Diabetes mellitus type 1 pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]; Cafer Zorkun, M.D., Ph.D. [3]
Pathophysiology
The cause of Type 1 diabetes is still not understood. Type 1 diabetes could be a virally induced autoimmune response. Autoimmunity is a condition where one's own immune system "attacks" structures in one's own body either destroying the tissue or decreasing its functionality. In the proposed scenario, pancreatic beta cells in the Islets of Langerhans are destroyed or damaged sufficiently to abolish endogenous insulin production. This etiology makes type 1 distinct from type 2 diabetes mellitus. It should also be noted that the use of insulin in a patient's diabetes treatment protocol does not render them as having type 1 diabetes, the type of diabetes a patient has is determined only by disease etiology. The autoimmune attack may be triggered by reaction to an infection, for example by one of the viruses of the Coxsackie virus family or German measles, although the evidence is inconclusive.
This vulnerability is not shared by everyone, for not everyone infected by these organisms develops Type 1 diabetes. This has suggested a genetic vulnerability[1] and there is indeed an observed inherited tendency to develop Type 1. It has been traced to particular HLA phenotypes, though the connection between them and the triggering of an auto-immune reaction is poorly understood.
Some researchers believe that the autoimmune response is influenced by antibodies against cow's milk proteins. A large retrospective controlled study published in 2006 strongly suggests that infants who were never breast fed had twice the risk for developing Type 1 diabetes as infants who were breast fed for at least three months. The mechanism, if any, is not understood. No connection has been established between autoantibodies, antibodies to cow's milk proteins, and Type 1 diabetes. A subtype of Type 1 (identifiable by the presence of antibodies against beta cells) typically develops slowly and so is often confused with Type 2. In addition, a small proportion of Type 1 cases have the hereditary condition maturity onset diabetes of the young (MODY) which can also be confused with Type 2.
Vitamin D in doses of 2000 IU per day given during the first year of a child's life has been connected in one study in Northern Finland (where intrinsic production of Vitamin D is low due to low natural light levels) with a reduction in the risk of getting Type 1 diabetes later in life (by 80%).
Some suggest that Vitamin D3 (one of several related chemicals with Vitamin D activity) may be an important pathogenic factor in Type 1 diabetes independent of geographical latitude.
Some chemicals and drugs specifically destroy pancreatic cells. Vacor (N-3-pyridylmethyl-N'-p-nitrophenyl urea), a rodenticide introduced in the United States in 1976, selectively destroys pancreatic beta cells, resulting in Type 1 diabetes after accidental or intentional ingestion. Vacor was withdrawn from the U.S. market in 1979. Zanosar is the trade name for streptozotocin, an antibiotic and antineoplastic agent used in chemotherapy for pancreatic cancer, that kills beta cells, resulting in loss of insulin production.
Other pancreatic problems, including trauma, pancreatitis or tumors (either malignant or benign), can also lead to loss of insulin production. The exact cause(s) of Type 1 diabetes are not yet fully understood, and research on those mentioned, and others, continues.
In December 2006, researchers from Toronto Hospital for Sick Children revealed research that shows a link between type 1 diabetes and the immune and nervous system. Using mice, the researchers discovered that a control circuit exists between insulin-producing cells and their associated sensory (pain-related) nerves [2]. It's being suggested that faulty nerves in the pancreas could be a cause of type 1 diabetes.
References
- ↑ "Donner", "Horst" ("2007"). ["http://jcem.endojournals.org/cgi/content/abstract/82/1/143" ""CTLA4 Alanine-17 Confers Genetic Susceptibility to Graves' Disease and to Type 1 Diabetes Mellitus""] Check
|url=value (help). "The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 1 143-146". "The Journal of Clinical Endocrinology & Metabolism". Retrieved 2008-02-06. Unknown parameter|coauthors=ignored (help); Check date values in:|date=(help) - ↑ "Canadian scientists reverse diabetes in mice". Retrieved 2007-06-04.