**12. Conclusion**

The evolution of T2DM requires the presence of defects in both insulin secretion and insulin action, and both of these defects can have a genetic and an acquired component. There are many discovered complex alterations in adipose tissue secretion of cytokines, adipokines, and chemokines and immune cell composition observed in adipose tissue-related pathologies such as obesity and IR. The later is a nearly universal finding in patients with established disease. There are many recognized genes involved in β-cell development, function and regulation. These could lead to disorders in insulin secretion, IR and glucose sensing. Physicians should be aware about the potential drugs contribute to the development of hyperglycemia and diabetes. Ladies at high risk of GDM should be identified and screened for diabetes before conception and to be followed after delivery. Early identification and diagnosis of many medical conditions and other risk factors could induce hyperglycemia or precipitate a preexisting condition of DM.

The above demonstrated a wide range of research in this area that should be encouraged to improve our understanding of the disease. T2DM is a complex interaction between genetics, cytokines, immune cells and tissues during inflammatory responses with obesity, insulin function, IR and β-cells failure. Subsequently this could help in discovery new drugs to treat T2DM that could interfere or stop any stage of these mechanisms at molecular or genetic level.
