As we mentioned in our previous blog post, insulin is the key that unlocks the door to allow glucose to enter cells to be used as energy. In type 1 diabetes mellitus (T1DM), the pancreas doesn’t produce enough insulin. Insulin is produced in the beta cells within the islets of Langerhans within the pancreas. The beta cells are destroyed by the body’s own immune response in whats called a type IV hypersensitivity reaction. The immune system contains T cells which react with antigens, which are small molecules the T cells can attached to. These might be on bacteria or another foreign body or they could be on our own cells. This is where the problem comes in in T1DM, usually T cells would undergo a mechanism known as self-tolerance when a T cell attached to an antigen that is part of a normal body cell, and this results in the destruction of that T cell. However, in T1DM a genetic abnormality results in this loss of self-tolerance therefore these T cells aren’t lost, specifically those that attack the beta cell antigens via an immune response. The human leukocyte antigen system are a group of genes on chromosome 6, and these are commonly affected in T1DM. These group of genes result in the major histocompatibility complex which is important in the recognition of foreign molecules and involved in self-tolerance. These major histocompatibility complexes present self-antigens to immune cells; therefore, a mutation might cause the immune system to recognise the antigen are foreign.
T1DM makes up about 10% of the amount of people with diabetes in the world. In people with T1DM the destruction of beta cells starts early on in life, however around 90% of cells needs to be destroyed before symptoms of the condition start to appear. Weight loss is a common symptom in someone with T1DM, this is a result of the glucose not being able to get into the cells to be used as energy so adipose tissue breaks down, called lipolysis and also muscles break down protein, leading to a catabolic state. This catabolic state results in the patient feeling hungry or polyphagia. Polyuria, or an increased frequency of urination, is another classic symptom of T1DM and this is due to excess glucose in the blood, causing glucose to spill out into the urine. This increased concentration of glucose in the urine upsets the equilibrium so more water stays in the urine instead of being reabsorbed by the kidney, resulting in increased urination. Polydipsia is another cardinal symptom, increased thirst, this is due to the dehydrated state that results from this increased urination.
Treatment for T1DM is lifelong insulin as this isn’t being produced in the body. This can be administered under various different regimes, but diet and fluid intake have to be carefully monitored in order to control the diabetes.
Watch out for a post of diabetes ketoacidosis in the coming weeks, this is a life-threatening complication of T1DM, and is actually how a lot of patients present to hospital and T1DM is diagnosed.