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Type 1 (T1DM) proceeds from a complete absence of insulin due to an autoimmuneassociated degradation of the insulin-secreting pancreatic ┚-cell. An islet autoimmune response seems to be regulated by the T-helper lymphocyte and its cytokine products including IL-2, IFN-┛, and TNF-┚, causing a cascade of inflammatory processes, known as insulitis and consequently gradual ┚-cell degradation (Rabinovitch and Suarez-Pinzon 2003). Therefore, T1DM etiology follows two stages. First, insulitis appears when various leukocytes attack the pancreas islets. Second, diabetes develops when most ┚-cells have been degraded, and there is no longer adequate insulin secretion to regulate blood glucose levels, leading to hyperglycemia (Mathis, Vence et al. 2001). Chronic hyperglycemia is believed to cause insulin resistance in T1DM (Patti, Maffettone et al. 1999). Thus, people can have concealed insulitis for years before it finally induces overt diabetes. Although most of diabetic patients suffer from T2DM, compelling evidence demonstrated that a proportion of people initially diagnosed with T2DM may in fact have a gradually progressing and less severe category of T1DM (Bell and Polonsky 2001). People affected by T1DM are constrained to insulin administration on a regular basis either through injections, pumps, or by inhalation. Outwardly, T1DM patients appear predominantly healthy; however failure to adhere to the appropriate treatment to effectively control blood glucose levels could lead to increased fatigue, neuropathies and long-term organ damages. The consequences of the autoimmunological destruction of pancreatic ┚-cells are clear, the causes are not, and the identification of the environmental factors that induce this destruction in genetically susceptible children, adolescents, and even adults still eludes us (Mathis, Vence et al. 2001).

Type I Diabetes and the Role of Inflammatory-Related Cellular Signaling