**1. Introduction**

The natural history of type 2 diabetes (T2DM) has been well described in multiple populations. Patients with T2DM have inherited genes from parents that make their tissues resistant to insulin. Insulin resistance (IR) in muscle and liver and β-cell failure represent the core pathophysiologic defects in development of T2DM. Age, genes, IR, lipotoxicity, glucotoxicity, amyloid deposition and abnormal incretin are factors playing a role in progressive β-cells dysfunction. The progressive decline in insulin secretion, decrease of the pancreatic β- cell mass and function and the presence of IR will contribute in changing the state of the dysgly‐ cemia from normal to, impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and end with overt diabetes [1].
