Diabetes mellitus is a growing health issue worldwide. The prevalence of diabetes was estimated to be 382 million people in 2013, and is projected to increase to 592 million by 20351. In 2012, diabetes was directly attributed as the cause of death in 1.5 million individuals, and mortality due to diabetes and associated complications is estimated to be 3.7 million deaths2. This places diabetes mellitus as the 8th leading cause of mortality worldwide according to The World Health Organization estimates in 20153. In addition to the impact of this chronic disease on the quality of life of patients, it also presents a dramatic economic burden. In the United States of America, the estimated cost of diagnosed diabetes was $176 billion in direct medical
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Prior to the purification of insulin for therapeutic use, these two forms of diabetes presented with different progression and outcomes. The first form was characterized as a rapid wasting disease where the condition of patients declined over the course of months. The second form was associated with overweight, older patients with much slower progression that could often be prolonged through alterations in diet10. The isolation of insulin from canine islets of Langerhans followed by the administration of bovine insulin extracts in diabetic patients ushered in a new era of understanding of diabetes mellitus11. The response to insulin treatment became a differentiating factor to separate patients broadly into insulin-sensitive and insulin-resistant diabetes mellitus10. Insulin-sensitive patients would respond similar to healthy individuals upon administration of a bolus of glucose followed by intravenous insulin. This led to the hypothesis that insulin-sensitive diabetes is due to the deficiency of insulin12. Eventually the insulin-dependent form of diabetes would be referred to as type 1 diabetes mellitus10. Currently the American Diabetes Association further divides this category based on etiology. Type 1A diabetes is immune mediated and type 1B diabetes is non-immune mediated13. This work will focus on type 1A diabetes mellitus …show more content…
These antoantibodies develop sequentially with IAA antibodies often presenting first. High affinity antibodies in patients are reactive to resides the N-terminal region (residues 8-13) of proinsulin21. Despite autoantibodies against GAD65 often developing after IAA antibodies, GAD65 antibodies are still detectable several years before metabolic diagnosis of T1D22,23. While IAA is specific to T1D, GAD65 antibodies may be a more general marker of autoimmunity19. The detection of autoantibodies represents a good marker for individuals who may progress to T1D and allow for early therapeutic
Prior to the purification of insulin for therapeutic use, these two forms of diabetes presented with different progression and outcomes. The first form was characterized as a rapid wasting disease where the condition of patients declined over the course of months. The second form was associated with overweight, older patients with much slower progression that could often be prolonged through alterations in diet10. The isolation of insulin from canine islets of Langerhans followed by the administration of bovine insulin extracts in diabetic patients ushered in a new era of understanding of diabetes mellitus11. The response to insulin treatment became a differentiating factor to separate patients broadly into insulin-sensitive and insulin-resistant diabetes mellitus10. Insulin-sensitive patients would respond similar to healthy individuals upon administration of a bolus of glucose followed by intravenous insulin. This led to the hypothesis that insulin-sensitive diabetes is due to the deficiency of insulin12. Eventually the insulin-dependent form of diabetes would be referred to as type 1 diabetes mellitus10. Currently the American Diabetes Association further divides this category based on etiology. Type 1A diabetes is immune mediated and type 1B diabetes is non-immune mediated13. This work will focus on type 1A diabetes mellitus …show more content…
These antoantibodies develop sequentially with IAA antibodies often presenting first. High affinity antibodies in patients are reactive to resides the N-terminal region (residues 8-13) of proinsulin21. Despite autoantibodies against GAD65 often developing after IAA antibodies, GAD65 antibodies are still detectable several years before metabolic diagnosis of T1D22,23. While IAA is specific to T1D, GAD65 antibodies may be a more general marker of autoimmunity19. The detection of autoantibodies represents a good marker for individuals who may progress to T1D and allow for early therapeutic