly-coordinated and lifelong process of replacing old damaged bone with newly-synthesized healthy bone. In the bone remodelling cycle, bone resorption is coupled with bone formation to maintain the bone volume and microarchitecture. This process is a result of communication between bone cells (osteoclasts, osteoblasts, and osteocytes) with paracrine and endocrine regulators, such as cytokines, reactive oxygen species, growth factors, and hormones. The essential signalling pathways responsible for osteoclastic bone resorption and osteoblastic bone formation include the receptor activator of nuclear factor kappa-B (RANK)/receptor activator of nuclear factor kappa-B ligand (RANKL)/osteoprotegerin (OPG), Wnt/β-catenin, and oxidative stress signalling. The imbalance between bone formation and degradation, in favour of resorption, leads to the occurrence of osteoporosis. Intriguingly, vitamin E has been extensively reported for its anti-osteoporotic properties using various male and female animal models. Thus, understanding the underlying cellular and molecular mechanisms contributing to the skeletal action of vitamin E is vital to promote its use as a potential bone-protecting agent. This review aims to summarize the current evidence elucidating the molecular actions of vitamin E in regulating the bone remodelling cycle.

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Section: Molecular Actions Of Vitamin E On Bonementioning

confidence: 90%

The Molecular Mechanism of Vitamin E as a Bone-Protecting Agent: A Review on Current Evidence

Wong

Mohamad

Ibrahim

et al. 2019

IJMS

View full text Add to dashboard Cite

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“…On the other hand, Odai et al’s cross-sectional study showed that dietary intake of vitamin E was associated with higher bone mineral density in premenopausal women but had no effect in postmenopausal women [ 202 ]. Yang et al found no effect of vitamin E on bone turnover markers or bone mineral density in peri- or postmenopausal women in the UK [ 203 ]. The antioxidant properties of vitamin E and their beneficial effects on other bone cells such as osteoblasts might be the confounding factors leading to these conflicting results [ 204 ].…”

Section: Recent Pre-clinical Studiesmentioning

confidence: 99%

Osteoclast Multinucleation: Review of Current Literature

Kodama

Kaito

2020

IJMS

112

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Multinucleation is a hallmark of osteoclast maturation. The unique and dynamic multinucleation process not only increases cell size but causes functional alterations through reconstruction of the cytoskeleton, creating the actin ring and ruffled border that enable bone resorption. Our understanding of the molecular mechanisms underlying osteoclast multinucleation has advanced considerably in this century, especially since the identification of DC-STAMP and OC-STAMP as “master fusogens”. Regarding the molecules and pathways surrounding these STAMPs, however, only limited progress has been made due to the absence of their ligands. Various molecules and mechanisms other than the STAMPs are involved in osteoclast multinucleation. In addition, several preclinical studies have explored chemicals that may be able to target osteoclast multinucleation, which could enable us to control pathogenic bone metabolism more precisely. In this review, we will focus on recent discoveries regarding the STAMPs and other molecules involved in osteoclast multinucleation.

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“…However, subsequent studies demonstrated that 1) aged αTTP knockout mice had reduced cortical bone mass, 2) low dietary Vitamin E intake did not increase bone mass in mature rats, 3) high dietary Vitamin E intake did not reduce cortical bone mass in mature rats, and 4) high Vitamin E intake did not affect cortical bone mass in maturing rats [5,6]. Human studies, likewise, have shown conflicting results regarding the beneficial or detrimental effects of Vitamin E on bone health [7][8][9][10][11][12][13]. Thus, the role of Vitamin E in bone remains unclear and somewhat controversial.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Osteocyte Membrane Repair Activity via Dietary Vitamin E Deprivation Impairs Osteocyte Survival

et al. 2018

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Osteocytes experience plasma membrane disruptions (PMD) that initiate mechanotransduction both in vitro and in vivo in response to mechanical loading, suggesting that osteocytes use PMD to sense and adapt to mechanical stimuli. PMD repair is crucial for cell survival; antioxidants (e.g., alpha-tocopherol, also known as Vitamin E) promote repair while reactive oxygen species (ROS), which can accumulate during exercise, inhibit repair. The goal of this study was to determine whether depleting Vitamin E in the diet would impact osteocyte survival and bone adaptation with loading. Male CD-1 mice (3 wk old) were fed either a regular diet (RD) or Vitamin E-deficient diet (VEDD) for up to 11 weeks. Mice from each dietary group either served as sedentary controls with normal cage activity, or were subjected to treadmill exercise (one bout of exercise or daily exercise for 5 weeks). VEDD-fed mice showed more PMD-affected osteocytes (+50%) after a single exercise bout suggesting impaired PMD repair following Vitamin E deprivation. After 5 weeks of daily exercise, VEDD mice failed to show an exercise-induced increase in osteocyte PMD formation, and showed signs of increased osteocytic oxidative stress and impaired osteocyte survival. Surprisingly, exercise-induced increases in cortical bone formation rate were only significant for VEDD-fed mice. This result may be consistent with previous studies in skeletal muscle, where myocyte PMD repair failure (e.g., with muscular dystrophy) initially triggers hypertrophy but later leads to widespread degeneration. In vitro, mechanically wounded MLO-Y4 cells displayed increased post-wounding necrosis (+40 fold) in the presence of H 2 O 2 , which could be prevented by Vitamin E pre-treatment. Taken together, our data support the idea that antioxidant-influenced osteocyte membrane repair is a vital aspect of bone mechanosensation in the osteocytic control of PMD-driven bone adaptation.

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Vitamin E homologues α- and γ-tocopherol are not associated with bone turnover markers or bone mineral density in peri-menopausal and post-menopausal women

Abstract: We did not find biologically meaningful results between dietary and tocopherol homologues with BTMs or BMD.

Cited by 23 publications

References 46 publications

The Molecular Mechanism of Vitamin E as a Bone-Protecting Agent: A Review on Current Evidence

The Molecular Mechanism of Vitamin E as a Bone-Protecting Agent: A Review on Current Evidence

Osteoclast Multinucleation: Review of Current Literature

Inhibition of Osteocyte Membrane Repair Activity via Dietary Vitamin E Deprivation Impairs Osteocyte Survival

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