الفهرس 
Effect of SLC30A8 rs13266634 genetic polymorphism on zinc supplementation and glycemic control in Egyptian patients with type 2 diabetes mellitus
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Abstract
Background Type 2 diabetes mellitus (T2DM) is a progressive disorder with variable degrees of insulin resistance and pancreatic Ý-cell dysfunction characterized by chronic hyperglycemia which leads to oxidative insult.Vitamins A and E have antioxidant potentials and may be of interest in controlling diabetes.Zinc, besides being an antioxidant trace element, plays an essential role in the synthesis, storage, and secretion of insulin by pancreatic Ý-tissue.The combined effect of high-dose vitamin A plus E supplementation with and without zinc in managing diabetes has never been examined. The SLC30A8 gene, encodes an essential zinc transporter 8 (ZnT8) protein in insulin synthesis and secretion. Rs13266634 polymorphism is a non-synonymous SNP encodinga C {u2192} T base substitution in the SLC30A8 gene that causes an amino acid code change from arginine to tryptophan at position 325, which in turn, affects zinc transport activity and causes a decrease in intragranular zinc levels.SNP rs13266634 has frequently been shown to be associated with the onset and development of T2DM in several populations.Clinical trials showed a diverse zinc response based on rs13266634 genetic polymorphism. Considering the beneficial effects of zinc supplementation and the genetic varied zinc response, zinc might be a possible new candidate molecule for personalized diabetes prevention and therapy in patients with T2DM. Aims To assess the association between SLC30A8 rs13266634 polymorphism and T2DM in Egyptian population and to study the potential effect of SLC30A8 rs13266634 genetic polymorphism on zinc supplementation and glycemic control in Egyptian patients withT2DM. In addition,weassessed and compared the effect of high-dose vitamin A plus E supplementation (AE) versus combined high-dose vitamin A plus E with the zinc (AEZ) versus control, on different diabetic parameters