Vitamin D status and vitamin D receptor gene polymorphisms and susceptibility to type 1 diabetes in Egyptian children

Type 1 diabetes mellitus (T1DM) is recognized as a T-cell-mediated autoimmune disease. Vitamin D compounds are known to suppress T-cell activation by binding to vitamin D receptor (VDR); and thus, VDR gene polymorphisms may be related to T-cell-mediated autoimmune diseases. The aim of this study was...

Full description

Saved in:
Bibliographic Details
Published in:Gene 2014-02, Vol.536 (2), p.430-434
Main Authors: Abd-Allah, Somia H., Pasha, Heba F., Hagrass, Hoda A., Alghobashy, Ashgan A.
Format: Article
Language:English
Subjects:
Adolescent
Alleles
Child
European Continental Ancestry Group - genetics
Female
Gene polymorphism
Genetic Predisposition to Disease - genetics
Genotype
Humans
Male
Polymorphism, Genetic - genetics
Receptors, Calcitriol - genetics
Risk
Type 1 diabetes mellitus
Vitamin D
Vitamin D - analogs & derivatives
Vitamin D - blood
Vitamin D - genetics
Vitamin D receptor
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Type 1 diabetes mellitus (T1DM) is recognized as a T-cell-mediated autoimmune disease. Vitamin D compounds are known to suppress T-cell activation by binding to vitamin D receptor (VDR); and thus, VDR gene polymorphisms may be related to T-cell-mediated autoimmune diseases. The aim of this study was to investigate the association between vitamin D status and VDR gene polymorphisms and T1DM. One hundred and twenty patients with T1DM and one hundred and twenty controls were enrolled in the study. VDR gene BsmI, FokI, ApaI and TaqI polymorphisms were determined using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). Serum 25-hydroxyvitamin D (25(OH)D) was determined using ELISA. Serum 25(OH)D levels revealed a vitamin D deficiency or insufficiency in 75% of the patients. The mean levels of vitamin D were significantly lower in patients as compared to their controls (P=
ISSN:0378-1119
1879-0038
DOI:10.1016/j.gene.2013.12.032