Journal articles: 'Bone physiology and vitamin A'

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White, C. P., N. A. Morrison, E. M. Gardiner, and J. A. Eisman. "Vitamin D receptor alleles and bone physiology." Journal of Cellular Biochemistry 56, no. 3 (November 1994): 307–14. http://dx.doi.org/10.1002/jcb.240560306.

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Larmonier, C. B., R. M. T. McFadden, F. M. Hill, R. Schreiner, R. Ramalingam, D. G. Besselsen, F. K. Ghishan, and P. R. Kiela. "High vitamin D3 diet administered during active colitis negatively affects bone metabolism in an adoptive T cell transfer model." American Journal of Physiology-Gastrointestinal and Liver Physiology 305, no. 1 (July 1, 2013): G35—G46. http://dx.doi.org/10.1152/ajpgi.00065.2013.

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Decreased bone mineral density (BMD) represents an extraintestinal complication of inflammatory bowel disease (IBD). Vitamin D3 has been considered a viable adjunctive therapy in IBD. However, vitamin D3 plays a pleiotropic role in bone modeling and regulates the bone formation-resorption balance, depending on the physiological environment, and supplementation during active IBD may have unintended consequences. We evaluated the effects of vitamin D3 supplementation during the active phase of disease on colonic inflammation, BMD, and bone metabolism in an adoptive IL-10−/− CD4+ T cell transfer model of chronic colitis. High-dose vitamin D3 supplementation for 12 days during established disease had negligible effects on mucosal inflammation. Plasma vitamin D3 metabolites correlated with diet, but not disease, status. Colitis significantly reduced BMD. High-dose vitamin D3 supplementation did not affect cortical bone but led to a further deterioration of trabecular bone morphology. In mice fed a high vitamin D3 diet, colitis more severely impacted bone formation markers (osteocalcin and bone alkaline phosphatase) and increased bone resorption markers, ratio of receptor activator of NF-κB ligand to osteoprotegrin transcript, plasma osteoprotegrin level, and the osteoclast activation marker tartrate-resistant acid phosphatase (ACp5). Bone vitamin D receptor expression was increased in mice with chronic colitis, especially in the high vitamin D3 group. Our data suggest that vitamin D3, at a dose that does not improve inflammation, has no beneficial effects on bone metabolism and density during active colitis or may adversely affect BMD and bone turnover. These observations should be taken into consideration in the planning of further clinical studies with high-dose vitamin D3 supplementation in patients with active IBD.

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Mazurais, D., M. J. Darias, M. F. Gouillou-Coustans, M. M. Le Gall, C. Huelvan, E. Desbruyères, P. Quazuguel, C. Cahu, and J. L. Zambonino-Infante. "Dietary vitamin mix levels influence the ossification process in European sea bass (Dicentrarchus labrax) larvae." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 2 (February 2008): R520—R527. http://dx.doi.org/10.1152/ajpregu.00659.2007.

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The influence of dietary vitamins on growth, survival, and morphogenesis was evaluated until day 38 of posthatching life in European sea bass larvae ( Dicentrarchus labrax). A standard vitamin mix (VM), at double the concentration of the U.S. National Research Council's recommendations, was incorporated into larval feeds at 0.5%, 1.5%, 2.5%, 4.0%, and 8.0% to give treatments VM 0.5, VM 1.5, VM 2.5, VM 4.0, and VM 8.0, respectively. The group fed the VM 0.5 diet all died before day 30. At day 38, the larvae group fed VM 1.5 had 33% survival, while the other groups, with higher vitamin levels, showed at least 50% survival. The higher the percentage VM in the diet, the lower the percentage of column deformities. High dietary vitamin levels positively influenced the formation of mineralized bone in larvae: the higher the dietary vitamin level, the higher the ossification status. In the larvae group fed at the highest vitamin levels, we observed a temporal sequence of coordinated growth factor expression, in which the expression of bone morphometric protein (BMP-4) preceded the expression of IGF-1, which stimulated the maturation of osteoblasts (revealed by high osteocalcin expression levels). In groups fed lower proportions of vitamins, elevated proliferator peroxisome-activated receptors (PPAR-γ) expression coincided with low BMP-4 expression. Our results suggest that high levels of PPAR-γ transcripts in larvae-fed diets with a low VM content converted some osteoblasts into adipocytes during the first two weeks of life. This loss of osteoblasts is likely to have caused skeletal deformities.

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Abegg, Kathrin, Nicole Gehring, Carsten A. Wagner, Annette Liesegang, Marc Schiesser, Marco Bueter, and Thomas A. Lutz. "Roux-en-Y gastric bypass surgery reduces bone mineral density and induces metabolic acidosis in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 305, no. 9 (November 1, 2013): R999—R1009. http://dx.doi.org/10.1152/ajpregu.00038.2013.

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Roux-en-Y gastric bypass (RYGB) surgery leads to bone loss in humans, which may be caused by vitamin D and calcium malabsorption and subsequent secondary hyperparathyroidism. However, because these conditions occur frequently in obese people, it is unclear whether they are the primary causes of bone loss after RYGB. To determine the contribution of calcium and vitamin D malabsorption to bone loss in a rat RYGB model, adult male Wistar rats were randomized for RYGB surgery, sham-operation–ad libitum fed, or sham-operation–body weight-matched. Bone mineral density, calcium and phosphorus balance, acid-base status, and markers of bone turnover were assessed at different time points for 14 wk after surgery. Bone mineral density decreased for several weeks after RYGB. Intestinal calcium absorption was reduced early after surgery, but plasma calcium and parathyroid hormone levels were normal. 25-hydroxyvitamin D levels decreased, while levels of active 1,25-dihydroxyvitamin D increased after surgery. RYGB rats displayed metabolic acidosis due to increased plasma lactate levels and increased urinary calcium loss throughout the study. These results suggest that initial calcium malabsorption may play a key role in bone loss early after RYGB in rats, but other factors, including chronic metabolic acidosis, contribute to insufficient bone restoration after normalization of intestinal calcium absorption. Secondary hyperparathyroidism is not involved in postoperative bone loss. Upregulated vitamin D activation may compensate for any vitamin D malabsorption.

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Massé, P. G., E. E. Delvin, P. V. Hauschka, S. M. Donovan, M. D. Grynpas, J. D. Mahuren, B. A. Watkins, and D. S. Howell. "Perturbations in factors that modulate osteoblast functions in vitamin B6 deficiency." Canadian Journal of Physiology and Pharmacology 78, no. 11 (November 1, 2000): 904–11. http://dx.doi.org/10.1139/y00-072.

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It was hypothesized that the widespread structural defect of collagen in connective tissue of vitamin B6deficient-animals and the consequent alteration in bone biomechanical properties cause an additional stress to their inflammed swollen tibiotarsometatarsal joints. The present study showed a 32% elevation (P &lt 0.02) in mean plasma free cortisol concentration. Vitamin D metabolism was impaired but without changing plasma calcium homeostasis and bone mineral content. Mean plasma calcitriol [1,25(OH)2D] concentration was significantly reduced (P < 0.001). Because plasma calcidiol concentration did not change, we speculated that either renal 25-hydroxycalciferol-1α-hydroxylase activity was reduced or 1,25(OH)2D turnover was increased. Plasma osteocalcin, an index of osteoblast function related to bone formation, was significantly decreased (P < 0.05). This adverse effect on osteoblasts was consistent with the reduction of bone specific alkaline phosphatase activity (another index of bone formation) found in a previous study. The excess of cortisol may have impaired these bone cells functions directly and (or) indirectly via the decline in calcitriol synthesis. Plasma hydroxyproline concentrations in B6-deficient animals were found to be significantly reduced (P < 0.001), suggesting that cortisol in excess had also a suppressive effect on another hydroxylase, namely tissue (mainly bone and liver) prolyl hydroxylase. The bone uncoupling (in formation and resoption) associated with vitamin B6deficiency seems to be due to secondary hypercortisolism and (or) another unknown factors but not related to a change in bone modulators such as IGF-1 and eicosanoids.Key words: collagen, vitamin B6, vitamin D, cortisol, osteocalcin, IGF-1, eicosanoids, PGE2.

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Lane, Ginny, Christine Nisbet, Susan J. Whiting, and Hassan Vatanparast. "Canadian newcomer children’s bone health and vitamin D status." Applied Physiology, Nutrition, and Metabolism 44, no. 7 (July 2019): 796–803. http://dx.doi.org/10.1139/apnm-2018-0705.

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Adequate calcium intake and supply of vitamin D during childhood play important roles in ensuring adequate bone mass gain to achieve optimal peak bone mass. The Healthy Immigrant Children study employed a mixed-method cross-sectional study design to characterize the health and nutritional status of 300 immigrant and refugee children aged 3–13 years who had been in Canada for less than 5 years. This paper presents bone mineral content and vitamin D status data along with qualitative data that deepen the understanding of newcomer bone health status. A significantly higher percentage of refugee children (72.3%) had insufficient (<50 nmol/L) or deficient (<30 nmol/L) serum vitamin D compared with immigrants (53.2%). Vitamin D deficiency was most common among ethnic minority girls. Newcomer children with higher intakes of vitamin D, younger newcomer children, and those from western Europe or the United States had higher serum vitamin D levels. Immigrants had significantly higher mean total body bone mineral content compared with refugees. Total body fat, serum vitamin D, calcium intake, height, height by calcium intake, total body fat by calcium intake, and total body fat by height predicted total body bone mineral content levels. Vitamin D deficiency among newcomer children may be related to lack of knowledge regarding children’s vitamin D requirements in the Canadian environment, dietary habits established in country of origin, low income that limits healthy dietary choices, and lifestyle habits that limit exposure to sunlight. Results suggest a need to screen newcomer children and pregnant women for vitamin D deficiency and support early intervention.

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Rangel, Letícia Batista Azevedo, Daniel de Siqueira, Olívia do Rosário Soares, Higor Scardini Santana, Emílio de Castro Miguel, Maura da Cunha, Andre Lacerda de Abreu Oliveira, et al. "Vitamin K Supplementation Modulates Bone Metabolism and Ultra-Structure of Ovariectomized Mice." Cellular Physiology and Biochemistry 51, no. 1 (2018): 356–74. http://dx.doi.org/10.1159/000495234.

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Background/Aims: Osteoporosis is a bone metabolic disease that affects mostly post-menopausal women. There has been shown that vitamin K (VK) supplementation during menopause may decrease bone loss as well as risk of bone breaking. Aiming to clarify the beneficial role of VK in bone metabolism during menopause, we investigated mineral metabolism and bone ultrastructure of ovariectomized (OVX) mice. Methods: To determine the effects chronic use of VK in bone structure and mineral metabolism in OVX mice, we used several methods, such as DXA, µCTScan, and SEM as well as biomolecular techniques, such as ELISA and qRT-PCR. In addition, complete analysis of serum hormonal and other molecules associated to bone and lipid metabolism were evaluated overview the effects of VK in menopause murine model. Results: VK treatment significantly affects Pi metabolism independently of OVX, changing Pi plasma, urinary output, balance, and Pi bone mass. Interestingly, VK also increased VLDL in mice independently of castration. In addition, VK increased compact bone mass in OVX mice when we evaluated it by DXA, histomorphometry, µCTScanning. VK increased bone formation markers, osteocalcin, HYP- osteocalcin, and AP whereas it decreased bone resorption markers, such as urinary DPD/creatinine ratio and plasmatic TRAP. Surprisingly, SEM images revealed that VK treatment led to amelioration of microfractures observed in OVX untreated controls. In addition, SHAM operated VK treated mice exhibited higher number of migrating osteoblasts and in situ secretion of AP. OVX led to decreased to in situ secretion of AP that was restored by VK treatment. Moreover, VK treatment increased mRNA expression of bone Calbindin 28KDa independently of OVX. Conclusion: VK treatment in OVX mice exhibited beneficial effects on bone ultrastructure, mostly by altering osteoblastic function and secretion of organic bone matrix. Therefore, VK could be useful to treat osteopenic/osteoporotic patients.

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Kelly, James, Audrey Lin, Chiachien J. Wang, Sil Park, and Ichiro Nishimura. "Vitamin D and Bone Physiology: Demonstration of Vitamin D Deficiency in an Implant Osseointegration Rat Model." Journal of Prosthodontics 18, no. 6 (August 2009): 473–78. http://dx.doi.org/10.1111/j.1532-849x.2009.00446.x.

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Tajima, Orie, Noriko Ashizawa, Tomoo Ishii, Hitoshi Amagai, Tomoko Mashimo, Li Jing Liu, Shinichi Saitoh, Kumpei Tokuyama, and Masashige Suzuki. "Interaction of the effects between vitamin D receptor polymorphism and exercise training on bone metabolism." Journal of Applied Physiology 88, no. 4 (April 1, 2000): 1271–76. http://dx.doi.org/10.1152/jappl.2000.88.4.1271.

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Bone metabolism is strongly influenced by heredity and environmental factors. To investigate interaction of the effects between vitamin D receptor polymorphism by Fok I and resistance exercise training on bone metabolism, young male subjects with FF genotype (F, n = 10) and Ff or ff genotypes (f, n = 10) followed 1 mo of weight training, and changes in bone metabolism were compared. An additional 14 subjects served as a sedentary control. Biomarkers of bone formation, bone-specific alkaline phosphatase, and osteocalcin were significantly increased by training in both F and f groups. 1,25-Dihydroxyvitamin D3, known to upregulate bone formation, was also increased by the training in the f but not in the F group. Bone resorption assessed by cross-linked NH2-terminal teropeptide of type I collagen was significantly suppressed by the training, and the decrease in F was greater and longer lasting than that in f group. In conclusion, stimulation of bone formation and suppression of bone resorption occurred within 1 mo in young men. Despite a significant increase in 1,25-dihydroxyvitamin D3 in the f group but not in the F group, the response of bone metabolism to the training in the F was similar to or greater than that in f group, suggesting a functional difference between vitamin D receptor genotypes f and F.

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Bouillon, Roger. "Vitamin D: Basic and clinical research in vitamin D, vitamin D analogs and bone health." Bone 47 (October 2010): S355. http://dx.doi.org/10.1016/j.bone.2010.09.049.

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Hagino, Hiroshi. "Vitamin D3 analogs for the treatment of osteoporosis." Canadian Journal of Physiology and Pharmacology 93, no. 5 (May 2015): 327–32. http://dx.doi.org/10.1139/cjpp-2014-0419.

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Vitamin D supplementation is recommended whenever patients are given therapeutic drugs for osteoporosis, to make their calcium (Ca) balance positive. Vitamin D is converted to 25-hydroxyvitamin D in the liver, and then activated to become 1α,25-dihydroxyvitamin D in the kidneys. The active vitamin D acts in the intestine to stimulate Ca absorption and maintain the Ca balance. 2β-(3-Hydroxypropyloxy)-1α,25-dihydroxyvitamin D3 (eldecalcitol) and 2-methylene-19-nor-(20S)-1α,25-dihydroxyvitamin D3 (2MD) are newly developed vitamin D analogs, with a substitution at the 2 position of 1α,25-dihydroxyvitamin D3 (calcitriol). Eldecalcitol and 2MD share common structural and biological characteristics. Both compounds increase serum Ca levels more markedly than calcitriol, increase bone mineral density (BMD), and improve bone strength in ovariectomized (OVX) rats. In a randomized, placebo-controlled, double-blind, 1 year clinical trial, eldecalcitol dose-dependently increased lumbar and hip BMD and suppressed bone turnover markers in patients with osteoporosis. Whereas, 2MD markedly increased the bone turnover markers, but it did not change the BMD of postmenopausal women with osteopenia in a 1 year clinical trial. After a randomized, double-blind, 3 year fracture-prevention trial comparing it with alfacalcidol, eldecalcitol was approved for the treatment of osteoporosis in Japan. On the other hand, the manufacturer discontinued the clinical development of 2MD. In this review, we discuss the similarities and differences between these 2 compounds, and the reasons why different outcomes resulted from their clinical trials.

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Gross, M., and R. Kumar. "Physiology and biochemistry of vitamin D-dependent calcium binding proteins." American Journal of Physiology-Renal Physiology 259, no. 2 (August 1, 1990): F195—F209. http://dx.doi.org/10.1152/ajprenal.1990.259.2.f195.

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The vitamin D-dependent calcium binding proteins (calbindins) are members of the troponin-C superfamily of proteins that occur in a number of calcium-transporting tissues such as the intestine, the distal tubule of the kidney, and the placenta. They are also present in other tissues such as the brain, peripheral nervous system, pancreas, parathyroid gland, and bone. In some tissues, such as the adult brain, the proteins occur in the absence of the vitamin. The proteins bind calcium in "EF" hand structures and are "calcium-sensitive" in that they undergo a conformational change on binding calcium. They appear to enhance transcellular calcium transport and are frequently present in tissues that contain the plasma membrane calcium pump.

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Kaisermann, Morrys C. "Vitamin K family effects on bone growth." Bone 48, no. 6 (June 2011): 1427. http://dx.doi.org/10.1016/j.bone.2011.03.757.

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Taylor, Sarah N. "Vitamin D in Toddlers, Preschool Children, and Adolescents." Annals of Nutrition and Metabolism 76, no. 2 (2020): 30–41. http://dx.doi.org/10.1159/000505635.

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Background: Vitamin D supplementation is known to both prevent and treat rickets, a disease of hypomineralized bone. Childhood is a period of great bone development and, therefore, attention to the vitamin D needed to optimize bone health in childhood is imperative. Summary: Observational studies have pointed to a vitamin D status, as indicated by a 25-hydroxyvitamin D concentration, of 50 nmol/L to ensure avoidance of rickets and of 75 nmol/L to optimize health. However, the benefits of achieving these levels of vitamin D status are less evident when pediatric randomized, controlled trials are performed. In fact, no specific pediatric vitamin D supplementation has been established by the existing evidence. Yet, study of vitamin D physiology continues to uncover further potential benefits to vitamin D sufficiency. This disconnection between vitamin D function and trials of supplementation has led to new paths of investigation, including establishment of the best method to measure vitamin D status, examination of genetic variation in vitamin D metabolism, and consideration that vitamin D status is a marker of another variable, such as physical activity, and its association with bone health. Nevertheless, vitamin D supplementation in the range of 10–50 μg/day appears to be safe for children and remains a promising intervention that may yet be supported by clinical trials as a method to optimize pediatric health. Key Message: Pediatric vitamin D status is associated with avoidance of rickets. Randomized, controlled trials of vitamin D supplementation for pediatric bone health are limited and equivocal in their results. Beyond bone, decreased risk for autoimmune, infectious, and allergic diseases has been associated with higher vitamin D status. The specific vitamin D supplementation to optimize toddler, child, and adolescent outcomes is unknown, but doses 10–50 μg/day are safe and may be beneficial.

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Popa, Daniela-Saveta, Galya Bigman, and Marius Emil Rusu. "The Role of Vitamin K in Humans: Implication in Aging and Age-Associated Diseases." Antioxidants 10, no. 4 (April 6, 2021): 566. http://dx.doi.org/10.3390/antiox10040566.

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As human life expectancy is rising, the incidence of age-associated diseases will also increase. Scientific evidence has revealed that healthy diets, including good fats, vitamins, minerals, or polyphenolics, could have antioxidant and anti-inflammatory activities, with antiaging effects. Recent studies demonstrated that vitamin K is a vital cofactor in activating several proteins, which act against age-related syndromes. Thus, vitamin K can carboxylate osteocalcin (a protein capable of transporting and fixing calcium in bone), activate matrix Gla protein (an inhibitor of vascular calcification and cardiovascular events) and carboxylate Gas6 protein (involved in brain physiology and a cognitive decline and neurodegenerative disease inhibitor). By improving insulin sensitivity, vitamin K lowers diabetes risk. It also exerts antiproliferative, proapoptotic, autophagic effects and has been associated with a reduced risk of cancer. Recent research shows that protein S, another vitamin K-dependent protein, can prevent the cytokine storm observed in COVID-19 cases. The reduced activation of protein S due to the pneumonia-induced vitamin K depletion was correlated with higher thrombogenicity and possibly fatal outcomes in COVID-19 patients. Our review aimed to present the latest scientific evidence about vitamin K and its role in preventing age-associated diseases and/or improving the effectiveness of medical treatments in mature adults ˃50 years old.

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Dusso, Adriana S., Alex J. Brown, and Eduardo Slatopolsky. "Vitamin D." American Journal of Physiology-Renal Physiology 289, no. 1 (July 2005): F8—F28. http://dx.doi.org/10.1152/ajprenal.00336.2004.

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The vitamin D endocrine system plays an essential role in calcium homeostasis and bone metabolism, but research during the past two decades has revealed a diverse range of biological actions that include induction of cell differentiation, inhibition of cell growth, immunomodulation, and control of other hormonal systems. Vitamin D itself is a prohormone that is metabolically converted to the active metabolite, 1,25-dihydroxyvitamin D [1,25(OH)2D]. This vitamin D hormone activates its cellular receptor (vitamin D receptor or VDR), which alters the transcription rates of target genes responsible for the biological responses. This review focuses on several recent developments that extend our understanding of the complexities of vitamin D metabolism and actions: the final step in the activation of vitamin D, conversion of 25-hydroxyvitamin D to 1,25(OH)2D in renal proximal tubules, is now known to involve facilitated uptake and intracellular delivery of the precursor to 1α-hydroxylase. Emerging evidence using mice lacking the VDR and/or 1α-hydroxylase indicates both 1,25(OH)2D3-dependent and -independent actions of the VDR as well as VDR-dependent and -independent actions of 1,25(OH)2D3. Thus the vitamin D system may involve more than a single receptor and ligand. The presence of 1α-hydroxylase in many target cells indicates autocrine/paracrine functions for 1,25(OH)2D3in the control of cell proliferation and differentiation. This local production of 1,25(OH)2D3is dependent on circulating precursor levels, providing a potential explanation for the association of vitamin D deficiency with various cancers and autoimmune diseases.

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Vogelsang, H., P. Ferenci, W. Woloszczuk, H. Resch, C. Herold, S. Frotz, and A. Gangl. "Bone disease in vitamin D-deficient patients with Crohn's disease." Digestive Diseases and Sciences 34, no. 7 (July 1989): 1094–99. http://dx.doi.org/10.1007/bf01536381.

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Norman, Anthony W. "Bone biochemistry and physiology from the perspectives of the vitamin D endocrine system." Current Opinion in Rheumatology 4, no. 3 (June 1992): 375–82. http://dx.doi.org/10.1097/00002281-199206000-00016.

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Minola, E., G. Colussi, M. E. De Ferrari, and R. Brusamolino. "Characterization by bone histology of hypophosphatemic vs vitamin-D deficiency bone disease." Bone 19, no. 3 (September 1996): 153. http://dx.doi.org/10.1016/s8756-3282(96)90822-4.

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Marcinkowska, Ewa. "The Vitamin D System in Humans and Mice: Similar but Not the Same." Reports — Medical Cases, Images, and Videos 3, no. 1 (January 10, 2020): 1. http://dx.doi.org/10.3390/reports3010001.

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Vitamin D is synthesized in the skin from 7-dehydrocholesterol subsequently to exposure to UVB radiation or is absorbed from the diet. Vitamin D undergoes enzymatic conversion to its active form, 1,25-dihydroxyvitamin D (1,25D), a ligand to the nuclear vitamin D receptor (VDR), which activates target gene expression. The best-known role of 1,25D is to maintain healthy bones by increasing the intestinal absorption and renal reuptake of calcium. Besides bone maintenance, 1,25D has many other functions, such as the inhibition of cell proliferation, induction of cell differentiation, augmentation of innate immune functions, and reduction of inflammation. Significant amounts of data regarding the role of vitamin D, its metabolism and VDR have been provided by research performed using mice. Despite the fact that humans and mice share many similarities in their genomes, anatomy and physiology, there are also differences between these species. In particular, there are differences in composition and regulation of the VDR gene and its expression, which is discussed in this article.

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Jorde, Rolf, Astrid Kamilla Stunes, Julia Kubiak, Ragnar Joakimsen, Guri Grimnes, Per Medbøe Thorsby, and Unni Syversen. "Effects of vitamin D supplementation on bone turnover markers and other bone-related substances in subjects with vitamin D deficiency." Bone 124 (July 2019): 7–13. http://dx.doi.org/10.1016/j.bone.2019.04.002.

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Brown, Ronald B., Afrozul Haq, Charles F. Stanford, and Mohammed S. Razzaque. "Vitamin D, phosphate, and vasculotoxicity." Canadian Journal of Physiology and Pharmacology 93, no. 12 (December 2015): 1077–82. http://dx.doi.org/10.1139/cjpp-2015-0083.

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Vascular calcification is a complex process that results in the ectopic deposition of calcium-phosphate hydroxyapatite. Medial and intimal vascular calcification is frequently present in patients with diabetes mellitus and chronic kidney disease (CKD), and markedly increases the morbidity and mortality of these patients. Increased serum levels of calcium and phosphate, along with the use of active vitamin D metabolites, are commonly implicated in the evolvement of vascular wall mineralization in CKD patients. Because CKD patients have lower serum levels of vitamin D, they are routinely prescribed vitamin D supplements that exert a dualistic role that is both healthful and harmful in these patients, perhaps protecting bone health, but at the expense of promoting vascular pathology. This review briefly explains how reducing the phosphate burden in CKD patients could minimize vitamin-D-associated vascular wall calcification.

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Jiang, Xiaorui, Botao Huang, Huiying Yang, Guishi Li, Chunlei Zhang, Guangshi Yang, Feng Lin, and Guodong Lin. "TGF-β1 is Involved in Vitamin D-Induced Chondrogenic Differentiation of Bone Marrow-Derived Mesenchymal Stem Cells by Regulating the ERK/JNK Pathway." Cellular Physiology and Biochemistry 42, no. 6 (2017): 2230–41. http://dx.doi.org/10.1159/000479997.

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Background/Aims: Osteoarthritis (OA) is characterized by degradation of cartilage, sole cell type of which is chondrocytes. Bone marrow-derived mesenchymal stem cells (BMSCs) possess multipotency and can be directionally differentiated into chondrocytes under stimulation. This study was aimed to explore the possible roles of vitamin D and transforming growth factor-β1 (TGF-β1) in the chondrogenic differentiation of BMSCs. Methods: BMSCs were isolated from femurs and tibias of rats and characterized by flow cytometry. After stimulation with vitamin D, BMSC proliferation and migration were measured by Cell Counting Kit-8 (CCK-8) and Transwell assays, respectively. Chondrogenic differentiation was estimated through expression levels of specific markers by qRT-PCR and Western blot analysis. After stable transfection, the effects of aberrantly expressed TGF-β1 on vitamin D-induced alterations, including BMSC viability, migration and chondrogenic differentiation, were all evaluated utilizing CCK-8 assay, Transwell assay, qRT-PCR and Western blot analysis. Finally, the phosphorylation levels of key kinases in the extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) pathways were determined by Western blot analysis. Results: Vitamin D remarkably promoted BMSC viability, migration and chondrogenic differentiation. These alterations of BMSCs induced by vitamin D were reinforced by TGF-β1 overexpression while were reversed by TGF-β1 silencing. Additionally, the phosphorylation levels of ERK, JNK and c-Jun were enhanced by TGF-β1 overexpression but were reduced by TGF-β1 knockdown. Conclusion: Vitamin D promoted BMSC proliferation, migration and chondrogenic differentiation. TGF-β1 might be implicated in the vitamin D-induced alterations of BMSCs through regulating ERK/JNK pathway.

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Granjon, David, Olivier Bonny, and Aurélie Edwards. "A model of calcium homeostasis in the rat." American Journal of Physiology-Renal Physiology 311, no. 5 (November 1, 2016): F1047—F1062. http://dx.doi.org/10.1152/ajprenal.00230.2016.

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We developed a model of calcium homeostasis in the rat to better understand the impact of dysfunctions such as primary hyperparathyroidism and vitamin D deficiency on calcium balance. The model accounts for the regulation of calcium intestinal uptake, bone resorption, and renal reabsorption by parathyroid hormone (PTH), vitamin D3, and Ca2+itself. It is the first such model to incorporate recent findings regarding the role of the calcium-sensing receptor (CaSR) in the kidney, the presence of a rapidly exchangeable pool in bone, and the delayed response of vitamin D3synthesis. Accounting for two (fast and slow) calcium storage compartments in bone allows the model to properly predict the effects of bisphophonates on the plasma levels of Ca2+([Ca2+]p), PTH, and vitamin D3. Our model also suggests that Ca2+exchange rates between plasma and the fast pool vary with both sex and age, allowing [Ca2+]pto remain constant in spite of sex- and age-based hormonal and other differences. Our results suggest that the inconstant hypercalciuria that is observed in primary hyperparathyroidism can be attributed in part to counterbalancing effects of PTH and CaSR in the kidney. Our model also correctly predicts that calcimimetic agents such as cinacalcet bring down [Ca2+]pto within its normal range in primary hyperparathyroidism. In addition, the model provides a simulation of CYP24A1 inactivation that leads to a situation reminiscent of infantile hypercalcemia. In summary, our model of calcium handling can be used to decipher the complex regulation of calcium homeostasis.

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Levy, David S., Rickinder Grewal, and Thu H. Le. "Vitamin K deficiency: an emerging player in the pathogenesis of vascular calcification and an iatrogenic consequence of therapies in advanced renal disease." American Journal of Physiology-Renal Physiology 319, no. 4 (October 1, 2020): F618—F623. http://dx.doi.org/10.1152/ajprenal.00278.2020.

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Vascular calcification is a known complication of chronic kidney disease (CKD). The prevalence of vascular calcification in patients with non-dialysis-dependent CKD stages 3–5 has been shown to be as high as 79% ( 20 ). Vascular calcification has been associated with increased risk for mortality, hospital admissions, and cardiovascular disease ( 6 , 20 , 50 , 55 ). Alterations in mineral and bone metabolism play a pivotal role in the pathogenesis of vascular calcification in CKD. As CKD progresses, levels of fibroblast growth factor-23, parathyroid hormone, and serum phosphorus increase and levels of 1,25-(OH)2 vitamin D decrease. These imbalances have been linked to the development of vascular calcification. More recently, additional factors have been found to play a role in vascular calcification. Matrix G1a protein (MGP) in its carboxylated form (cMGP) is a potent inhibitor of vascular calcification. Importantly, carboxylation of MGP is dependent on the cofactor vitamin K. In patients with CKD, vitamin K deficiency is prevalent and is exacerbated by warfarin, which is frequently used for anticoagulation. Insufficient bioavailability of vitamin K reduces the amount of cMGP available, and, therefore, it may lead to increased risk of vascular calcification. In vitro studies have shown that in the setting of a high-phosphate environment and vitamin K antagonism, human aortic valve interstitial cells become calcified. In this article, we discuss the pathophysiological consequence of vitamin K deficiency in the setting of altered mineral and bone metabolism, its prevalence, and clinical implications in patients with CKD.

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Kim, G. K., and J. Q. Del Rosso. "Does isotretinoin have effect on vitamin D physiology and bone metabolism in acne patients?" Yearbook of Dermatology and Dermatologic Surgery 2012 (January 2012): 161–62. http://dx.doi.org/10.1016/j.yder.2012.02.001.

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Mathews, C. H., R. Brommage, and H. F. DeLuca. "Role of vitamin D in neonatal skeletal development in rats." American Journal of Physiology-Endocrinology and Metabolism 250, no. 6 (June 1, 1986): E725—E730. http://dx.doi.org/10.1152/ajpendo.1986.250.6.e725.

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The role of vitamin D in rat pup growth and skeletal development without the influence of nutritional factors was investigated. Pups from vitamin D-replete and vitamin D-deficient dams receiving identical amounts of milk for 20 days were compared. Body weight gain, femur ash content and histomorphometric analyses of diaphysial and distal femur were determined. Up to 20 days of age, growth and skeletal development of the pups were completely normal in the absence of vitamin D. Skeletal changes found in vitamin D deficiency were not observed, i.e., there was no increased volume of osteoid or lack of bone mineralization as demonstrated by tetracycline labeling and ash content. Only increased cortical porosity was found in vitamin D-deficient pups. Therefore, abnormalities previously attributed to vitamin D deficiency in neonatal rats can be corrected by sufficient milk consumption and are thus not a direct function of vitamin D.

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Hauschka, P. V., J. B. Lian, D. E. Cole, and C. M. Gundberg. "Osteocalcin and matrix Gla protein: vitamin K-dependent proteins in bone." Physiological Reviews 69, no. 3 (July 1, 1989): 990–1047. http://dx.doi.org/10.1152/physrev.1989.69.3.990.

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Pigarova, Ekaterina A., and Alexandra A. Petrushkina. "Non-classical effects of vitamin D." Osteoporosis and Bone Diseases 20, no. 3 (April 24, 2018): 90–101. http://dx.doi.org/10.14341/osteo2017390-101.

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Since the discovery of vitamin D, interest in role of vitamin D in human body is consistently growing, and there is increasing evidence that vitamin D is not only essential to bone health but may also be involved in physiology of many other tissues. Thus understanding of its aspects in particular tissues appears to be important because of possible contribution to pathophysiologic processes. Intracrine regulatory systems associated with widely expressed vitamin D metabolizing enzymes, ways of cellular intake and signal pathways involved are of particular interest. Association of local effects with vitamin D level in blood is under investigation on animal models as well as in clinical studies; values of vitamin D level that mediate extraskeletal effects should be determined. In this review, we discuss impact of vitamin D on immune function and its association with skin, nervous system, cardiovascular system, obesity and diabetes mellitus, cancer, reproductive function, prevention of falls and quality of life improvement.

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Ardawi, M. S., M. H. Qari, and A. A. Rouzi. "Vitamin-D receptor gene polymorphisms and bone mineral density." Bone 47 (June 2010): S150—S151. http://dx.doi.org/10.1016/j.bone.2010.04.347.

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Meir, Tomer, Ronen Levi, Liesbet Lieben, Steven Libutti, Geert Carmeliet, Roger Bouillon, Justin Silver, and Tally Naveh-Many. "Deletion of the vitamin D receptor specifically in the parathyroid demonstrates a limited role for the receptor in parathyroid physiology." American Journal of Physiology-Renal Physiology 297, no. 5 (November 2009): F1192—F1198. http://dx.doi.org/10.1152/ajprenal.00360.2009.

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1,25(OH)2D3 decreases parathyroid hormone (PTH) gene transcription through the vitamin D receptor (VDR). Total body VDR−/− mice have high PTH levels, hypocalcemia, hypophosphatemia, and bone malformations. To investigate PTH regulation by the VDR specifically in the parathyroid, we generated parathyroid-specific VDR knockout mice ( PT-VDR−/−). In both strains, there was a decrease in parathyroid calcium receptor (CaR) levels. The number of proliferating parathyroid cells was increased in the VDR−/− mice but not in the PT-VDR−/− mice. Serum PTH levels were moderately but significantly increased in the PT-VDR−/− mice with normal serum calcium levels. The sensitivity of the parathyroid glands of the PT-VDR−/− mice to calcium was intact as measured by serum PTH levels after changes in serum calcium. This indicates that the reduced CaR in the PT-VDR−/− mice enables a physiologic response to serum calcium. Serum C-terminal collagen crosslinks, a marker of bone resorption, were increased in the PT-VDR−/− mice with no change in the bone formation marker, serum osteocalcin, consistent with a resorptive effect due to the increased serum PTH levels in the PT-VDR−/− mice. Therefore, deletion of the VDR specifically in the parathyroid decreases parathyroid CaR expression and only moderately increases basal PTH levels, suggesting that the VDR has a limited role in parathyroid physiology.

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Kito, Hiroaki, Haruka Morihiro, Yuka Sakakibara, Kyoko Endo, Junko Kajikuri, Takayoshi Suzuki, and Susumu Ohya. "Downregulation of the Ca2+-activated K+ channel KCa3.1 in mouse preosteoblast cells treated with vitamin D receptor agonist." American Journal of Physiology-Cell Physiology 319, no. 2 (August 1, 2020): C345—C358. http://dx.doi.org/10.1152/ajpcell.00587.2019.

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The maturity of osteoblasts by proliferation and differentiation in preosteoblasts is essential for maintaining bone homeostasis. The beneficial effects of vitamin D on bone homeostasis in mammals have been demonstrated experimentally and clinically. However, the direct actions of vitamin D on preosteoblasts remain to be fully elucidated. In this study, we found that the functional activity of intermediate-conductance Ca2+-activated K+ channels (KCa3.1) positively regulated cell proliferation in MC3T3-E1 cells derived from mouse preosteoblasts by enhancing intracellular Ca2+ signaling. We examined the effects of treatment with vitamin D receptor (VDR) agonist on the expression and activity of KCa3.1 by real-time PCR examination, Western blotting, Ca2+ imaging, and patch clamp analyses in mouse MC3T3-E1 cells. Following the downregulation of KCa3.1 transcriptional modulators such as Fra-1 and HDAC2, KCa3.1 activity was suppressed in MC3T3-E1 cells treated with VDR agonists. Furthermore, application of the KCa3.1 activator DCEBIO attenuated the VDR agonist-evoked suppression of cell proliferation rate. These findings suggest that a decrease in KCa3.1 activity is involved in the suppression of cell proliferation rate in VDR agonist-treated preosteoblasts. Therefore, KCa3.1 plays an important role in bone formation by promoting osteoblastic proliferation under physiological conditions.

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Zhang, Yan, Wan-Ping Lai, Chun-Fu Wu, Murray J. Favus, Ping-Chung Leung, and Man-Sau Wong. "Ovariectomy worsens secondary hyperparathyroidism in mature rats during low-Ca diet." American Journal of Physiology-Endocrinology and Metabolism 292, no. 3 (March 2007): E723—E731. http://dx.doi.org/10.1152/ajpendo.00445.2006.

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Estrogen deficiency impairs intestinal Ca absorption and induces bone loss, but its effects on the vitamin D-endocrine system are unclear. In the present study, calciotropic hormones levels, renal vitamin D metabolism, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]-dependent intestinal calcium absorption, and bone properties in 3-mo-old sham-operated (sham) or ovariectomized (OVX) rats fed either a normal-Ca (NCD; 0.6% Ca, 0.65% P) or a low-Ca (LCD; 0.1% Ca, 0.65% P) diet for 2 wk were determined. LCD increased serum 1,25(OH)2D3 levels in both sham and OVX rats. Serum parathyroid hormone [PTH(1–84)] levels were highest in OVX rats fed LCD. Renal 25-hydroxyvitamin D1α-hydroxylase (1-OHase) protein expression was induced in both sham and OVX rats during LCD, while renal 1-OHase mRNA expression was highest in OVX rats fed LCD. Renal vitamin D receptor (VDR) and mRNA expressions in rats were induced by ovariectomy in rats fed NCD but suppressed by ovariectomy in rats fed LCD. The induction of intestinal calcium transporter-1 and calbindin-D9k mRNA expressions by LCD were not altered by ovariectomy. As expected, bone Ca content, cancellous bone mineral density, and bone strength index in proximal metaphysis of rat tibia were reduced by both ovariectomy and LCD ( P < 0.05) as analyzed by two-way ANOVA. Taken together, the data demonstrate that ovariectomy alters the responses of circulating PTH levels, renal 1-OHase mRNA expression, and renal VDR expression to LCD. These results suggest that estrogen is necessary for the full adaptive response to LCD mediated by both PTH and 1,25(OH)2D3.

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Yanagi, Hisako, Shigeo Tomura, Satoshi Kurihara, Kei Yamana, Hideo Hamaguchi, and Shigeru Tsuchiya. "Vitamin D Receptor Gene Polymorphisms and Bone Mineral Density in Hemodialysis Patients." Nephron 77, no. 1 (1997): 114–15. http://dx.doi.org/10.1159/000190258.

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Denis, I., G. Cournot, H. Lacroix, C. Colin, E. Zerath, and A. Pointillart. "In vivo bone metabolism and ex vivo bone marrow osteoprogenitors in vitamin D-deprived pigs." Bone 26, no. 5 (May 2000): 491–98. http://dx.doi.org/10.1016/s8756-3282(00)00257-x.

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Van Pottelbergh, I., S. Goemaere, D. De Bacquer, A. De Paepe, and M. Kaufman. "Vitamin D receptor gene allelic variants, bone density, and bone turnover in community-dwelling men." Bone 31, no. 5 (November 2002): 631–37. http://dx.doi.org/10.1016/s8756-3282(02)00867-0.

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Mølgaard, C., A. Larnkjær, K. D. Cashman, C. Lamberg-Allardt, J. Jakobsen, and K. F. Michaelsen. "Does vitamin D supplementation of healthy Danish Caucasian girls affect bone turnover and bone mineralization?" Bone 46, no. 2 (February 2010): 432–39. http://dx.doi.org/10.1016/j.bone.2009.08.056.

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Verma, Divij, Rahul Kumar, Raquel S. Pereira, Christina Karantanou, Costanza Zanetti, Valentina R. Minciacchi, Keertik Fulzele, et al. "Vitamin K antagonism impairs the bone marrow microenvironment and hematopoiesis." Blood 134, no. 3 (July 18, 2019): 227–38. http://dx.doi.org/10.1182/blood.2018874214.

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Abstract Vitamin K antagonists (VKAs) have been used in 1% of the world’s population for prophylaxis or treatment of thromboembolic events for 64 years. Impairment of osteoblast function and osteoporosis has been described in patients receiving VKAs. Given the involvement of cells of the bone marrow microenvironment (BMM), such as mesenchymal stem cells (MSCs) and macrophages, as well as other factors such as the extracellular matrix for the maintenance of normal hematopoietic stem cells (HSCs), we investigated a possible effect of VKAs on hematopoiesis via the BMM. Using various transplantation and in vitro assays, we show here that VKAs alter parameters of bone physiology and reduce functional HSCs 8-fold. We implicate impairment of the functional, secreted, vitamin K-dependent, γ-carboxylated form of periostin by macrophages and, to a lesser extent, MSCs of the BMM and integrin β3-AKT signaling in HSCs as at least partly causative of this effect, with VKAs not being directly toxic to HSCs. In patients, VKA use associates with modestly reduced leukocyte and monocyte counts, albeit within the normal reference range. VKAs decrease human HSC engraftment in immunosuppressed mice. Following published examples that alteration of the BMM can lead to hematological malignancies in mice, we describe, without providing a causal link, that the odds of VKA use are higher in patients with vs without a diagnosis of myelodysplastic syndrome (MDS). These results demonstrate that VKA treatment impairs HSC function via impairment of the BMM and the periostin/integrin β3 axis, possibly associating with increased MDS risk.

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Shimada, Takashi, Yuji Yamazaki, Motoo Takahashi, Hisashi Hasegawa, Itaru Urakawa, Takeshi Oshima, Kaori Ono, et al. "Vitamin D receptor-independent FGF23 actions in regulating phosphate and vitamin D metabolism." American Journal of Physiology-Renal Physiology 289, no. 5 (November 2005): F1088—F1095. http://dx.doi.org/10.1152/ajprenal.00474.2004.

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FGF23 suppresses both serum phosphate and 1,25-dihydroxyvitamin D [1,25D] levels in vivo. Because 1,25D itself is a potent regulator of phosphate metabolism, it has remained unclear whether FGF23-induced changes in phosphate metabolism were caused by a 1,25D-independent mechanism. To address this issue, we intravenously administered recombinant FGF23 to vitamin D receptor (VDR) null (KO) mice as a rapid bolus injection and evaluated the early effects of FGF23. Administration of recombinant FGF23 further decreased the serum phosphate level in VDR KO mice, accompanied by a reduction in renal sodium-phosphate cotransporter type IIa (NaPi2a) protein abundance and a reduced renal 25-hydroxyvitamin D-1α-hydroxylase (1αOHase) mRNA level. Thus FGF23-induced changes in NaPi2a and 1αOHase expression are independent of the 1,25D/VDR system. However, 24-hydroxylase (24OHase) mRNA expression remained undetectable by the treatment with FGF23. We also analyzed the regulatory mechanism for FGF23 expression. The serum FGF23 level was almost undetectable in VDR KO mice, whereas dietary calcium supplementation significantly increased circulatory levels of FGF23 and its mRNA abundance in bone. This finding indicates that calcium is another determinant of FGF23 production that occurs independently of the VDR-mediated mechanism. In contrast, dietary phosphate supplementation failed to induce FGF23 expression in the absence of VDR, whereas marked elevation in circulatory FGF23 was observed in wild-type mice fed with a high-phosphate diet. Taken together, FGF23 works, at least in part, in a VDR-independent manner, and FGF23 production is also regulated by multiple mechanisms involving VDR-independent pathways.

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Abdellaoui, Selma, Bilal Bengana, Abdenour Boukabous, and Salima Lefkir-Tafiani. "Vitamin D deficiency pandemic and extra bone effects." Batna Journal of Medical Sciences (BJMS) 7, no. 2 (November 9, 2020): 142–47. http://dx.doi.org/10.48087/bjmsra.2020.7217.

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Le phénomène de déficit en vitamine D a pris une grande ampleur aujourd’hui, ce déficit connaît un effet de « pandémie » mondiale, il n’épargne aucune frontière ni catégorie d’âge. Les connaissances de la physiologie de cette vitamine ont progressé de manière considérable, faisant passer sa conception d’une hormone purement osseuse à une hormone ayant un rôle sur la santé globale. En effet, son double rôle d’immunomodulateur et de contrôle de la prolifération cellulaire est possible grâce à son métabolite actif secrété de façon autocrine par certains tissus, et la répartition ubiquitaire de ses récepteurs. En plus de cette description d’effets pléiotropes à la fois dans des modèles cellulaires, expérimentales et cliniques, de plus en plus d’études épidémiologiques ont montré l’importance de la carence en vitamine D dans la population générale, adulte, comme pédiatrique. Sur le plan diagnostic, la mesure du taux de la 25-hydroxy-vitamine D (25-OHD) est une méthode très fiable pour évaluer les réserves. D’autre part, beaucoup de facteurs de risque ont été mis en évidence et des populations à risque ont été identifiées. En ce qui concerne la supplémentation, il a été récemment suggéré que la stabilité de la concentration de la 25-OHD ne peut être obtenue lors de la supplémentation intermittente que si l’espacement entre les prise est inférieur à 3 mois (de l’ordre de 1 mois) . Quelques travaux récents montrent, que l’utilisation de doses journalières modérées de vitamine D plutôt que de fortes doses administrées de manière intermittente serait à privilégier.

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Granjon, David, Olivier Bonny, and Aurélie Edwards. "Coupling between phosphate and calcium homeostasis: a mathematical model." American Journal of Physiology-Renal Physiology 313, no. 6 (December 1, 2017): F1181—F1199. http://dx.doi.org/10.1152/ajprenal.00271.2017.

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We developed a mathematical model of calcium (Ca) and phosphate (PO4) homeostasis in the rat to elucidate the hormonal mechanisms that underlie the regulation of Ca and PO4balance. The model represents the exchanges of Ca and PO4between the intestine, plasma, kidneys, bone, and the intracellular compartment, and the formation of Ca-PO4-fetuin-A complexes. It accounts for the regulation of these fluxes by parathyroid hormone (PTH), vitamin D3, fibroblast growth factor 23, and Ca2+-sensing receptors. Our results suggest that the Ca and PO4homeostatic systems are robust enough to handle small perturbations in the production rate of either PTH or vitamin D3. The model predicts that large perturbations in PTH or vitamin D3synthesis have a greater impact on the plasma concentration of Ca2+([Ca2+]p) than on that of PO4([PO4]p); due to negative feedback loops, [PO4]pdoes not consistently increase when the production rate of PTH or vitamin D3is decreased. Our results also suggest that, following a large PO4infusion, the rapidly exchangeable pool in bone acts as a fast, transient storage PO4compartment (on the order of minutes), whereas the intracellular pool is able to store greater amounts of PO4over several hours. Moreover, a large PO4infusion rapidly lowers [Ca2+]powing to the formation of CaPO4complexes. A large Ca infusion, however, has a small impact on [PO4]p, since a significant fraction of Ca binds to albumin. This mathematical model is the first to include all major regulatory factors of Ca and PO4homeostasis.

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Heaney, Robert P. "Vitamin D and Bone Health—Discussion Points Following the Recent Institute of Medicine Recommendations." US Endocrinology 07, no. 02 (2011): 137. http://dx.doi.org/10.17925/use.2011.07.02.137.

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The 2011 Institute of Medicine recommendations for vitamin D—both the recommended daily amount (RDA) and the vitamin D status judged adequate for bone health—are too low. Calcium absorption, osteoporotic fracture risk reduction, and healing of histological osteomalacia all require values above 30 ng/ml, and probably even 40 ng/ml. Furthermore, the proposed RDA (600 international units per day up to the age of 70) is not compatible with the blood level of 25-hydroxyvitamin D (i.e., 20 ng/ml) recommended in the same report. Concerns regarding adverse consequences of higher intakes or status levels can be dismissed, in view of our extensive experience with outdoor summer workers (who regularly have values of 60 ng/ml or more) and the virtual certainty that human physiology evolved in—and is attuned to—an environment providing 10,000 IU/day or more.

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Genever, P. G., and I. R. Dickson. "Influence of vitamin D status on hyaluronan localization in bone." Bone 18, no. 5 (May 1996): 429–35. http://dx.doi.org/10.1016/8756-3282(96)00046-4.

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Dickson, I., and J. Walls. "Influence of vitamin a on bone collagen synthesis in vitro." Bone 6, no. 4 (1985): 277. http://dx.doi.org/10.1016/8756-3282(85)90018-3.

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Dickson, I. R., and J. Walls. "Influence of vitamin A on bone matrix formation in vitro." Bone 6, no. 6 (January 1985): 480. http://dx.doi.org/10.1016/8756-3282(85)90276-5.

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Hodges, SJ, S. Petursson, D. Harrington, C. Hopper, B. Henderson, and M. Harris. "P28. Phylloquinone (vitamin K1) content of bone in young adults." Bone 15, no. 4 (July 1994): 458. http://dx.doi.org/10.1016/8756-3282(94)90862-1.

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Wong, Dickson, Dana N. Broberg, Jagroop Doad, Joseph U. Umoh, Miranda Bellyou, Chris J. D. Norley, David W. Holdsworth, et al. "Effect of Memantine Treatment and Combination with Vitamin D Supplementation on Body Composition in the APP/PS1 Mouse Model of Alzheimer’s Disease Following Chronic Vitamin D Deficiency." Journal of Alzheimer's Disease 81, no. 1 (May 4, 2021): 375–88. http://dx.doi.org/10.3233/jad-201137.

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Background: Vitamin D deficiency and altered body composition are common in Alzheimer’s disease (AD). Memantine with vitamin D supplementation can protect cortical axons against amyloid-β exposure and glutamate toxicity. Objective: To study the effects of vitamin D deprivation and subsequent treatment with memantine and vitamin D enrichment on whole-body composition using a mouse model of AD. Methods: Male APPswe/PS1dE9 mice were divided into four groups at 2.5 months of age: the control group (n = 14) was fed a standard diet throughout; the remaining mice were started on a vitamin D-deficient diet at month 6. The vitamin D-deficient group (n = 14) remained on the vitamin D-deficient diet for the rest of the study. Of the remaining two groups, one had memantine (n = 14), while the other had both memantine and 10 IU/g vitamin D (n = 14), added to their diet at month 9. Serum 25(OH)D levels measured at months 6, 9, 12, and 15 confirmed vitamin D levels were lower in mice on vitamin D-deficient diets and higher in the vitamin D-supplemented mice. Micro-computed tomography was performed at month 15 to determine whole-body composition. Results: In mice deprived of vitamin D, memantine increased bone mineral content (8.7% increase, p < 0.01) and absolute skeletal tissue mass (9.3% increase, p < 0.05) and volume (9.2% increase, p < 0.05) relative to controls. This was not observed when memantine treatment was combined with vitamin D enrichment. Conclusion: Combination treatment of vitamin D and memantine had no negative effects on body composition. Future studies should clarify whether vitamin D status impacts the effects of memantine treatment on bone physiology in people with AD.

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Krahenbühl, Tathyane, Juliano Henrique Borges, Antonio de Azevedo Barros-Filho, Gil Guerra-Junior, and Ezequiel Moreira Gonçalves. "Assessment of bone mineral density in young female handball players." Brazilian Journal of Kinanthropometry and Human Performance 20, no. 1 (March 14, 2018): 102–13. http://dx.doi.org/10.5007/1980-0037.2018v20n1p102.

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Optimizing bone mass gain during childhood and adolescence may help prevent bone diseases in advanced ages. The aim of this study was to verify the bone mineral density (BMD) and bone mineral content (BMC) in female adolescent’s handball players. This is a cross-sectional study where 68 female adolescents (12–17 years) were allocated into two groups: handball players (n = 29) (HG) and control group (n = 39) (CG). BMC and BMD from total body (TB), total body less head (TBLH), lumbar spine (L1–L4), femoral neck (FN), Ward’s triangle (WT) and respectively Z-scores were measured using dual-energy X-ray absorptiometry (DXA). Sexual maturity, menarche, PHV, time of sun exposure, physical activity level and Calcium and vitamin D intake were assessed. The HG showed significantly higher BMC, BMD as well Z-scores values (p≤0.05) of total body, TBLH, femoral neck, hip and lumbar spine than the CG. When the values were adjusted for lean soft tissue (LST) the HG showed significantly higher BMC of femoral neck (p≤0.05), as well as BMD of TBLH and femoral neck (p≤0.05) and Z-score values all bone sites except hip, than the CG. We conclude that handball players have significantly higher bone mass values compared to group of girls of the same age.

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Dikker, Okan, Seldag Bekpinar, Gul Ozdemirler, Mujdat Uysal, Muberra Vardar, Sevgi Atar, Murat Usta, and Berrin Huner. "Evaluation of the Relation Between Omentin-1 and Vitamin D in Postmenopausal Women With or Without Osteoporosis." Experimental and Clinical Endocrinology & Diabetes 126, no. 05 (November 8, 2017): 316–20. http://dx.doi.org/10.1055/s-0043-120110.

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Abstract Introduction Crosstalk between bone and adipose tissues is implicated in several pathologic conditions related to bone metabolism. Omentin-1, a 34-kD protein, is released from omental adipose tissue. A few studies indicated the effect of omentin-1 on bone health and bone mineral density (BMD) and the interaction of omentin-1 with vitamin D. Therefore, this study aimed to investigate the relationship between omentin-1, vitamin D, and BMD in postmenopausal women with osteoporosis compared with non-osteoporotic counterparts. Materials and methods Forty postmenopausal women with osteoporosis (OP), 40 counterparts without OP, and 30 premenopausal women were enrolled. Dual-energy X-ray Absorptiometry results, body mass index, and some demographic and biochemical data were recorded. Vitamin D (25-hydroxyvitamin D3) levels were measured using liquid chromatography-tandem mass spectrometry. Serum omentin-1 was determined using an enzyme-linked immunosorbent assay. Results Omentin-1 levels tended to increase in both postmenopausal women groups compared with the control group, but this increase was significant only in women with osteoporosis. Vitamin D levels were not different between the groups. When women were categorized according to vitamin D levels, women with normal vitamin D levels had significantly higher omentin-1 levels. A positive correlation was found between omentin-1 and vitamin D levels in all groups (r=0.197, p=0.041, n=110). Conclusion The tendency to an increase in omentin-1 levels in postmenopausal women with osteoporosis may be due to a physiologic compensation against bone loss after menopause. The linear relationship between omentin-1 and vitamin D suggests that adipose tissue is one of the target tissues for the vitamin D effect.

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Okuda, N., S. Takeda, K. Shinomiya, T. Muneta, S. Itoh, M. Noda, and Y. Asou. "ED-71, a novel vitamin D analog, promotes bone formation and angiogenesis and inhibits bone resorption after bone marrow ablation." Bone 40, no. 2 (February 2007): 281–92. http://dx.doi.org/10.1016/j.bone.2006.08.017.

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Journal articles on the topic 'Bone physiology and vitamin A'

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