**2. Type 1 diabetes**

T1D represents only around 10% of the DM cases worldwide but is increasingly occurring earlier in life. It results from autoimmune destruction of the beta cells (β-cells) of the endocrine pancreas. As with cancer, obesity, and autoimmune diseases, T1D results from the interaction of genetic and non-genetic factors [2]. In autoimmune diseases, due to an immunological malfunction and lack of tolerance of self-antigens, the immune system destroys the body's own tissues. More than 80 different diseases are considered autoimmune and affect approximately 100 million people worldwide [3]. T1D is one such example that results in the slow degeneration and destruction of the pancreas. However, approximately 10% of the affected patients are classified as subtype 1B, and the pathogenesis in these cases is considered idiopathic since there is no evidence of autoimmunity [4]. T1D can be correlated to ethnicity, gender, genetics, and environmental influences. For instance, it occurs more in children and those under the age of 20 and affects both male and female children equally. However, studies have found that males are disproportionally affected in areas with a high prevalence of T1D, whereas females are disproportionally affected in areas with a low prevalence of the disease. It is highest in non-Hispanic White people and lowest in Navajo groups. Moreover, T1D is common in families with a history of the disease. Epidemiological studies have found an association between T1D and environmental factors, and dietary and nutritional habits [5].

Essential mediators leading to β-cell destruction in T1D include the following pro-inflammatory cytokines: interleukin-1β (IL-1β); interferon-γ (IFN-γ); and tumor necrosis factor-α (TNF-α). These cytokines induce the overexpression of iNOS in β-cells, leading to an overproduction of NO that causes cytotoxicity. This suggests an important role for NO in the pathogenesis of DM [6].
