It destroys the body’s own immune system as part of an inflammatory response known as insulitis, the insulin-producing beta cells in the pancreas itself. This inflammatory reaction is probably present already in early childhood.
The ensuing destruction of the insulin-producing beta cells leads to a gradually increasing deficiency of insulin. Only when about 80-90% of the beta cells are destroyed, can type-1 diabetes manifest. In the early stages of the disease there is quite a small residual insulin production.
The lack of glucose within the cells accumulates in the blood. The formation of glucose in the liver proceeds unabated. It will be making up to 500g of glucose per day in the blood. Because of this the cells can not be exploited it remains in the blood and increases the blood sugar level.
There will be a flood of blood with free fatty acids. As for the metabolism of fatty acid substrates from the carbohydrate metabolism, they can not be reduced in the normal way, but be transformed via a side road to ketone bodies (acetone, and acetoacetic acid).
The free fatty acids and these ketone (acetone exception) acids, leads to an acidification of the blood (ketoacidosis), through which all the metabolic processes are affected in the body. Presuming a healthy renal function, after crossing the threshold of impaired renal reabsorption in the tubules, the glucose is excreted in the urine (glucosuria). For the same reason, water and vital substances increased in urine (polyuria appear = constant urination) are caused by constant drinking = polydipsia.
The emergence of diabetes mellitus type 1 is associated with genetic and environmental factors. There are currently more than 20 genes which have been identified that could be related to the development of type 1 diabetes. Most described gene mutations are caused by a polygenic origin, i.e. several genetic changes have to be present so that type-1 diabetes arises.
Only in rare cases is a monogenic disorder is present. In particular, genetic modifications of the short arm of chromosome 6, called the MHC region, could be held responsible for the development of diabetes mellitus type 1. The genes HLA-A and HLA-B in this region contain the hereditary information for proteins on the surface of body cells, which serve the body’s own immune system as a basis for discrimination against foreign cells.
Genes outside the HLA complex, probably play a much smaller role in the aetiology of type 1 diabetes. Among them we find the gene for insulin (INS) and the CTLA4 gene, which is responsible for the T-lymphocyte regulation.
An autoimmune reaction occurs when the immune system is exposed to exogenous antigen, which is similar to a body’s surface protein. The resulting immune response is directed against both the foreign antigen as well as against the existing body’s own proteins in the pancreatic islet cells (cross-reactivity, molecular mimicry).
The following environmental factors could be documented relationships: The consumption of cow’s milk in the first three months of life in children with only a short lactation. Very early exposure to the protein gluten, which occurs in various cereals. Diabetic (diabetes inducing) viruses: Coxsackie B viruses (especially B4), intrauterine (in the uterus during pregnancy), rubella infection with the Rubivirus (leading to diabetes in 50%), echo viruses, cytomegalovirus (CMV), herpes viruses.
Insulin-like structures to solve the antigens of the immune system attack on the pancreas. Lymphocytes from Type 1 diabetic patients demonstrated to respond to a specific part of the insulin protein.
Bafilomycine, in particular, to the rotten bodies of root vegetables (potatoes, carrots) are formed by streptomycetes: Bafilomycin A1 caused on animals already in nanogram quantities of glucose intolerance and damages the islets of Langerhans in the pancreas.
Characteristic of the type-1 diabetes is the pronounced weight loss within a very short time, coupled with desiccation (dehydration), constant thirst, frequent urination, vomiting and sometimes abdominal pain and cramps. Common symptoms include fatigue and weakness, blurred vision and difficulty with concentration. Headaches are not uncommon.
Be fed artificially in type 1 diabetes. The aim of this insulin therapy is not a cure for Type 1 diabetes, but compensation for the lack of endogenous insulin. Therefore, the treatment must be carried out continuously until the end of life. A therapy to cure is not yet available.
Continuously measuring glucose sensors alone or in combination with an insulin pump as an artificial pancreas, allowing it to guide therapy by the patient himself or through an automatic control algorithm using an insulin pump which can be time-consuming and possibly administer insulin as needed and carbohydrates. The latter is still in its experimental stage.
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