الفهرس 
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Abstract
Diabetes mellitus (DM) is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion and/or action (Mestry et al., 2017). One of the most important complications of this metabolic disease is diabetic nephropathy (DN). DN is damage to the kidney which can lead to chronic renal failure, eventually requiring dialysis, it is now considered the principal cause of end-stage renal disease (ESRD) in most of countries worldwide (Sharaf El-Din et al., 2017).
Metformin is a biguanide compound that is characterized by its glucose-lowering effect through enhancing insulin sensitivity of both hepatic and peripheral tissues. This allows for increased uptake of glucose into these insulin-sensitive tissues (Rena et al., 2017). Recent studies discovered that metformin reduces insulin requirement in type 1 diabetes, it also plays essential roles in pancreatic β-cells. It restores insulin secretion activities and protects pancreatic β-cells from lipotoxicity or glucotoxicity (Yang et al., 2017). Despite decades of use of metformin as a first line therapy for type 2 diabetes. Metformin has previously been demonstrated to control hepatic glucose production through mechanisms that involve adenosine monophosphate-activated protein kinase (AMPK), and mitochondrial metabolism (Koffert et.