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RESEARCH PRODUCT

Genetic Variability in Selected ZnT8 SNPs in the Opolskie Voivodeship (Poland) - Relationship with Type 2 Diabetes and its Complications and Accompanying Diseases

subject

Opolskie voivodeship; Type-2 diabetes mellitus; Leukocytes; Obesity; Hypertension; Strokes

description

Introduction: Type-2 Diabetes Mellitus (DM2) is of multigeneous origin, and its course may be modified by autoimmune mechanisms. It can be assumed that the clinically different course of diabetes depends, among others, on the genetically determined efficiency of the mechanisms of zinc homeostasis maintenance. The study of the relationship of mutations in the gene encoding ZnT8 with the tendency to the occurrence of diabetes and its course may result in new therapeutic possibilities in the future. It is also interesting because in leukocytes only ZnT8 shows significant individual variability in expression under physiological and pathological conditions, which indicates its genetic determinants. Selection of SNP SLC30A8 GENE polymorphisms: In the study group, Single Nucleotide Polymorphism (SNP) was determined in the following ZnT8 alleles: rs2466293, rs2466294, rs2466295, rs3802177, rs10282940, rs11558471, rs13266634. Study group: A group of 467 people was examined, including 45 subjects constituting the control group. The group of 422 people were patients with type 2 diabetes. The group of people subjected to the study are randomly selected representatives of the population of the Opolskie Voivodeship, specific in terms of origin- indigenous and immigrant population from the today's Ukraine territory that prior to Second World War belonged to Poland. The control group consisted of healthy people with no family history of type 2 diabetes, type 1 diabetes, obesity, hypertension and early symptoms of atherosclerosisstrokes and heart attacks before the age of 50. The group of patients with DM2 was additionally divided into subgroups depending on the presence of other health problems. Results: As to rs13266634, the C/C mutation seems to predispose to DM2 development. The mutation does not contribute to occurrence of additional clinical problems in DMt2 patients besides a predisposition to heart failure. In rs11558471, the A/A mutation predisposes to the development of DM2. The mutation does not contribute to the development of additional clinical problems in patients with DM2 with the exception of dilated cardiomyopathy where it may be protective. In rs2466294, rs3802177, rs2466293 and rs10282940 SNP mutations in these alleles did not affect the development of DM2 in the study population. Conclusion: The present study should be treated as the successive, little appendix to the needed widened research and observations explaining the complexity of the processes leading to the disclosure of DM2 and the progression of organ changes. Such studies will allow the development of new curation methods and more individualized treatment in the future

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