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Matti Narkia

The Relevance of Vitamin D Receptor (VDR) Gene Polymorphisms for Cancer: A Review of th... - 0 views

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    The relevance of vitamin D receptor (VDR) gene polymorphisms for cancer: a review of the literature. Köstner K, Denzer N, Müller CS, Klein R, Tilgen W, Reichrath J. Anticancer Res. 2009 Sep;29(9):3511-36. Review. PMID: 19667145 CONCLUSION: Significant associations with VDR polymorphisms have been reported in cancer of the breast (Fok1, Bsm1, Taq1, Apa1, poly (A)), prostate (Fok1, Bsm1, Taq1, poly (A)), skin (Fok1, Bsm1, A-1210), colorectum (Fok1, Bsm1), ovary (Fok1, Apa1) and bladder (Fok1), and in renal cell carcinoma (Taq1, Apa1). However, conflicting data have been reported for most malignancies. After careful evaluation of the actual literature, it can be summarized that data indicating an association of VDR polymorphisms and cancer risk are strongest for breast cancer (Bsm1, Fok1), prostate cancer (Fok1) and malignant melanoma (MM) (Fok1). Data indicating an association of VDR polymorphisms and cancer prognosis are strongest for prostate cancer (Fok1), breast cancer (Bsm1, Taq1), MM (Bsm1) and renal cell carcinoma (Taq1).
Matti Narkia

Take or avoid vitamin D supplements? - ImmInst.org Forums - 0 views

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    "Hi! This is Amy Proal. I wrote the article referenced at the start of the thread about vitamin D. Dr. Marshall is not concerned with vitamin D toxicity. Rather his molecular modeling research has clarified the actions of the two vitamin D metabolites 25-D and 1,25-D. The Vitamin D Receptor (VDR) is a fundamental receptor of the body - it controls the expression thousands of genes, as well as the activity of the innate immune system and the antimicrobial peptides. If you think of the VDR as a switch, 25-D (which is a corticosteroid) turns it off (inactivates it) and 1,25-D turn it on (activates it). What is commonly believed among vitamin D researchers is that if people supplement with extra vitamin D it will be converted into 1,25-D and activate the VDR. Unfortunately, Marshall's work revealed that the type of vitamin D derived from supplements and sun remains, for the most part, in it's precursor form 25-D. This means that the extra vitamin D we get from fortified food products and supplements is turning the VDR off, not on. That causes a decrease in immune function and gene transcription."
Matti Narkia

Calcitriol receptor - Wikipedia, the free encyclopedia - 0 views

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    The calcitriol receptor, also known as the vitamin D receptor (VDR) and also known as NR1I1 (nuclear receptor subfamily 1, group I, member 1), is a member of the nuclear receptor family of transcription factors.[1] Upon activation by vitamin D, the VDR forms a heterodimer with the retinoid-X receptor and binds to hormone response elements on DNA resulting in expression or transrepression of specific geneproducts. In humans, the vitamin D receptor is encoded by the VDR gene.[2]
Matti Narkia

Vitamin D receptor (VDR) gene polymorphisms and haplotypes, interactions with plasma 25... - 0 views

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    Vitamin D receptor (VDR) gene polymorphisms and haplotypes, interactions with plasma 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, and prostate cancer risk. Mikhak B, Hunter DJ, Spiegelman D, Platz EA, Hollis BW, Giovannucci E. Prostate. 2007 Jun 15;67(9):911-23. PMID: 17440943 DOI: 10.1002/pros.20570 RESULTS No association was found between these SNPs or their associated haplotypes and all PC subtypes except that haplotype 2 (A-f-b) with Cdx2 A, Fok1 f, and Bsm1 b alleles and haplotype 3 (A-F-B) with Cdx2 A, Fok1 F and Bsm1 B alleles compared to the most common haplotype (A-F-b), were associated with reduced risk of aggressive PC (high stage or Gleason sum 7; P = 0.02), both with two alleles suspected of being low risk. Carriers of the variant Cdx2 A allele who were deficient in plasma 25-hydroxyvitamin D (15 ng/ml) compared to non-carriers with normal 25-hydroxyvitamin D, had a lower risk of total and poorly differentiated PCs (Gleason sum 7) (P for interaction = 0.02 and 0.04, respectively). Plasma 1,25-dihydroxyvitamin D deficiency (26 pg/ml) was associated with a threefold risk of poorly differentiated PC (P for interaction = 0.01) when comparing carriers of the Cdx2 A allele to non-carriers with normal 1,25-dihydroxyvitamin D. CONCLUSION In this population of men, none of the VDR polymorphisms studied was associated with susceptibility to PC. Carriers of the variant Cdx2 A allele with low plasma 25-hydroxyvitamin D may experience a reduction in risk of total and poorly differentiated prostate cancers compared to non-carriers with adequate 25-hydroxyvitamin D.
Matti Narkia

Association study on two vitamin D receptor gene polymorphisms and vitamin D metabolite... - 0 views

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    Association study on two vitamin D receptor gene polymorphisms and vitamin D metabolites in multiple sclerosis. Smolders J, Damoiseaux J, Menheere P, Tervaert JW, Hupperts R. Ann N Y Acad Sci. 2009 Sep;1173:515-20. PMID: 19758194 DOI: 10.1111/j.1749-6632.2009.04656.x Discussion: We found no association of the Apal and Taql VDR gene SNPs with MS or with vitamin D metabolism in our population. Further research should assess the complex interaction between vitamin D, the VDR, and susceptibility to MS.
Matti Narkia

The Heart Scan Blog: Vitamin D for Peter, Paul, and Mary - 0 views

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    Why is it that vitamin D deficiency can manifest in so many different ways in different people? One big reason is something called vitamin D receptor (VDR) genotypes, the variation in the receptor for vitamin D. Why is it that the dose of vitamin D necessary to reach a specific level differs so widely from one person to the next? VDR genotype, again. Variation in blood levels of 25-hydroxy vitamin D from a specific dose of vitamin D can vary three-fold, as shown by a University of Toronto study. In other words, a dose of 4000 units per day may yield a 25-hydroxy vitamin D blood level of 30 ng/ml in Mary, 60 ng/ml in Paul, and 90 ng/ml in Pete--same dose, different blood levels
Matti Narkia

OMIM - VITAMIN D RECEPTOR; VDR - 0 views

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    The vitamin D3 receptor (VDR) is an intracellular hormone receptor that specifically binds the active form of vitamin D (1,25-dihydroxyvitamin D3 or calcitriol) and interacts with target-cell nuclei to produce a variety of biologic effects
Matti Narkia

D-vitamiini - Wikipedia - 0 views

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    D-vitamiini on yksi ihmisen tarvitsemista rasvaliukoisista vitamiineista. D-vitamiinin muotoja ovat kolekalsiferoli (D3) ja ergokalsiferoli (D2). Ihminen pystyy itsekin tuottamaan D-vitamiinia riittävässä auringonvalossa UVB-säteilyn vaikutuksesta. D-vitamiini on steroidihormoni, jonka esimuotoa muodostuu ihossa tai saadaan ruoasta. D-vitamiinin vaikutukset välittyvät vitamiinireseptorin (VDR) kautta. Reseptoreita on kaikissa soluissa keskushermosto mukaan lukien. Useat kliiniset ja kokeelliset tulokset osoittavat D-vitamiinin vaikuttavan aivojen toimintaan. D-vitamiini voi vähentää riskiä sairastua tyypin 2 diabetekseen[6]. Kansanterveyslaitoksen tutkijat seurasivat 17 vuotta noin 4000 suomalaisen naisen ja miehen terveydentilaa. Niillä henkilöillä, joiden veressä oli eniten D-vitamiinia, oli 40 % pienempi sairastumisriski verrattuna niihin, joiden veressä vitamiinia oli vähiten. Maailman terveysjärjestön (WHO:n) syöväntutkimuslaitos IARC Lyonissa analysoi 18 suurta D-vitamiinitutkimusta, joihin oli osallistunut 57 311 ihmistä[7]. Heidän terveydentilaansa oli seurattu lähes kuusi vuotta. Sinä aikana 4 777 heistä kuoli. D-vitamiinia ravintolisänä käyttäneiden kuolleisuus oli kahdeksan prosenttia pienempi kuin muiden. D-vitamiinilisän päiväannos vaihteli 7,5:stä 50 µg:aan; keskimäärin se oli 14 µg. D-vitamiinilisää käyttävien ihmisten veressä oli 1,5-5,2 kertaa enemmän tätä vitamiinia kuin muilla[8]. Lontoon King's Collegessa tehdyn tutkimuksen mukaan D-vitamiini lisää keuhkoissa tulehdusta vaimentavan tulehdussytokiinin, interleukiini 10:n (IL10:n) tuotantoa. Silloin astman oireet vähenevät, jopa sellaisilla potilailla, joihin kortisoni (deksametasoni) ei ole tehonnut[
Matti Narkia

Vitamin D Receptor Expression in Normal, Premalignant, and Malignant Human Lung Tissue ... - 0 views

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    Vitamin D receptor expression in normal, premalignant, and malignant human lung tissue. Menezes RJ, Cheney RT, Husain A, Tretiakova M, Loewen G, Johnson CS, Jayaprakash V, Moysich KB, Salgia R, Reid ME. Cancer Epidemiol Biomarkers Prev. 2008 May;17(5):1104-10. PMID: 18483332 doi: 10.1158/1055-9965.EPI-07-2713 onclusions: VDR expression spanned the lung carcinogenesis spectrum. Nuclear expression was similar across various histologies, whereas cytoplasmic expression decreased with increasing histologic grade. These results indicate that there is potential for the use of calcitriol as a chemopreventive agent against the development of lung cancer. (Cancer Epidemiol Biomarkers Prev 2008;17(5):1104-10)
Matti Narkia

Novel role of the vitamin D receptor in maintaining the integrity of the intestinal muc... - 0 views

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    Novel role of the vitamin D receptor in maintaining the integrity of the intestinal mucosal barrier. Kong J, Zhang Z, Musch MW, Ning G, Sun J, Hart J, Bissonnette M, Li YC. Am J Physiol Gastrointest Liver Physiol. 2008 Jan;294(1):G208-16. Epub 2007 Oct 25. PMID: 17962355 These observations suggest that VDR plays a critical role in mucosal barrier homeostasis by preserving the integrity of junction complexes and the healing capacity of the colonic epithelium. Therefore, vitamin D deficiency may compromise the mucosal barrier, leading to increased susceptibility to mucosal damage and increased risk of IBD.
Matti Narkia

Vitamin D and the vitamin D receptor are critical for control of the innate immune resp... - 0 views

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    Conclusion The data point to a critical role for the VDR and 1,25(OH)2D3 in control of innate immunity and the response of the colon to chemical injury. Vitamin D and the vitamin D receptor are critical for control of the innate immune response to colonic injury. Froicu M, Cantorna MT. BMC Immunol. 2007 Mar 30;8:5. PMID: 17397543 doi:10.1186/1471-2172-8-5
Matti Narkia

Polymorphisms in the Vitamin D Receptor and Risk of Ovarian Cancer in Four Studies -- T... - 0 views

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    Our results of an association with the Fok1 VDR polymorphism further support a role of the vitamin D pathway in ovarian carcinogenesis. Polymorphisms in the vitamin D receptor and risk of ovarian cancer in four studies. Tworoger SS, Gates MA, Lee IM, Buring JE, Titus-Ernstoff L, Cramer D, Hankinson SE. Cancer Res. 2009 Mar 1;69(5):1885-91. Epub 2009 Feb 17. Erratum in: Cancer Res. 2009 Jun 15;69(12):5267. Gate, Margaret A [corrected to Gates, Margaret A]. PMID: 19223536 doi: 10.1158/0008-5472.CAN-08-3515
Matti Narkia

Improved Cholecalciferol Nutrition in Rats Is Noncalcemic, Suppresses Parathyroid Hormo... - 0 views

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    Improved cholecalciferol nutrition in rats is noncalcemic, suppresses parathyroid hormone and increases responsiveness to 1, 25-dihydroxycholecalciferol. Vieth R, Milojevic S, Peltekova V. J Nutr. 2000 Mar;130(3):578-84. PMID: 10702588 We conclude suppression of 1,25(OH)(2)D and PTH, and higher renal VDR mRNA and 24-hydroxylase did not involve higher free 1,25(OH)(2)D concentration or a first pass effect at the gut. Thus, 25(OH)D or a metabolite other than 1,25(OH)(2)D is a physiological, transcriptionally and biochemically active, noncalcemic vitamin D metabolite. When viewed from a perspective that starts with higher vitamin D nutrition, the results indicate that low vitamin D nutrition may bring about a form of resistance to 1,25(OH)2D. This situation would explain why, in humans, nutritional rickets and osteomalacia are commonly associated with normal or increased levels of 1,25(OH)2D (Chesney et al. 1981Citation , Eastwood et al. 1979Citation , Garabedian et al. 1983Citation ,Rasmussen et al. 1980Citation )-these are not like the low hormone levels associated with any other endocrine-deficiency disorder. A connection between lower vitamin D nutrition and vitamin D resistance helps to explain why the supposedly inactive compound 25(OH)D is more relevant in diagnosing nutritional rickets than is the active hormone 1,25(OH)2D. If the features of improved vitamin D nutrition shown here were demonstrated for any newly synthesized compound, the compound would be classified as a noncalcemic 1,25(OH)2D analogue (Brown et al. 1989Citation , Finch et al. 1999Citation , Goff et al. 1993Citation , Koshizuka et al. 1999Citation ). Thus, we contend that 25(OH)D or a metabolite of it other than 1,25(OH)2D exists as a physiological and biologically-active noncalcemic vitamin D metabolite whose effects require further examination, particularly in relationship to studies involving the synthetic analogs of 1,25(OH)2D.
Matti Narkia

Vitamin D: the alternative hypothesis. - Autoimmun Rev. 2009 Jul;8(8):639-44. (full tex... - 0 views

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    Vitamin D: the alternative hypothesis. Albert PJ, Proal AD, Marshall TG. Autoimmun Rev. 2009 Jul;8(8):639-44. Epub 2009 Feb 12. Review. PMID: 19393200 Emerging molecular evidence suggests that symptomatic improvements among those administered vitamin D is the result of 25-D's ability to temper bacterial-induced inflammation by slowing VDR activity. While this results in short-term palliation, persistent pathogens that may influence disease progression, proliferate over the long-term.
Matti Narkia

Vitamin D and calcium insufficiency-related chronic diseases: molecular and cellular pa... - 0 views

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    Vitamin D and calcium insufficiency-related chronic diseases: molecular and cellular pathophysiology. Peterlik M, Cross HS. Eur J Clin Nutr. 2009 Dec;63(12):1377-86. Epub 2009 Sep 2. PMID: 19724293 doi:10.1038/ejcn.2009.105 A compromised vitamin D status, characterized by low 25-hydroxyvitamin D (25-(OH)D) serum levels, and a nutritional calcium deficit are widely encountered in European and North American countries, independent of age or gender. Both conditions are linked to the pathogenesis of many degenerative, malignant, inflammatory and metabolic diseases. Studies on tissue-specific expression and activity of vitamin D metabolizing enzymes, 25-(OH)D-1alpha-hydroxylase and 25-(OH)D-24-hydroxylase, and of the extracellular calcium-sensing receptor (CaR) have led to the understanding of how, in non-renal tissues and cellular systems, locally produced 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) and extracellular Ca2+ act jointly as key regulators of cellular proliferation, differentiation and function. Impairment of cooperative signalling from the 1,25-(OH)2D3-activated vitamin D receptor (VDR) and from the CaR in vitamin D and calcium insufficiency causes cellular dysfunction in many organs and biological systems, and, therefore, increases the risk of diseases, particularly of osteoporosis, colorectal and breast cancer, inflammatory bowel disease, insulin-dependent diabetes mellitus type I, metabolic syndrome, diabetes mellitus type II, hypertension and cardiovascular disease. Understanding the underlying molecular and cellular processes provides a rationale for advocating adequate intake of vitamin D and calcium in all populations, thereby preventing many chronic diseases worldwide.
Matti Narkia

Evolution and function of vitamin D. [Recent Results Cancer Res. 2003] - PubMed Result - 0 views

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    Evolution and function of vitamin D. Holick MF. Recent Results Cancer Res. 2003;164:3-28. Review. PMID: 12899511
Matti Narkia

Vitamin D and autoimmune rheumatic diseases -- Cutolo 48 (3): 210 -- Rheumatology - 0 views

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    Vitamin D and autoimmune rheumatic diseases. Cutolo M. Rheumatology (Oxford). 2009 Mar;48(3):210-2. Epub 2008 Oct 17. PMID: 18930963 doi:10.1093/rheumatology/ken394
Matti Narkia

JNNP -- eLetters for Soilu-Hänninen et al., 79 (2) 152-157 - 0 views

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    Vitamin D may suppress infections which lead to development of Multiple Sclerosis Steven R Brenner, None (16 August 2007) J Neurol Neurosurg Psychiatry 2008 I read the article with reference to the inverse relationship between multiple sclerosis clinical activity and deficiency of vitamin D by Soilu-Hannienen (1) with interest, and was considering what mechanism could be in play to cause such a relationship. 25-hydroxylated metabolites of vitamin D act as intracellular regulators of the synthesis and action of defensin (2) molecules against bacterial antigens, defensin being an endogenously synthesized antimicrobial substance (2). Human cathelicidin antimicrobial peptide gene is a target of vitamin D receptor and is strongly up-regulated by 1,25-dihydroxyvitamin D3, indicating vitamin D receptor and the 1,25-dihydroxyvitaminD3 regulate primate innate immunity (3)
Matti Narkia

Vitamin D receptor gene polymorphism: association with Crohn's disease susceptibility -... - 0 views

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    Vitamin D receptor gene polymorphism: association with Crohn's disease susceptibility.\nSimmons JD, Mullighan C, Welsh KI, Jewell DP.\nGut. 2000 Aug;47(2):211-4.\nPMID: 10896912 \ndoi:10.1136/gut.47.2.211
Matti Narkia

Role of vitamin D in the pathogenesis of type 2 diabetes mellitus. - Wiley InterScience... - 0 views

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    Role of vitamin D in the pathogenesis of type 2 diabetes mellitus. Palomer X, González-Clemente JM, Blanco-Vaca F, Mauricio D. Diabetes Obes Metab. 2008 Mar;10(3):185-97. Review. PMID: 18269634 DOI: 10.1111/j.1463-1326.2007.00710.x Vitamin D deficiency has been shown to alter insulin synthesis and secretion in both humans and animal models. It has been reported that vitamin D deficiency may predispose to glucose intolerance, altered insulin secretion and type 2 diabetes mellitus. Vitamin D replenishment improves glycaemia and insulin secretion in patients with type 2 diabetes with established hypovitaminosis D, thereby suggesting a role for vitamin D in the pathogenesis of type 2 diabetes mellitus.
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