Type 1 diabetes occurs as a result of the body's immune system attacking the insulin producing beta cells of the pancreas, although it is not clear why this happens. A lack of insulin in the blood means inadequate amounts of glucose are taken up by cells of the body to provide energy for cellular functions. Consequently, glucose remains in the blood leading to a high blood sugar level. Exactly what causes the immune system to do this is not yet clearly understood but some hypotheses include:
Viral infection - Some research has suggested that the immune system is activated in response to viral infection. As the immune cells are activated against the virus particles, they are also activated against the beta cells of the pancreas. Viruses that have been implicated in the causation of type 1 diabetes include the coxsackie and rubella viruses.
Genetic tendency - Type 1 diabetes seems to run in families which suggests a genetic basis to the pathology of the condition. Some HLA genotypes are known to raise the risk of developing type 1 diabetes.
Development of antibodies - Some researchers have suggested that the development of antibodies against proteins in cow's milk may also lead to the development of antibodies that attack the beta cells of the pancreas. The presence of antibodies against pancreatic beta cells is seen in a subtype of type 1 diabetes mellitus.
There is speculation that lack of vitamin D in the first year of a child's life may raise the risk of type 1 diabetes developing.
Certain drugs and chemicals may also play a role in the development of type 1 diabetes by destroying the pancreatic beta cells. These include chemicals such as pyrinuron (Vacor, N-3-pyridylmethyl-N'-p-nitrophenyl urea) which is used as a rat poison and is no longer used in the USA. An anticancer and antibiotic agent called streptozotocin used to treat pancreatic cancer also destroys the pancreatic beta cells.
Further Reading
Gene expression signature associated with rapid progression of type 1 diabetes