الفهرس 
• Introduction and rationaleOnly 14 pages are availabe for public view
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Abstract
Type 2 diabetes mellitus accounts for more than 90% of diabetes and is documented as a global epidemic by the World Health Organization. Though the etiology of T2DM is poorly understood, risk factors that may influence the development of this complex metabolic illness include ethnicity, life style and genetic factors. T2DM is associated with micro and macrovasacular complications, among which diabetic nephropathy (DN) is the most serious microvascular complication.
Diabetic nephropathy is a progressive kidney disease caused by damage to the capillaries in the renal glomeruli. It is due to longstanding diabetes mellitus. Hyperglycemia, increased blood pressure levels, and genetic predisposition are the main risk factors for the development of DN. The main histological event linked to DN is Glomerular mesangial enlargement due to glumeruloesclerosis and accumulation of extracellular matrix proteins. Moreover, the glucose transporter 1 (Glut1), the major glucose carrier in mesangial cells, is increased in renal cortex, and more elevated glucose concentrations over-express the Glut1 protein concentration.
Identifying the genes associated with the risk or protection of T2DM is vital for understanding the mechanisms underlying the disease to provide the potential profits of personalized prevention and treatment programs.
Solute carrier family 2 facilitated glucose transporter member 1 (SLC2A1) (GLUT1 gene), is located at 1p34.2. The SLC2A1 encodes the membrane transport protein Glut1, a carrier protein that is in charge of the low-level of basal glucose uptake needed to maintain respiration in all cells, especially in erythrocytes.