Vitamin A decreases the anabolic bone response to mechanical loading by suppressing bone formation

Lionikaite, Vikte; Henning, Petra; Drevinge, Christina; Shah, Furqan A.; Palmquist, Anders; Wikström, Pernilla; Lerner, Ulf H.

doi:10.1096/fj.201802040r

Cited by 18 publications

(14 citation statements)

References 59 publications

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“…For control animals not subjected to tibial loading, retinyl acetate supplementation induced no changes in trabecular bone microstructure and osteogenic gene expression. However, retinyl acetate supplementation promoted BFR, mineralising surface (MS) and MAR at endocortical region but decreased Ct.Ar, Ma.Ar, Ec.Pm, and Ps.Pm [ 18 ]. In another study involving mature female Sprague Dawley rats, retinyl palmitate (natural alternative of retinyl acetate) and retinyl acetate were enriched in the diet (120 or 600 IU/g pellet) and given to the animals for 12 weeks.…”

Section: Effects Of Vitamin a On Bone Health In Animalsmentioning

confidence: 99%

Vitamin A and Bone Health: A Review on Current Evidence

et al. 2021

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Vitamin A is a fat-soluble micronutrient essential for growth, immunity, and good vision. The preformed retinol is commonly found in food of animal origin whereas provitamin A is derived from food of plant origin. This review summarises the current evidence from animal, human and cell-culture studies on the effects of vitamin A towards bone health. Animal studies showed that the negative effects of retinol on the skeleton were observed at higher concentrations, especially on the cortical bone. In humans, the direct relationship between vitamin A and poor bone health was more pronounced in individuals with obesity or vitamin D deficiency. Mechanistically, vitamin A differentially influenced the stages of osteogenesis by enhancing early osteoblastic differentiation and inhibiting bone mineralisation via retinoic acid receptor (RAR) signalling and modulation of osteocyte/osteoblast-related bone peptides. However, adequate vitamin A intake through food or supplements was shown to maintain healthy bones. Meanwhile, provitamin A (carotene and β-cryptoxanthin) may also protect bone. In vitro evidence showed that carotene and β-cryptoxanthin may serve as precursors for retinoids, specifically all-trans-retinoic acid, which serve as ligand for RARs to promote osteogenesis and suppressed nuclear factor-kappa B activation to inhibit the differentiation and maturation of osteoclasts. In conclusion, we suggest that both vitamin A and provitamin A may be potential bone-protecting agents, and more studies are warranted to support this hypothesis.

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Section: Effects Of Vitamin a On Bone Health In Animalsmentioning

confidence: 99%

Vitamin A and Bone Health: A Review on Current Evidence

et al. 2021

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“…Previous studies in vivo and in vitro have indicated that a high concentration of preformed VA negatively affects both osteoblast differentiation and mineralization, owing to the effects of VA on osteogenic gene inhibition, osteoclastogenic gene activation, and osteocyte or osteoblast-related peptides modulation [ 9 ]. Through an animal experiment using female C57BL6/J mouse models, researchers reported a significant increase in the osteoclast number and the osteoclastogenic gene expression in mice that were treated with high doses of dietary retinyl acetate [ 35 ]. Moreover, VA antagonizes vitamin D (VD) by increasing calcium absorption and maintaining a steady-state serum calcium concentration.…”

Section: Discussionmentioning

confidence: 99%

Vitamin A Nutritional Status Is a Key Determinant of Bone Mass in Children

et al. 2022

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The bone mass increases that occur during the period of childhood are of great significance for maximizing the peak bone mass in adults and preventing for osteoporosis. Studies have reported that VA can improve the bone health in adults. Moreover, limited studies have assessed such associations in children. In this cross-sectional study including 426 children, we assessed the children’s plasma retinol concentration by liquid chromatography–mass spectrometry and the dietary intake of VA and carotenoids using a structured Food Frequency Questionnaire. Their bone mineral content and bone mineral density (BMD) were measured using dual-energy X-ray absorptiometry. After adjusting for potential confounders, the restricted cubic spline revealed an inverted U-shaped association between plasma retinol concentration and BMD; the estimated effects on the TBLH BMD per μmol/L increase in the plasma retinol concentration were 1.79 × 10−2 g/cm2 below 1.24 μmol/L and −5.78 × 10−3 g/cm2 above this point (p for non-linearity = 0.046). A multiple linear regression analysis revealed a positive association between the plasma retinol concentration and the TBLH BMC (β = 1.89, 95% CI: 1.64 × 10−1–3.62, p = 0.032). In conclusion, an appropriate plasma retinol concentration and greater intakes of dietary VA and β-carotene may enhance the bone mineral status of children who are aged 6–9 years.

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“…We have previously demonstrated that vitamin A-induced resorption initially occurs in the periosteal bone, and subsequently in the endosteal bone [ 12 ]. In addition to decreased periosteal bone thickness, retinol has also been shown to reduce mechanical loading-induced bone formation in mice after 6-weeks of treatment, largely through decreasing the bone formation rate (BFR) of osteoblasts [ 22 ]. In future studies, it will be important to extend the treatment period to determine whether the osteoclasts would be detectable in response to COD treatment.…”

Section: Discussionmentioning

confidence: 99%

Cod Liver Oil, but Not Retinoic Acid, Treatment Restores Bone Thickness in a Vitamin A-Deficient Rat

et al. 2022

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Vitamin A plays a prominent role for maintaining optimal bone status, but its impact upon the bone in response to vitamin A deficiency is not well defined. The purpose of this study was to evaluate how replenishing vitamin A by either whole food cod liver oil (COD) or the active metabolite of vitamin A, retinoic acid (RA), altered bone thickness of vitamin A-deficient (VAD) rats. Weanling rats were administered a control diet (CTRL) or VAD diet for 9 weeks. This was followed by four weeks of treatment in which the VAD group was divided into the following 4 subgroups: (1) VAD (9 weeks)-VAD (4 weeks); (2) VAD-CTRL; (3) VAD-COD; and (4) VAD-RA. Compared to controls, VAD rats had thicker bones which showed marked dysplasia. VAD-rats treated with COD produced a thinner bone that was not significantly different from that of untreated rats. In contrast, RA did not significantly change the thicker bone, and also had significantly greater periosteal and endosteal osteoblast numbers compared to VAD-COD. Active osteoclasts were not detected in VAD rats, nor during the treatment period. These findings suggest that the abnormal bone thickness in VAD rats appears to be more effectively restored to bone thickness of untreated control rats when treated with COD.

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Vitamin A decreases the anabolic bone response to mechanical loading by suppressing bone formation

Cited by 18 publications

References 59 publications

Vitamin A and Bone Health: A Review on Current Evidence

Vitamin A and Bone Health: A Review on Current Evidence

Vitamin A Nutritional Status Is a Key Determinant of Bone Mass in Children

Cod Liver Oil, but Not Retinoic Acid, Treatment Restores Bone Thickness in a Vitamin A-Deficient Rat

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