Vitamin D: A master example of nutrigenomics

Nutrigenomics attempts to characterize and integrate the relation between dietary molecules and gene expres- sion on a genome-wide level. One of the biologically active nutritional compounds is vitamin D3 , which activates via its metabolite 1 alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3) the nuclear receptor VDR (vitamin D receptor). Vitamin D3 can be synthesized endogenously in our skin, but since we spend long times indoors and often live at higher latitudes where for many winter months UV-B radiation is too low, it became a true vitamin. The ligand- inducible transcription factor VDR is expressed in the majority of human tissues and cell types, where it mod- ulates the epigenome at thousands of genomic sites. In a tissue-specific fashion this results in the up- and downregulation of primary vitamin D target genes, some of which are involved in attenuating oxidative stress. Vitamin D affects a wide range of physiological functions including the control of metabolism, bone formation and immunity. In this review, we will discuss how the epigenome- and transcriptome-wide effects of 1,25 (OH)2D3 and its receptor VDR serve as a master example in nutrigenomics. In this context, we will outline the basis of a mechanistic understanding for personalized nutrition with vitamin D3.

Automated summary

Nutrigenomics aims to study and integrate the relationship between dietary molecules and gene expression on a genome-wide level. Vitamin D3, an active nutritional compound, activates the nuclear receptor VDR through its metabolite 1 alpha,25-dihydroxyvitamin D3. Vitamin D3 can be synthesized internally but has become a true vitamin due to limited UV-B radiation from spending long hours indoors and living at higher latitudes. VDR, an inducible transcription factor, modulates the epigenome at numerous genomic sites, resulting in the regulation of vitamin D target genes and affecting various physiological functions.