الفهرس 
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Abstract
Diabetes mellitus is a group of metabolic disorders characterized by hyperglycemia resulting from defect of insulin secretion and/or increased cellular resistance to insulin.
The prevalence of DM is expected to increase by 55% in 2035 to reach 592 million adults affected worldwide. Most of people with diabetes live in low and middle-income countries and these will experience the greatest increase in cases of diabetes over the next 22 years. Therefore, it is crucial to understand the mechanisms that contribute to the pathogenesis of DM.
The metabolic disturbances of DM and chronic hyperglycemia lead to long term tissue and organ damage involving eyes, kidneys, neurons and vascular system. The vast majority of cases of diabetes fall into two broad etiopathogenetic categories of which 90% have type 2 diabetes mellitus (T2D) and no more than 10% have type 1 diabetes.
Transcription factor 7-like 2 protein is a transcription factor which has been implicated in blood glucose homeostasis. It is involved in Wnt signaling pathway which plays a substantial role in beta-cell proliferation and insulin secretion. It influences synthesis of glucagon-like peptide 1 (GLP-1) in intestinal cells which plays an important role in blood glucose homeostasis, and it has been assumed that TCF7L2 gene variants may influence the susceptibility to T2D by indirectly altering GLP-1 levels.
Our study aimed to evaluate the role of TCF7L2 rs12255372 gene polymorphism in the development of T2D and to evaluate the impact of TCF7L2 rs12255372 polymorphism on glycemic control in diabetic patients.
The study was conducted on forty seven (47) diabetic patients who were recruited from the out-patient clinic and in-patient Department of Endocrinology at Ain Shams University Hospitals; in addition, twenty three (23) age- and sex- matched healthy subjects taken as healthy control group. Assay of TCF7L2 rs12255372 gene polymorphism was performed by real-time PCR analysis and the glycemic control in diabetic patients was monitored by measuring baseline HbA1c at the start of the study and before treatment with sulphonylurea, recent HbA1c after three months of treatment with sulphonylurea and ΔHbA1c which is the difference between recent HbA1c (after 3-months therapy) and baseline HbA1c.
The study had demonstrated that there was no significant association between TCF7L2 rs12255372 G>T gene polymorphism and T2D. However, there was significant association between the concordance of risk T allele and the occurrence of dyslipidemia and poor therapeutic response to hypoglycemic agents.
The non-significance of our results may be due to the small sample size compared to other studies, ethnic variation and different population. Further large, multi-ethnic, linkage and haplotype studies on larger sample sizes should be performed to confirm the role of TCF7L2 gene polymorphism in T2D susceptibility and pathogenesis.