**3. Type 2 diabetes**

In contrast to T1D, T2D is a defect in insulin secretion, insulin action, or both that leads to the development of a multifactorial and heterogeneous group of disorders. Changes in diet and physical activity levels have led to an increased worldwide prevalence of T2D over the past several decades. There is also strong evidence supporting a genetic component of T2D susceptibility, and several genes underlying monogenic forms of DM have already been identified. However, T2D likely results from the contribution of many genes interacting with different environmental factors to produce wide variations in the clinical course [7].

Regarding this process, there is a decrease in β-cell mass in T2D with the primary implicated mechanism being the apoptosis of the cells. This type of dynamic cell death is increased in all diabetic individuals; β-cell mass depends on many factors, including cell size, cell renewal rate from proliferation of pre-existing cells or neogenesis (differentiation from other precursor cells), and speed of apoptosis. Also, β-cell failure during the progression to T2D can be caused by either chronic exposure of the β-cell to glucose, which is called "glucotoxicity," or exposure to fatty acids, which is known as "lipotoxicity" [8].
