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Malachi J McKenna and Barbara F Murray

Introduction Two conflicting reports on vitamin D intake requirements were published in 2011: Institute of Medicine (IOM) report on Dietary Reference Intakes for Calcium and Vitamin D and the Endocrine Society's Clinical Practice Guideline (CPG

Open access

Melissa Braga, Zena Simmons, Keith C Norris, Monica G Ferrini and Jorge N Artaza

Introduction Vitamin D is universally recognized for its classical effects on calcium regulation and phosphate homeostasis, in relation to bone development and maintenance ( 1 , 2 ). However, vitamin D deficiency has also been linked to the

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Suma Uday, Ardita Kongjonaj, Magda Aguiar, Ted Tulchinsky and Wolfgang Högler

Introduction Vitamin D deficiency and its complications such as osteomalacia, rickets, hypocalcaemic seizures, dilated cardiomyopathy and skeletal myopathy are a growing concern worldwide in high-, medium- and low-income countries regardless

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Gunjan Garg, Garima Kachhawa, Rekha Ramot, Rajesh Khadgawat, Nikhil Tandon, V Sreenivas, Alka Kriplani and N Gupta

Introduction Vitamin D deficiency (VDD) was once thought to exclusively affect bone metabolism. Currently, however, there is ample evidence of its role in many extra-skeletal conditions including metabolic syndrome, autoimmune diseases, and cancer

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Karoline Winckler, Lise Tarnow, Louise Lundby-Christensen, Thomas P Almdal, Niels Wiinberg, Pia Eiken, Trine W Boesgaard and the CIMT trial group

detect more subtle changes in the relative proportions of the layering of the arterial wall (9, 10) . A number of studies indicate a high prevalence of vitamin D deficiency in the general population and diabetic cohorts (11, 12) . Several

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Ozlem Atan Sahin, Damla Goksen, Aysel Ozpinar, Muhittin Serdar and Huseyin Onay

Introduction Type 1 diabetes (DM1) is a complex disease characterized by the autoimmune destruction of pancreatic β cells. Vitamin D is an immune regulatory hormone that exerts its effects through highly polymorphic VDR that belongs to

Open access

Amarjit Saini, LInda Björkhem Bergman, Johan Boström, Mats Lilja, Michael Melin, Karl Olsson, Lena Ekström, Peter Bergman, Mikael Altun, Eric Rullman and Thomas Gustafsson

The CC-genotype of the VDR polymorphism TaqI rs731236 has previously been associated with a higher risk of developing myopathy compared to TT-carriers. However, the mechanistic role of this polymorphism in skeletal muscle is not well defined. The effects of vitamin D on patients genotyped for the VDR polymorphism TaqI rs731236, comparing CC and TT-carriers were evaluated. Primary human myoblasts isolated from 4 CC-carriers were compared with myoblasts isolated from 4 TT-carriers and treated with vitamin D in vitro. A dose-dependent inhibitory effect on myoblast proliferation and differentiation was observed concurrent with modifications of key myogenic regulatory factors. RNA-sequencing revealed a Vitamin D dose-response gene signature enriched with a higher number of VDR-responsive elements (VDREs) per gene. Interestingly, the greater the expression of muscle differentiation markers in myoblasts the more pronounced was the Vitamin D-mediated response to suppress genes associated with myogenic fusion and myotube formation. This novel finding provides a mechanistic explanation to the inconsistency regarding previous reports of the role of vitamin D in myoblast differentiation. No effects in myoblast proliferation, differentiation or gene expression were related to CC vs. TT carriers. Our findings suggest that the VDR polymorphism TaqI rs731236 comparing CC vs. TT carriers did not influence the effects of vitamin D on primary human myoblasts and that vitamin D inhibits myoblast proliferation and differentiation through key regulators of cell cycle progression. Future studies need to employ strategies to identify the primary responses of vitamin D that drive the cellular response towards quiescence.

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R Perchard, L Magee, A Whatmore, F Ivison, P Murray, A Stevens, M Z Mughal, S Ehtisham, J Campbell, S Ainsworth, M Marshall, M Bone, I Doughty and P E Clayton

and Care Excellence (NICE) HbA1c target of <6.5%. The incidence of vitamin D deficiency, as reliably defined by serum 25-hydroxyvitamin D [25(OH)D] <50 nmol/L ( 3 , 4 , 5 , 6 ), has been estimated at 8–24% in UK children ( 7 ), with particularly

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Søs Dragsbæk Larsen, Christine Dalgård, Mathilde Egelund Christensen, Sine Lykkedegn, Louise Bjørkholt Andersen, Marianne Andersen, Dorte Glintborg and Henrik Thybo Christesen

-hydroxyvitamin D (s-25OHD) <50 nmol/L, was suggested to be a risk factor for cardiovascular events ( 4 ). The potential cardioprotective properties of vitamin D stem from its biological actions including its ability to inhibit vascular smooth muscle cell

Open access

June Young Choi, Jin Wook Yi, Jun Hyup Lee, Ra-Yeong Song, Hyeongwon Yu, Hyungju Kwon, Young Jun Chai, Su-jin Kim and Kyu Eun Lee

epidemiological reports show that higher levels of vitamin D3 are associated with a lower risk of developing cancer ( 3 ). The active form of vitamin D3, 1,25-dihydroxyvitamin D3 (1,25D) exerts antitumor activity by binding to the vitamin D receptor ( VDR ). The