Common genetic variants of the vitamin D binding protein (DBP) predict differences in response of serum 25-hydroxyvitamin D [25(OH)D] to vitamin D supplementation

Vitamin D and inflammation in the prevention of type 2 diabetes: public health relevance

“…Similar results were obtained in another meta-analysis of GWAS studies, which evaluated serum levels of 25(OH)D and genetic variation in a pooled sample of cohorts consisting of ~34,000 individuals of European origin [25]. A recent candidate gene study examined the relationship between common genetic variants of GC and the response of serum levels of 25(OH)D to vitamin D supplementation [24]. This group found that a common functional variant of this gene, T436K (rs4588, c.1307C> A) predicted differences in response of 25(OH)D levels to supplementation.…”

“…As mentioned above, there is evidence in favor of a relationship between vitamin D status and predisposition to T2DM, which may be a result of the immunomodulatory and anti-inflammatory properties of vitamin D. However, the association remains inconsistent and this may reflect confounding factors, such as genetic variation affecting the individual responses to vitamin D. The role of common genetic variants on vitamin D status has recently begun to be elucidated [24][25][26]. A meta-analysis of genome wide association studies (GWAS) combined results from ~4,500 individuals of European ancestry and found significant associations between 25(OH)D concentrations and SNPs in the following genetic loci: GC (the gene coding for VDBP), NADSYN1 (encoding nicotinamide adenine dinucleotide synthetase), which is in high linkage disequilibrium with a SNP in DHCR7 (encoding 7-dehydrocholesterol reductase, which synthesizes cholesterol from 7-dehydrocholesterol), and CYP2R1 (encoding cytochrome P450, family 2, subfamily R, polypeptide 1, a C-25 hydroxylase that converts cholecalciferol to 1α,25(OH) 2 D) [26].…”

“…The elderly, certain ethnocultural groups, and individuals with malabsorption diseases are at risk of becoming vitamin D deficient [22,23]. In addition, recent genome-wide association studies suggest that common genetic variations, e.g, in CYP2R1, may also affect vitamin D status [24][25][26]. Dietary factors such as fish liver oil, fatty fish, including sardines and salmon, egg yolks and fortified milk are important nutritional sources of vitamin D [27].…”

Utility of vitamins in the prevention of type 2 diabetes mellitus and its complications: A public health perspective

“…In these cells, the biologically active metabolite of vitamin D (i.e., 1,25-dihydroxy-vitamin D; 1,25[OH]D) [64] enhances insulin production and secretion via its action on the VDR [63]. Indeed, the presence of vitamin D binding protein (DBP), a major predictor of serum levels of 25(OH)D and response to vitamin D supplementation [65,66], and VDR initiated several studies demonstrating a relationship between single nucleotide polymorphisms (SNPs) in the genes regulating VDR and DBP and glucose intolerance and insulin secretion [67][68][69]. This further supports a role for vitamin D in T2DM and may explain the reduced overall risk of the disease in subjects who ingest >800 IU/d of vitamin D [61,70].…”

Lifestyle and Other Factors Explain One-Half of the Variability in the Serum 25-Hydroxyvitamin D Response to Cholecalciferol Supplementation in Healthy Adults

“…The NAM provides intake recommendations by age and sex, but it is unclear whether supplementation should be varied according to vitamin D status, weight, or other factors (7). In addition, although common genetic variants have been associated with circulating serum 25(OH)D concentrations in genome-wide association studies (29,30), their role in affecting the magnitude of serum response to supplementation is also less clear (31)(32)(33).…”