Type I Diabetes Mellitus (TIDM) is a chronic, autoimmune disease where pancreatic beta cells are destroyed, thus little to no insulin is produced.
This renders the patient unable to use glucose at the cellular level. There is no cure available, with the gold standard of treatment being lifelong insulin therapy. TIDM accounts for 10% of all diabetes cases globally (1), and is the most common type of diabetes in children. Incidence of TIDM worldwide has been increasing by 2-5%, with prevalence at 1 in 300 by 18 years of age (2). In the United States, the costs due to TIDM are estimated to be $14.4 billion annually.
The classical presentation of type 1 diabetes includes polyuria polydipsia, xerostomia, polyphagia, fatigue, and weight loss (3)(4), with the strongest association being with IDDM1, the gene encoding the major histocompatibility complex type 2 (MHCII) on chromosome 6. Certain variants of this gene seem to be associated with increased risk, while others may be protective (5). Although certain chemicals are known to destroy the insulin producing beta cells in the pancreas, no environmental factors have been convincing linked to T1DM. The development of autoantibodies to a number of antigens found on beta cells is associated with increasing risk of T1DM. Not all individuals with antibodies to beta-islet cells, insulin, glutamate decarboxylase, IA-2 or ZnT8 will develop T1DM, but as the number of these proteins to which an individual produces antibodies increases, so their risk of T1DM increases, though the time interval is highly variable (6).
T1DM is not currently preventable, and does not have the same association with obesity that type 2 diabetes has. T1DM does respond to insulin, unlike type 2 diabetes, and individuals with T1DM are generally dependent on insulin. There are currently no approved treatments for T1DM, and potential treatments are focused on transplantation (pancreas, beta-islet cells, stem cells) or vaccines designed to induce tolerance. The complications of T1DM are largely due to excessive glycosylation of proteins due to the elevated levels of blood glucose. While the impact of poorly controlled blood glucose is monitored by the glycosylation of hemoglobin, the pathological impact is seen on basement membrane proteins in the kidney (diabetic nephropathy), the retina (diabetic retinopathy), and blood vessels generally (cardiovascular disease, diabetic ulcer, diabetic vascular dementia, diabetic neuropathy) (7, 8).