Статті в журналах: "Vitamin D Metabolism"

1

Goodman, William G. "Vitamin D metabolism." Current Opinion in Orthopaedics 5, no. 5 (October 1994): 60–65. http://dx.doi.org/10.1097/00001433-199410000-00010.

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2

Swaminathan, R. "Vitamin D Metabolism." Annals of Clinical Biochemistry: An international journal of biochemistry and laboratory medicine 32, no. 1 (January 1, 1995): 98–100. http://dx.doi.org/10.1177/000456329503200114.

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3

Christakos, Sylvia, Dare V. Ajibade, Puneet Dhawan, Adam J. Fechner, and Leila J. Mady. "Vitamin D: Metabolism." Rheumatic Disease Clinics of North America 38, no. 1 (February 2012): 1–11. http://dx.doi.org/10.1016/j.rdc.2012.03.003.

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4

Christakos, Sylvia, Dare V. Ajibade, Puneet Dhawan, Adam J. Fechner, and Leila J. Mady. "Vitamin D: Metabolism." Endocrinology and Metabolism Clinics of North America 39, no. 2 (June 2010): 243–53. http://dx.doi.org/10.1016/j.ecl.2010.02.002.

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5

Lehmann, Bodo, and Michael Meurer. "Vitamin D metabolism." Dermatologic Therapy 23, no. 1 (January 2010): 2–12. http://dx.doi.org/10.1111/j.1529-8019.2009.01286.x.

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6

Salle, B. L., F. H. Glorieux, and N. Bishop. "Perinatal vitamin D metabolism." Seminars in Neonatology 3, no. 2 (May 1998): 143–47. http://dx.doi.org/10.1016/s1084-2756(98)80032-8.

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7

Salle, B. L., F. H. Glorieux, and E. E. Delvin. "Perinatal Vitamin D Metabolism." Neonatology 54, no. 4 (1988): 181–87. http://dx.doi.org/10.1159/000242850.

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8

Ramasamy, Indra. "Vitamin D Metabolism and Guidelines for Vitamin D Supplementation." Clinical Biochemist Reviews 41, no. 3 (December 8, 2020): 103–26. http://dx.doi.org/10.33176/aacb-20-00006.

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Анотація:

Vitamin D is essential for bone health and is known to be involved in immunomodulation and cell proliferation. Vitamin D status remains a significant health issue worldwide. However, there has been no clear consensus on vitamin D deficiency and its measurement in serum, and clinical practice of vitamin D deficiency treatment remains inconsistent. The major circulating metabolite of vitamin D, 25-hydroxyvitamin D (25(OH)D), is widely used as a biomarker of vitamin D status. Other metabolic pathways are recognised as important to vitamin D function and measurement of other metabolites may become important in the future. The utility of free 25(OH)D rather than total 25(OH)D needs further assessment. Data used to estimate the vitamin D intake required to achieve a serum 25(OH)D concentration were drawn from individual studies which reported dose-response data. The studies differ in their choice of subjects, dose of vitamin D, frequency of dosing regimen and methods used for the measurement of 25(OH)D concentration. Baseline 25(OH)D, body mass index, ethnicity, type of vitamin D (D2 or D3) and genetics affect the response of serum 25(OH)D to vitamin D supplementation. The diversity of opinions that exist on this topic are reflected in the guidelines. Government and scientific societies have published their recommendations for vitamin D intake which vary from 400–1000 IU/d (10–25 µg/d) for an average adult. It was not possible to establish a range of serum 25(OH)D concentrations associated with selected non-musculoskeletal health outcomes. To recommend treatment targets, future studies need to be on infants, children, pregnant and lactating women.

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9

Thomas, Melissa K., and Marie B. Demay. "VITAMIN D DEFICIENCY AND DISORDERS OF VITAMIN D METABOLISM." Endocrinology and Metabolism Clinics of North America 29, no. 3 (September 2000): 611–27. http://dx.doi.org/10.1016/s0889-8529(05)70153-5.

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10

Jovičić, Snežana, Svetlana Ignjatović, and Nada Majkić-Singh. "Biochemistry and metabolism of vitamin D / Biohemija i metabolizam vitamina D." Journal of Medical Biochemistry 31, no. 4 (October 1, 2012): 309–15. http://dx.doi.org/10.2478/v10011-012-0028-8.

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Summary Vitamin D is not technically a vitamin, since it is not an essential dietary factor. It is rather a prohormone produced photochemically in the skin from 7-dehydrocholesterol. Vitamin D and its metabolites may be categorized as either cholecalciferols or ergocalciferols. Cholecalciferol (vi - tamin D3) is the parent compound of the naturally occurring family and is produced in the skin from 7-dehydrocholesterol on exposure to the ultraviolet B portion of sunlight. Vitamin D2 (ergocalciferol), the parent compound of the other family, is manufactured by irradiation of ergosterol produced by yeasts and its potency is less than one-third of vitamin D3’s potency. The steps in the vitamin D endocrine system include the following: 1) the photoconversion of 7- dehydrocholesterol to vitamin D3 in the skin or dietary intake of vitamin D3; 2) metabolism of vitamin D3 by the liver to 25-hydroxyvitamin-D3 [25(OH)D3 ], the major form of vitamin D circulating in the blood compartment; 3) conversion of 25(OH)D3 by the kidney (functioning as an endocrine gland) to the hormone 1,25-dihydroxyvitamin D3 [1,25(OH)2D3 ]; 4) systemic transport of the dihydroxylated metabolite 1,25(OH)2D3 to distal target organs; and 5) binding of 1,25(OH)2D3 to a nuclear receptor (VDR) at target organs, followed by generation of appropriate biological responses. The activation of vitamin D to its hormonal form is mediated by cytochrome P450 enzymes. Six cytochrome P450 (CYP) isoforms have been shown to hydroxylate vitamin D. Four of these, CYP27A1, CYP2R1, CYP3A4 and CYP2J3, are candidates for the enzyme vitamin D 25-hy - droxylase that is involved in the first step of activation. The highly regulated, renal enzyme 25-hydroxyvitamin D-1a-hy - dro xylase contains the component CYP27B1, which completes the activation pathway to the hormonal form 1,25(OH)2D3. A five-step inactivation pathway from 1,25(OH)2D3 to calcitroic acid is attributed to a single multifunctional CYP, CYP24A1, which is transcriptionally in du - ced in vitamin D target cells by the action of 1,25(OH)2D3. An additional key component in the operation of the vitamin D endocrine system is the plasma vitamin D binding protein (DBP), which carries vitamin D3 and its metabolites to their metabolism and target organs. DBP is a specific, high-affinity transport protein. It is synthesized by the liver and circulates in great excess, with fewer than 5% of the binding sites normally occupied. 1,25(OH)2D3, acts as a ligand for a nuclear transcription factor, vitamin D receptor - VDR, which like all other nuclear receptors, regulates gene transcription and cell function. The widespread presence of VDR, and the key activating (1a-hydroxylase, CYP27B1) and inactivating (24-hydroxylase, CYP24A1) en - zy mes in most mammalian cells means that the cells in these tissues have the potential to produce biological res pon ses, depending on the availability of appropriate amounts of vi - tamin D3. Thanks to this widespread presence of elements of vitamin D endocrine system, its biological features are being recognized outside bone tissue, i.e. calcium and pho - sphate metabolism.

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11

Lawson-Matthew, Peter, Jill Clayton, Diane Guilland-Cumming, Ashley Yates, Eric Preston, Michael Greaves, and John A. Kanis. "Vitamin D metabolism in myeloma." British Journal of Haematology 73, no. 1 (September 1989): 57–60. http://dx.doi.org/10.1111/j.1365-2141.1989.tb00220.x.

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12

Salle, Bernard L., Edgar E. Delvin, Alexandre Lapillonne, Nicholas J. Bishop, and Francis H. Glorieux. "Perinatal metabolism of vitamin D." American Journal of Clinical Nutrition 71, no. 5 (May 1, 2000): 1317S—1324S. http://dx.doi.org/10.1093/ajcn/71.5.1317s.

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13

Mawer, E. B., and M. Davies. "Vitamin D metabolism in lymphoma." Bone 7, no. 4 (1986): 304. http://dx.doi.org/10.1016/8756-3282(86)90215-2.

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14

Henry, Helen L. "Regulation of vitamin D metabolism." Best Practice & Research Clinical Endocrinology & Metabolism 25, no. 4 (August 2011): 531–41. http://dx.doi.org/10.1016/j.beem.2011.05.003.

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15

Bouillon, R., G. Carmeliet, E. Daci, S. Segaert, and A. Verstuyf. "Vitamin D Metabolism and Action." Osteoporosis International 8, S2 (September 1998): S13—S19. http://dx.doi.org/10.1007/pl00022727.

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16

Smith, R. "Vitamin D metabolism—An update." Current Orthopaedics 2, no. 2 (April 1988): 90–93. http://dx.doi.org/10.1016/0268-0890(88)90007-2.

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17

Dawson-Hughes, B. "Calcium, vitamin D and vitamin D metabolites." Osteoporosis International 6, S1 (January 1996): 93. http://dx.doi.org/10.1007/bf02499912.

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18

Miller, Walter L., and Erik A. Imel. "Rickets, Vitamin D, and Ca/P Metabolism." Hormone Research in Paediatrics 95, no. 6 (2022): 579–92. http://dx.doi.org/10.1159/000527011.

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Rickets was a major public health problem dating from Roman times, and medical descriptions of rickets date from the 17th century. Sniadecki first advocated treatment by exposure to sunshine in 1822; contemporaneously, several British physicians advocated use of cod liver oil. Both approaches were successful. Work in 1924 showed that exposure to UV light endowed fats and other foods with antirachitic properties. Vitamins D2 and D3, the antirachitic agent in cod liver oil, were, respectively, produced by UV radiation of ergosterol and 7-dehydrocholesterol. Calcitriol (1,25[OH]2D3) was identified as the biologically active form of vitamin D in the early 1970s. The vitamin D 25-hydroxylase, 24-hydroxylase, and 1α-hydroxylase were cloned in the 1990s and their genetic defects were soon delineated. The vitamin D receptor was also cloned and its mutations identified in vitamin D-resistant rickets. Work with parathyroid hormone (PTH) began much later, as the parathyroids were not identified until the late 19th century. In 1925, James B. Collip (of insulin fame) identified PTH by its ability to correct tetany in parathyroidectomized dogs, but only in the 1970s was it clear that only a small fragment of PTH conveyed its activity. Congenital hypoparathyroidism with immune defects was described in 1968, eventually linked to microdeletions in chromosome 22q11.2. X-linked hypophosphatemic rickets was reported in 1957, and genetic linkage analysis identified the causative PHEX gene in 1997. Autosomal dominant hypophosphatemic rickets similarly led to the discovery of FGF23, a phosphate-wasting humoral factor made in bone, in 2000, revolutionizing our understanding of phosphorus metabolism.

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19

Kaminsky, O. V. "Vitamin D dosage." INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine) 17, no. 5 (January 4, 2022): 435–42. http://dx.doi.org/10.22141/2224-0721.17.5.2021.241524.

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Despite its historical name, vitamin D is not a vitamin at all but a hormone that, when activated, is a metabolically active steroid fat-soluble hormone that acts on cellular receptors. Vitamin D hormone is synthesized endogenously and then metabolized in the body, provi-ding that there are the necessary precursors and some factors — the effects of ultraviolet light on the skin. At the same time, vitamins themselves are nutrients, co-factors of biochemical reactions that are not synthesized in the body and cannot interact with receptors, consumed with food, so the hormone D is not a vitamin. Disputes about its use and dosage continue throughout the study period of vitamin D hormone. Most reputable experts in Europe and the USA support the need to replenish and maintain a normal level of vitamin D, believing it to be completely safe and useful. In 2011, the US Endocrine Society issued clinical practice guidelines for vitamin D, indicating that the desired serum concentration of 25(OH)D is > 75 nmol/l (> 30 ng/ml) to achieve the maximum effect of this vitamin on calcium metabolism, bone, and muscle metabolism. According to them, for a consistent increase in serum 25(OH)D above 75 nmol/l (30 ng/ml), adults may require at least 1,500-2,000 IU/day of additional vitamin D, at least 1,000 IU/day in children and adolescents. The most common form of thyroid dysfunction is secondary hyperparathyroidism, which develops due to vitamin D defect/deficiency (80–90 %). Non-optimal serum concentrations of 25(OH)D lead to secondary hyperparathyroidism, potentially leading to decreased bone mineralization and, ultimately, to an increased risk of osteopenia, osteoporosis and fractures, cardiac arrhythmia, and increased blood pressure. Vitamin D is most commonly used at a star-ting dose of 5,000 IU daily for 2–3 months, then transferring patients to maintenance doses of 2,000–4,000 IU/day daily that are consi-dered safe. However, it should be noted that some patients will need constant administration of 5,000 IU of vitamin D per day for a long time (years) to maintain the target optimal level of 25(OH)D in the blood, especially in patients with normocalcemic forms of secondary hyperparathyroidism.

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20

Karamali, Maryam, Mahnaz Ashrafi, Maryamalsadat Razavi, Mehri Jamilian, Maryam Akbari, and Zatollah Asemi. "The Effects of Calcium, Vitamins D and K co-Supplementation on Markers of Insulin Metabolism and Lipid Profiles in Vitamin D-Deficient Women with Polycystic Ovary Syndrome." Experimental and Clinical Endocrinology & Diabetes 125, no. 05 (April 13, 2017): 316–21. http://dx.doi.org/10.1055/s-0043-104530.

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Abstract Data on the effects of calcium, vitamins D and K co-supplementation on markers of insulin metabolism and lipid profiles among vitamin D-deficient women with polycystic ovary syndrome (PCOS) are scarce. This study was done to determine the effects of calcium, vitamins D and K co-supplementation on markers of insulin metabolism and lipid profiles in vitamin D-deficient women with PCOS. This randomized double-blind, placebo-controlled trial was conducted among 55 vitamin D-deficient women diagnosed with PCOS aged 18–40 years old. Subjects were randomly assigned into 2 groups to intake either 500 mg calcium, 200 IU vitamin D and 90 µg vitamin K supplements (n=28) or placebo (n=27) twice a day for 8 weeks. After the 8-week intervention, compared with the placebo, joint calcium, vitamins D and K supplementation resulted in significant decreases in serum insulin concentrations (−1.9±3.5 vs. +1.8±6.6 µIU/mL, P=0.01), homeostasis model of assessment-estimated insulin resistance (−0.4±0.7 vs. +0.4±1.4, P=0.01), homeostasis model of assessment-estimated b cell function (−7.9±14.7 vs. +7.0±30.3, P=0.02) and a significant increase in quantitative insulin sensitivity check index (+0.01±0.01 vs. −0.008±0.03, P=0.01). In addition, significant decreases in serum triglycerides (−23.4±71.3 vs. +9.9±39.5 mg/dL, P=0.03) and VLDL-cholesterol levels (−4.7±14.3 vs. +2.0±7.9 mg/dL, P=0.03) was observed following supplementation with combined calcium, vitamins D and K compared with the placebo. Overall, calcium, vitamins D and K co-supplementation for 8 weeks among vitamin D-deficient women with PCOS had beneficial effects on markers of insulin metabolism, serum triglycerides and VLDL-cholesterol levels.

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21

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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22

Saponaro, Federica, Alessandro Saba, and Riccardo Zucchi. "An Update on Vitamin D Metabolism." International Journal of Molecular Sciences 21, no. 18 (September 8, 2020): 6573. http://dx.doi.org/10.3390/ijms21186573.

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Vitamin D is a steroid hormone classically involved in the calcium metabolism and bone homeostasis. Recently, new and interesting aspects of vitamin D metabolism has been elucidated, namely the special role of the skin, the metabolic control of liver hydroxylase CYP2R1, the specificity of 1α-hydroxylase in different tissues and cell types and the genomic, non-genomic and epigenomic effects of vitamin D receptor, which will be addressed in the present review. Moreover, in the last decades, several extraskeletal effects which can be attributed to vitamin D have been shown. These beneficial effects will be here summarized, focusing on the immune system and cardiovascular system.

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23

Patil, Dr Vishakha S. "Vitamin D: A Review on Metabolism and Regulating Factors (Part I)." Journal of Medical Science And clinical Research 04, no. 12 (December 24, 2016): 14871–77. http://dx.doi.org/10.18535/jmscr/v4i12.92.

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24

Moriya, Aya, Tsutomu Fukuwatari, Mitsue Sano, and Katsumi Shibata. "Different variations of tissue B-group vitamin concentrations in short- and long-term starved rats." British Journal of Nutrition 107, no. 1 (June 27, 2011): 52–60. http://dx.doi.org/10.1017/s0007114511002339.

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Prolonged starvation changes energy metabolism; therefore, the metabolic response to starvation is divided into three phases according to changes in glucose, lipid and protein utilisation. B-group vitamins are involved in energy metabolism via metabolism of carbohydrates, fatty acids and amino acids. To determine how changes in energy metabolism alter B-group vitamin concentrations during starvation, we measured the concentration of eight kinds of B-group vitamins daily in rat blood, urine and in nine tissues including cerebrum, heart, lung, stomach, kidney, liver, spleen, testis and skeletal muscle during 8 d of starvation. Vitamin B1, vitamin B6, pantothenic acid, folate and biotin concentrations in the blood reduced after 6 or 8 d of starvation, and other vitamins did not change. Urinary excretion was decreased during starvation for all B-group vitamins except pantothenic acid and biotin. Less variation in B-group vitamin concentrations was found in the cerebrum and spleen. Concentrations of vitamin B1, vitamin B6, nicotinamide and pantothenic acid increased in the liver. The skeletal muscle and stomach showed reduced concentrations of five vitamins including vitamin B1, vitamin B2, vitamin B6, pantothenic acid and folate. Concentrations of two or three vitamins decreased in the kidney, testis and heart, and these changes showed different patterns in each tissue and for each vitamin. The concentration of pantothenic acid rapidly decreased in the heart, stomach, kidney and testis, whereas concentrations of nicotinamide were stable in all tissues except the liver. Different variations in B-group vitamin concentrations in the tissues of starved rats were found. The present findings will lead to a suitable supplementation of vitamins for the prevention of the re-feeding syndrome.

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25

Alshahrani, Fahad M., Mussa H. Almalki, Naji Aljohani, Abdullah Alzahrani, Yousef Alsaleh, and Michael F. Holick. "Vitamin D." Dermato-Endocrinology 5, no. 1 (January 2013): 177–80. http://dx.doi.org/10.4161/derm.23351.

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26

Gröber, Uwe, Jörg Spitz, Jörg Reichrath, Klaus Kisters, and Michael F. Holick. "Vitamin D." Dermato-Endocrinology 5, no. 3 (June 2013): 331–47. http://dx.doi.org/10.4161/derm.26738.

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27

Detopoulou, Paraskevi, Sousana K. Papadopoulou, Gavriela Voulgaridou, Vasileios Dedes, Despoina Tsoumana, Aristea Gioxari, George Gerostergios, Maria Detopoulou, and George I. Panoutsopoulos. "Ketogenic Diet and Vitamin D Metabolism: A Review of Evidence." Metabolites 12, no. 12 (December 19, 2022): 1288. http://dx.doi.org/10.3390/metabo12121288.

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The ketogenic diet (KD), which is low in carbohydrates and high to normal in fat and protein, has been traditionally used in epilepsy for the last 100 years. More recently, its application in obesity has been introduced. The present review aimed to investigate the effects of the KD on vitamin D. In total, five studies were done in healthy adults, one in subjects with type 2 diabetes, and seven in subjects with epilepsy that assessed the levels of vitamin D pre- and post-intervention. In the majority of studies, increases in circulating vitamin D were reported. The relationship of the KD with vitamin D was explained through several mechanisms: ketone bodies, macronutrient intake, the status levels of other fat-soluble vitamins, weight loss, changes in the hormonal milieu, and effects on gut microbiota. Moreover, potential nutrient–gene-related interactions were discussed. There is still a need to conduct multiple arm studies to compare the effects of the KD versus other diets and better decipher the particular effects of the KD on vitamin D levels and metabolism. Moreover, differentiations of the diet’s effects according to sex and genetic makeup should be investigated to prescribe KDs on a more personalized basis.

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28

Maylyan, E. A., N. A. Rheznichenko, and D. E. Maylyan. "VITAMIN D REGULATION OF BONE METABOLISM." Medical Herald of the South of Russia, no. 1 (January 1, 2017): 12–20. http://dx.doi.org/10.21886/2219-8075-2017-1-12-20.

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29

Kimura, Saburo, Yoshiki Seino, Tokuzo Harada, Osamu Nose, Kanji Yamaoka, Kazuo Shimizu, Hiroyuki Tanaka, et al. "Vitamin D Metabolism in Biliary Atresia." Journal of Pediatric Gastroenterology and Nutrition 7, no. 3 (May 1988): 341–46. http://dx.doi.org/10.1097/00005176-198805000-00005.

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30

KOBAYASHI, TADASHI. "Metabolism of vitamin D and calcium." Eisei kagaku 33, no. 5 (1987): 300–312. http://dx.doi.org/10.1248/jhs1956.33.300.

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31

Khokhar, Aditi, Salvador Castells, and Sheila Perez-Colon. "Genetic Disorders of Vitamin D Metabolism." Clinical Pediatrics 55, no. 5 (December 23, 2015): 404–14. http://dx.doi.org/10.1177/0009922815623231.

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32

Fraser, David R. "Vitamin D Deficiency and Energy Metabolism." Endocrinology 156, no. 6 (June 1, 2015): 1933–35. http://dx.doi.org/10.1210/en.2015-1298.

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33

Lagishetty, Venu, Nancy Q. Liu, and Martin Hewison. "Vitamin D metabolism and innate immunity." Molecular and Cellular Endocrinology 347, no. 1-2 (December 2011): 97–105. http://dx.doi.org/10.1016/j.mce.2011.04.015.

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34

Morris, Howard A., and Paul H. Anderson. "Vitamin D metabolism and biological activities." Molecular and Cellular Endocrinology 347, no. 1-2 (December 2011): 1–2. http://dx.doi.org/10.1016/j.mce.2011.06.018.

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35

Bosworth, Cortney, and Ian H. de Boer. "Impaired Vitamin D Metabolism in CKD." Seminars in Nephrology 33, no. 2 (March 2013): 158–68. http://dx.doi.org/10.1016/j.semnephrol.2012.12.016.

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36

Steinherz, R., A. Metzker, B. Eisenstein, and R. Samuel. "Vitamin D metabolism in tumoral calcinosis." European Journal of Pediatrics 148, no. 5 (February 1989): 475. http://dx.doi.org/10.1007/bf00595920.

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37

Chakhtoura, Marlene, Maya Rahme, and Ghada El-Hajj Fuleihan. "Vitamin D Metabolism in Bariatric Surgery." Endocrinology and Metabolism Clinics of North America 46, no. 4 (December 2017): 947–82. http://dx.doi.org/10.1016/j.ecl.2017.07.006.

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38

Carpenter, Thomas O. "Mineral regulation of vitamin D metabolism." Bone and Mineral 5, no. 3 (March 1989): 259–69. http://dx.doi.org/10.1016/0169-6009(89)90004-4.

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39

Berry, Jacqueline L., Michael Davies, and Andrew P. Mee. "Vitamin D Metabolism, Rickets, and Osteomalacia." Seminars in Musculoskeletal Radiology 06, no. 3 (2002): 173–82. http://dx.doi.org/10.1055/s-2002-36714.

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40

Kobayashi, Tadashi. "Metabolism of Vitamin D and Calcium." Japanese Journal of Nutrition and Dietetics 55, no. 5 (1997): 217–29. http://dx.doi.org/10.5264/eiyogakuzashi.55.217.

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41

Salle, B. L., J. Senterre, F. H. Glorieux, E. E. Delvin, and G. Putet. "Vitamin D Metabolism in Preterm Infants." Neonatology 52, no. 1 (1987): 119–30. http://dx.doi.org/10.1159/000242749.

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42

Landrier, Jean‐François, Lourdes Mounien, and Franck Tourniaire. "Obesity and Vitamin D Metabolism Modifications." Journal of Bone and Mineral Research 34, no. 7 (May 29, 2019): 1383. http://dx.doi.org/10.1002/jbmr.3739.

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43

Griffiths, Paul, and Angela Fairney. "Vitamin D metabolism in polar vertebrates." Comparative Biochemistry and Physiology Part B: Comparative Biochemistry 91, no. 3 (January 1988): 511–16. http://dx.doi.org/10.1016/0305-0491(88)90014-4.

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44

Kochneva, E. V., S. Yu Kalinchenko, and D. V. Makharoblishvili. "Vitamin D deficiency: a pandemic of the 21st century. Problems of standardization of diagnosis of vitamin D deficiency." Voprosy dietologii 11, no. 1 (2021): 33–43. http://dx.doi.org/10.20953/2224-5448-2021-1-33-43.

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Vitamin D deficiency is a noninfectious pandemic of the 21st century. Vitamin D, apart from its role in phosphorus-calcium metabolism, is vital for functioning of all organs and systems, and its deficiency is a risk factor of developing aging-associated extraskeletal diseases. Vitamin D deficiency is a multifactor process related to a decreased synthesis of endogenous cholecalcipherol, insufficient intake of exogenous vitamin D and its disordered metabolism. Improvement of the effectiveness of therapeutic and preventive measures for management of vitamin D deficiency is impossible without accurate laboratory diagnosis. Immunochemical methods (radioactive, enzymatic and chemiluminescent) overestimate the 25(ОН)D levels, a benchmark test for vitamin D status assessment is a high performance liquid chromatography tandem–mass spectrometry. In order to reduce the risk of socially significant diseases the adequate 25(ОН)D levels should be not less than 40 ng/mL (100 nmol/L). Key words: vitamin D, vitamin D deficiency, liquid chromatography tandem–mass spectrometry

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45

Marushko, Yu V., and T. V. Hyshchak. "Prevention of vitamin D deficiency in children. The state of the problem in the world and in Ukraine." Modern pediatrics. Ukraine, no. 4(116) (May 26, 2021): 36–45. http://dx.doi.org/10.15574/sp.2021.116.36.

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The article presents current data on the prevalence of vitamin D deficiency and criteria for its deficiency in children in different countries. Vitamin D is recognized as one of the most important vitamins involved in many biochemical processes in the body. Its active metabolites play a key role in calcium absorption, bone mineralization and promote phosphate and magnesium metabolism. At the same time, in addition to affecting mineral metabolism, there is a wide range of conditions in which vitamin D also plays a preventive role. Vitamin D has been shown to play a vital role in innate immunity maintenance and is important in prevention of several diseases, including infections, autoimmune diseases, certain forms of cancer, type 1 and 2 diabetes, and cardiovascular diseases. Vitamin D is of particular importance for newborns and young children. This vitamin is involved in important physiological regulatory processes such as bone metabolism, lung development, maturation of the immune system and differentiation of the nervous system. Vitamin D deficiency increases risks of neonatal sepsis, necrotizing enterocolitis, respiratory distress syndrome, and bronchopulmonary dysplasia. Adequate intake of vitamin D and calcium during childhood can reduce the risk of osteoporosis and other diseases associated with vitamin D deficiency in adults. Recently, vitamin D deficiency has shown to be a potential risk factor for COVID-19 propensity. It has been established that to date most scientific pediatric societies have recognized the need to prevent vitamin D deficiency in healthy children of all ages, but data on the dosage of vitamin D in its prophylactic use differ. Most scientific societies recommend an average of 400–600 IU per day of vitamin D for prophylactic purposes. The analysis of published data shows the need to follow a strategy based on an individual approach, taking into account physiological characteristics, individual requirements and lifestyle. No conflict of interest was declared by the authors. Key words: vitamin D, children, deficiency, prevention.

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46

Hurst, Emma A., Natalie Z. Homer, and Richard J. Mellanby. "Vitamin D Metabolism and Profiling in Veterinary Species." Metabolites 10, no. 9 (September 15, 2020): 371. http://dx.doi.org/10.3390/metabo10090371.

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The demand for vitamin D analysis in veterinary species is increasing with the growing knowledge of the extra-skeletal role vitamin D plays in health and disease. The circulating 25-hydroxyvitamin-D (25(OH)D) metabolite is used to assess vitamin D status, and the benefits of analysing other metabolites in the complex vitamin D pathway are being discovered in humans. Profiling of the vitamin D pathway by liquid chromatography tandem mass spectrometry (LC-MS/MS) facilitates simultaneous analysis of multiple metabolites in a single sample and over wide dynamic ranges, and this method is now considered the gold-standard for quantifying vitamin D metabolites. However, very few studies report using LC-MS/MS for the analysis of vitamin D metabolites in veterinary species. Given the complexity of the vitamin D pathway and the similarities in the roles of vitamin D in health and disease between humans and companion animals, there is a clear need to establish a comprehensive, reliable method for veterinary analysis that is comparable to that used in human clinical practice. In this review, we highlight the differences in vitamin D metabolism between veterinary species and the benefits of measuring vitamin D metabolites beyond 25(OH)D. Finally, we discuss the analytical challenges in profiling vitamin D in veterinary species with a focus on LC-MS/MS methods.

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MAWER, E. BARBARA, S. W. STANBURY, M. J. ROBINSON, J. JAMES, and C. CLOSE. "VITAMIN D NUTRITION AND VITAMIN D METABOLISM IN THE PREMATURE HUMAN NEONATE." Clinical Endocrinology 25, no. 6 (December 1986): 641–49. http://dx.doi.org/10.1111/j.1365-2265.1986.tb03619.x.

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48

Nicolaidou, Polyxeni, Anna Papadopoulou, Helen Georgouli, Y. G. Matsinos, Helen Tsapra, Andreas Fretzayas, Aglaia Giannoulia-Karantana, et al. "Calcium and Vitamin D Metabolism in Hypocalcemic Vitamin D-Resistant Rickets Carriers." Hormone Research in Paediatrics 65, no. 2 (2006): 83–88. http://dx.doi.org/10.1159/000091043.

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van Ballegooijen, Adriana J., Stefan Pilz, Andreas Tomaschitz, Martin R. Grübler, and Nicolas Verheyen. "The Synergistic Interplay between Vitamins D and K for Bone and Cardiovascular Health: A Narrative Review." International Journal of Endocrinology 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/7454376.

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Vitamins D and K are both fat-soluble vitamins and play a central role in calcium metabolism. Vitamin D promotes the production of vitamin K-dependent proteins, which require vitamin K for carboxylation in order to function properly. The purpose of this review is to summarize available evidence of the synergistic interplay between vitamins D and K on bone and cardiovascular health. Animal and human studies suggest that optimal concentrations of both vitamin D and vitamin K are beneficial for bone and cardiovascular health as supported by genetic, molecular, cellular, and human studies. Most clinical trials studied vitamin D and K supplementation with bone health in postmenopausal women. Few intervention trials studied vitamin D and K supplementation with cardiovascular-related outcomes. These limited studies indicate that joint supplementation might be beneficial for cardiovascular health. Current evidence supports the notion that joint supplementation of vitamins D and K might be more effective than the consumption of either alone for bone and cardiovascular health. As more is discovered about the powerful combination of vitamins D and K, it gives a renewed reason to eat a healthy diet including a variety of foods such as vegetables and fermented dairy for bone and cardiovascular health.

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Maltsev, S. V. "Current perspectives of using vitamin D in clinical practice." Russian Journal of Woman and Child Health 5, no. 3 (2022): 244–52. http://dx.doi.org/10.32364/2618-8430-2022-5-3-244-252.

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An approach to problem solving in public health has revived interest to the prevalence rate of vitamin D deficiency, its role in the pathogenesis of various disease, and strategies for treating vitamin D deficiency. The article presents updates on vitamin D metabolism — its classical and non-calcemic actions. The emphasis is made on the effects of its individual metabolites and other components of the vitamin D endocrine system, such as hydrolase, vitamin-D receptors, and vitamin-D-binding protein (VDBP). The functions of vitamin D are characterized as genomic and non-genomic, including immunomodulatory effect. In particular, the role of vitamin D in patients with COVID-19 is elucidated. The vitamin-D endocrine system plays a special role during pregnancy and in children of all age groups. The article highlights the latest data on vitamin D provision, individual variability in the responses to the same vitamin D dose, as well as the findings of a new research area relating to the content of vitamin D metabolites in food of animal origin. Also, it describes vitamin D intoxication which is usually linked to the impaired regulation of vitamin D metabolism. The clinical efficacy of cholecalciferol agents is demonstrated. KEYWORDS: cholecalciferol, vitamin D metabolism, vitamin D-endocrine system, pregnant women, children, adolescents, vitamin D provision, individual response to vitamin D, food of animal origin, vitamin D intoxication, hypervitaminosis D. FOR CITATION: Maltsev S.V. Current perspectives of using vitamin D in clinical practice. Russian Journal of Woman and Child Health. 2022;5(3):244–252 (in Russ.). DOI: 10.32364/2618-8430-2022-5-3-244-252.

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