缺乏維生素D會(huì)增加許多疾病的發(fā)病風(fēng)險(xiǎn),，但其深層原因過去并不清楚,。一項(xiàng)最新研究顯示,，缺乏維生素D會(huì)直接影響人類基因組中200多個(gè)基因的活性,，這些基因與風(fēng)濕性關(guān)節(jié)炎和糖尿病等許多疾病有關(guān),。
英國牛津大學(xué)等機(jī)構(gòu)的研究人員在新一期《基因組研究》雜志上報(bào)告說,，維生素D進(jìn)入人體后會(huì)激活一種名叫維生素D受體的蛋白質(zhì),，這種蛋白質(zhì)會(huì)與脫氧核糖核酸（DNA）結(jié)合。研究發(fā)現(xiàn),，在DNA鏈上有2776個(gè)可供維生素D受體蛋白質(zhì)結(jié)合的位點(diǎn),。
對(duì)這些位點(diǎn)進(jìn)行的分析顯示，維生素D可以影響229個(gè)基因的活性,。這些基因已經(jīng)被證明與一系列疾病有關(guān),，如多發(fā)性硬化癥、風(fēng)濕性關(guān)節(jié)炎、慢性淋巴細(xì)胞性白血病,、I型糖尿病和腸癌等,。研究人員安德烈亞斯·赫格爾說，這項(xiàng)結(jié)果顯示,，維生素D在人體健康系統(tǒng)中發(fā)揮著廣泛的作用,，提醒人們要注意補(bǔ)充維生素D。
據(jù)估計(jì),，全球約有10億人缺乏維生素D,，并因此罹患各種疾病。人們可以通過多吃魚油,、雞蛋等食物來補(bǔ)充維生素D,，多曬太陽也有助于人體自身合成維生素D，但研究人員也提醒說,，過多暴曬會(huì)增加患皮膚癌風(fēng)險(xiǎn),。（生物谷Bioon.com）
生物谷推薦原文出處：
Genome Res. doi:10.1101/gr.107920.110
A ChIP-seq defined genome-wide map of vitamin D receptor binding: Associations with disease and evolution
Sreeram V. Ramagopalan1,2,3,6,7, Andreas Heger4,6, Antonio J. Berlanga1,2, Narelle J. Maugeri1, Matthew R. Lincoln1,2, Amy Burrell1,2, Lahiru Handunnetthi1,2, Adam E. Handel1,2, Giulio Disanto1,2, Sarah-Michelle Orton1,2, Corey T. Watson5, Julia M. Morahan1,2, Gavin Giovannoni3, Chris P. Ponting4, George C. Ebers1,2,7 and Julian C. Knight1,7
1Wellcome Trust Centre for Human Genetics, University of Oxford, Headington, Oxford OX3 7BN, United Kingdom;
2Department of Clinical Neurology, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, United Kingdom;
3Blizard Institute of Cell and Molecular Science, Queen Mary University of London, Barts and The London School of Medicine and Dentistry, London E1 2AT, United Kingdom;
4MRC Functional Genomics Unit, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3QX, United Kingdom;
5Department of Biological Sciences, Simon Fraser University, Burnaby, British Columbia V5A 1S6, Canada
Initially thought to play a restricted role in calcium homeostasis, the pleiotropic actions of vitamin D in biology and their clinical significance are only now becoming apparent. However, the mode of action of vitamin D, through its cognate nuclear vitamin D receptor (VDR), and its contribution to diverse disorders, remain poorly understood. We determined VDR binding throughout the human genome using chromatin immunoprecipitation followed by massively parallel DNA sequencing (ChIP-seq). After calcitriol stimulation, we identified 2776 genomic positions occupied by the VDR and 229 genes with significant changes in expression in response to vitamin D. VDR binding sites were significantly enriched near autoimmune and cancer associated genes identified from genome-wide association (GWA) studies. Notable genes with VDR binding included IRF8, associated with MS, and PTPN2 associated with Crohn's disease and T1D. Furthermore, a number of single nucleotide polymorphism associations from GWA were located directly within VDR binding intervals, for example, rs13385731 associated with SLE and rs947474 associated with T1D. We also observed significant enrichment of VDR intervals within regions of positive selection among individuals of Asian and European descent. ChIP-seq determination of transcription factor binding, in combination with GWA data, provides a powerful approach to further understanding the molecular bases of complex diseases.
