Abstract
T1DM is an autoimmune disease that has CD4+ and CD8+ cells attacking islet cells. The destruction of islet cells disrupts the ability to produce insulin severely, causing hyperglycemia and insufficient energy production, leading to symptoms such as drowsiness and body weakness. Excessive bloodstream glucose is discharged through urination. While the trigger of this autoimmunity is unknown, HLA class II haplotypes HLA-DR3-DQ2 and HLA-DR4-DQ8 on chromosome 6 are thought to be responsible for T1DM development. Though T1DM incidence rate varies among countries, patients under 15 years old are drastically increasing. While insulin is the most well-established current treatment of T1DM, amylin helps to increase the effectiveness of glucose regulation by insulin. In pramlintide, amino acids 25, 28 and 29 are different from amylin, which solves the problem of amylin being self-aggregating and insoluble after injection. However, the injection dose of pramlintide needs to be carefully controlled to prevent hypoglycemia. Responding to the increasing number of T1DM patients, pramlintide increases the effectiveness of insulin treatment
Published Version
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