What Is The Purpose Of Vitamin D – Transgenic expression of Haemonchus contortus cytochrome P450 Hco-cyp-13A11 reduces sensitivity to specific but not all macrocyclic lactones

Open Access Policy Institutional Open Access Program Special Issue Guidelines Editorial Process Research and Publication Ethics Article Processing Fee Award Testimonials

What Is The Purpose Of Vitamin D

All articles published by are made immediately available worldwide under an open access license. No special permission is required to re-use all or part of the published article, including figures and tables. For articles published under the open access Creative Commons CC BY license, any part of the article may be reused without permission as long as the original article is clearly cited. For more information, please visit https:///openaccess.

The New Roche Vitamin D Total Assay: Fit For Its Purpose?

Feature papers represent the most advanced research with significant potential for high impact in the field. A feature paper should be a substantial original article that includes several techniques or approaches, provides an outlook for future research directions and describes potential research applications.

Feature papers are submitted by personal invitation or recommendation of scientific editors and must receive positive feedback from reviewers.

Editor’s Choice articles are based on recommendations by scientific editors of journals around the world. The editors select a small number of recently published articles in the journal that they believe will be particularly interesting to readers, or important in a related research area. The aim of the journal is to provide a snapshot of some of the most exciting work published in various research areas.

By Fulvia Zappulo Fulvia Zappulo Scilit Preprints.org Google Scholar , Maria Cappuccili Maria Cappuccili Scilit Preprints.org Google Scholar , Alessandra Cingolani Alessandra Cingolani Scilit Preprints.org Google Scholar , Anna Scrivo Anna Scrivo Scilit Preprints.org Google Scholar Laura Croci Chiocchini Scilit Preprints. org Google Scholar , Miriam Di Nunzio Miriam Di Nunzio Scilit Preprints.org Google Scholar , Chiara Donadei Chiara Donadei Scilit Preprints.org Google Scholar , Marianna Napoli Marianna Napoli Scilit Preprints.org , Google Scholar Preprints.org Google Scholar , Giuseppe Cianciolo Giuseppe Cianciolo Scilit Preprints.org Google Scholar and Gaetano La Manna Gaetano La Manna Scilit Preprints.org Google Scholar *

Hyperparathyroidism And Vitamin D

Nephrology, Dialysis and Renal Transplant Unit, IRCCS-Azienda Ospedaliero-Universitaria di Bologna, Alma Mater Studiorum University of Bologna, 40138 Bologna, Italy

Received: 29 June 2022 / Revised: 8 August 2022 / Accepted: 11 August 2022 / Published: 15 August 2022

(This article is related to the Role of Vitamin D in Human Health and Disease 2.0 Special Issue)

Vitamin D is a group of liposoluble steroids involved in bone metabolism by modulating to varying degrees calcium and phosphorus absorption or reabsorption, as well as parathyroid hormone production. Recent evidence has demonstrated extra-skeletal effects of vitamin D, including glucose homeostasis, cardiovascular protection, and anti-inflammatory and antiproliferative effects. This narrative review provides a holistic view of the role of vitamin D in various settings, with a particular focus on chronic kidney disease and kidney transplantation.

Vitamin D + K2 Liquid & Reviews

Calcium; heart disease; cholecalciferol; Chronic kidney disease – mineral and bone disorders; fibroblast growth factor 23; kidney transplant; parathyroid hormone; Vitamin D; Vitamin D receptor

The term “vitamin D” refers to a group of liposoluble, steroidal compounds important for intestinal absorption and regulation of calcium and phosphate metabolism [1]. The most important isoforms in human physiology are ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3), also known as calciol; While the first is only synthesized in plants and fungi (dietary intake), the second is exogenous and produced endogenously from the photolysis of 7-dehydrocholesterol by UVB radiation in the skin [2]. Calciols undergo two-step hydroxylation to convert to the biologically active form, calcitriol. First, vitamin D 25-hydroxylase in the liver mediates the conversion of D2/D3 to 25(OH)D (calcidiol), a quantitative form often used to determine serum vitamin D levels, and is defined as the parent form. . The next step is hydroxylation at carbon 1 in the renal proximal tubule to form calcitriol, also known as 1, 25-dihydroxyvitamin D [1, 25(OH)2D]. Serum 1, 25(OH)2D provides little information about vitamin D status, and it is usually normal or even elevated when hyperparathyroidism is associated with vitamin D deficiency [3].

1, 25(OH)2D reaches target organs in the systemic circulation via vitamin D-binding protein (VDBP), then binds to the local vitamin D receptor (VDR). It is known that VDR is related to a wide group of ligand-activated nuclear transcription factors, and it can boast almost ubiquitous and tissue-dependent expression in nucleated cells [4]. Besides triggering the absorption, output, and mobilization of both calcium and phosphorus, vitamin D also exerts several non-osteogenic and non-calcemic actions, thus representing a key player in extraskeletal health [3].

To avoid intoxication, calcidiol and calcitriol are tightly regulated by 25(OH)D 24-hydroxylase (CYP24A1), which is the primary vitamin D-inactivating enzyme for both compounds [ 5 ]. Furthermore, parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) also regulate vitamin D metabolism. PTH is produced by the parathyroid glands in response to low serum calcium levels; It stimulates bone turnover and increases 1, 25(OH)2D levels due to the induction of renal expression of the involved cytochrome (CYP27B1). FGF23 is instead produced by osteoblasts and osteoclasts in response to high phosphate and calcitriol serum levels and reduces calcitriol production by inhibiting CYP27B1 in the kidney [ 6 , 7 ]. In Figure 1, the main systemic effects of 1, 25(OH)2D are highlighted.

Vitomin D3 Granules 1 Gm Price, Uses, Side Effects, Composition

Vitamin D has direct and indirect control of bone-matrix formation, as its main physiological function is the modulation of calcium and phosphorus absorption or reabsorption at different levels. In this frame, the kidney has a major involvement: once calcium and inorganic phosphorus are filtered in preurein, 1, 25(OH) 2D, together with PTH, regulates their reabsorption through various channels and transporters in distant, tubular segments. Under conditions of normal renal function, approximately 98% of filtered calcium is reabsorbed by the kidney; In the proximal tubules, where the thiazide diuretics, 1, 25(OH)2D, and PTH have no effect, Na-dependent, paracellular mechanisms mediate the uptake of 50–60% of the total calcium load. The descending loop of the loop of Henle and the thin, ascending limb play a minor role in calcium homeostasis. On the other hand, significant percentages of filtered mineral reabsorption occur in the thick, ascending limb (20%), distal tubule (10–15%), and collecting duct (5%), where calcium reabsorption is ATP dependent and epithelial calcium channels, calbindin , and mediated by plasma membrane Ca

Another important function of vitamin D is the enhancement of intestinal calcium and phosphorus reabsorption. This is actually demonstrated by the large effect of vitamin D on the amount of internal calcium uptake: with 25(OH)D insufficiency, only 10-20% of dietary calcium intake finally enters the bloodstream, while adequate levels of the prohormone improve absorption. up to 30–40% [12, 13]. Many of the direct effects of vitamin D on skeletal tissue are not fully understood. However, there is much evidence to suggest that the involvement of vitamin D in bone tissue deposition and remodeling is represented not only through the regulation of Ca/P serum levels in close coordination with PTH, but also through a direct effect on bone. cells expressing VDR, osteoblasts, and osteoclasts [14]. 1α-hydroxylation of 25(OH)D to 1, 25(OH).

While D in bone cells was described many years ago, the discovery of its autocrine/paracrine activity for osteoblast and osteoclast maturation and proliferation is relatively recent [15]. It has been proved that 1, 25 (OH)

D promotes the expression of RANKL, osteocalcin, and osteopontin, associated with osteoblast maturation and mineralization. Furthermore, 1, 25 (OH) 2D also controls hyperactive osteoclastic resorptive activity and upregulates the expression of FGF23 and sclerostin via VDR [ 16 ].

High Dose Vitamin D3 Supplementation In Relapsing Remitting Multiple Sclerosis: A Randomised Clinical Trial

Patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD) have a higher prevalence of vitamin D deficiency and insufficiency than the healthy population. Different definitions of vitamin D deficiency and insufficiency have been provided over the years, resulting in heterogeneous guidelines, ranges, and cut-offs. However, most clinicians follow the recommendations of the Endocrine Society, where 25(OH)D concentrations 30 ng/mL are normal/adequate [16]. Given the severe dietary restrictions in subjects with impaired renal function and the presence of comorbidities that may affect hospitalization and mobility, CKD patients usually require vitamin D supplementation, mainly cholecalciferol and calcifediol-based supplementation [17]. Moreover, 1α-hydroxylation of 25(OH)D is impaired due to damaged renal tissue. As a result hypocalcemia and hyperphosphoremia, secondary to renal failure, secondary hyperparathyroidism and hyperphosphatemic, increased serum levels of osteocyte-derived fibroblast growth factor 23 (FGF23) [18]. PTH and FGF23 have opposite effects on the regulation of 1α-hydroxylase: while PTH increases its expression to reverse the tendency to calcium loss, FGF23, which is triggered by phosphate retention, inhibits renal 1α-hydroxylase expression [ 7 ]. Chronic 25(OH)D and 1, 25(OH)2D insufficiency and secondary hyperparathyroidism result in a broad spectrum of bone loss, commonly found in the CKD/ESRD population with chronic kidney disease-mineral and bone disorders (CKD-MBD) [19].

Chronic 25(OH)D and 1, 25(OH) 2D deficiency leads to decreased bone mineral density and progressive bone loss, which burdens the patient.

The purpose of vitamin c, what is the purpose of vitamin d, what is the purpose of vitamin e, what is the purpose of vitamin d3, the purpose of vitamin d, the purpose of vitamin d3, what is the purpose of vitamin b, what is the purpose of vitamin b complex, what is the purpose of vitamin b12, what is the purpose of vitamin c, what is the purpose of vitamin c serum, what is the purpose of vitamin k