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Type 1 Diabetes Mellitus is a syndrome characterized by hyperglycemia and insulin deficiency resulting from the loss of beta cells in pancreatic islets (Mapes & Faulds, 2014). The destruction of insulin-producing beta cells in the pancreas starts with the formation of autoantigens. Type 1 diabetes does not present clinically until 80-90% of the beta cells have been destroyed (McCance & Heuther, 2014).
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Nonimmune (type 1B diabetes), occurs secondary to other diseases and is much less common than autoimmune (type 1A).
These autoantigens are ingested by antigen-presenting cells which activate T helper 1 (Th1) and T helper 2 (Th2) lmphocytes. Activated Th1 lymphocytes secrete interluekin-2 (IL-2) and interferon.
Because insulin stimulates glucose uptake into tissues, stores glycose as glycogen, inhibits glucagon secretion and inhibits glucose production from the liver, the destruction of insulin-producing beta cells causes hyperglycemia (Mapes & Faulds, 2014).


Neither text, nor links to other websites, is reviewed or endorsed by The Ohio State University. The destruction of beta cells in Type 1A diabetes results from the interaction of both genetic and environmental factors. IL-2 activates autoantigen-specific T cytotoxic lymphocytes which destroy islet cells through the secretion of toxic perforins and granzymes. Type 1 diabetics may present with abrupt onset of diabetic ketoacidosis, polyuria, polyphagia, polydipsia, or rapid weight loss with marked hyperglycemia (Mapes & Faulds, 2014). Although the genetic susceptibility is not well understood, type 1 diabetes is most strongly associated with major histocompatibility complex (MHC), specifically histocompatibility leukocyte antigen (HLA) class II alleles (HLA-DQ and HLA-DR) (McCance & Heuther, 2014).
AntiGAD65 is an enzyme that helps control the release of insulin from beta cells and can be used to determine the cause of diabetes (McCance & Heuther, 2014).
Insulin autoantibodies [IAAs]) and zinc transporter 8 (Znt8) protein are also associated with type 1 diabetes mellitus.


Despite it’s complicated pathophysiology, it is important to understand the destruction of beta cells in type 1 diabetes because it leads to a lack of insulin and amylin. Without insulin or amylin the body cannot promote glucose disappearance or limit glucose appearance from the bloodstream, respectively, resulting in hyperglycemia (Mapes & Faulds, 2014). This is why the condition is sometimes called a€?juvenile diabetes.a€? The most common age of diagnosis is between 11 and 14 years old. People with type 1 diabetes regularly measure their blood sugar to figure out how much insulin they need. Diet and Exercise People with type 1 diabetes should eat regular meals and snacks to keep blood sugar stable.



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