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). The content of this site is published by the site owner(s) and is not a statement of advice, opinion, or information pertaining to The Ohio State University. The 10 parameters Urine Reagent Strips (URS-10) is a urinalysis CLIA Waived test, FDA approved product that provides rapid visual results for Leukocytes, Nitrite, Urobilinogen, Protein, pH, Blood, Specific Gravity, Ketone, Bilirubin and Glucose in human urine. 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).



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