So what exactly is diabetes? Let's explain: (Thank you wikipedia)
Part one:
Diabetes mellitus type 1 (Type 1 diabetes, Type I diabetes, T1D, IDDM) is a form of diabetes mellitus. Type 1 diabetes is an autoimmune disease that results in the permanent destruction of insulin producing beta cells of the pancreas. Type 1 is lethal unless treatment with exogenous insulin via injections replaces the missing hormone.
There is currently no preventive measure that can be taken against type 1 diabetes. Most people affected by type 1 diabetes are otherwise healthy and of a healthy weight when onset occurs, but they can lose weight quickly and dangerously, if not diagnosed in a relatively short amount of time. Diet and exercise cannot reverse or prevent type 1 diabetes. However, there are clinical trials ongoing that aim to find methods of preventing or slowing its development. There is no cure for type 1 diabetes. Type 2 is not as dangerous and can be prevented/cured depending on reasoning for it.
Part 2:
PathophysiologyThe 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 and there is indeed an observed inherited tendency to develop Type 1[citation needed]. 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.
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.
Part 3:
Treatment~
Type 1 is treated with insulin replacement therapy — usually by injection or insulin pump, dietary control, typically including carbohydrate tracking, and careful monitoring of blood glucose levels using Glucose meters.
Untreated Type 1 diabetes can lead to one form of diabetic coma, diabetic ketoacidosis, which can be fatal. At present, insulin treatment must be continued for a lifetime; this will change if better treatment, or a cure, is discovered. Continuous glucose monitors have been developed which alert to the presence of dangerously high or low blood sugar levels.
In some extreme cases, a pancreas transplant can help restore proper glucose regulation. However, the surgery and accompanying immunosuppression required is considered by many physicians to be more dangerous than continued insulin replacement therapy and is therefore often used only as a last resort (such as when a kidney must also be transplanted or in cases where the patient's blood glucose levels are extremely control resistant). Experimental replacement of beta cells (by transplant or from stem cells) is being investigated in several research programs and may become clinically available in the future. Thus far, beta cell replacement has only been performed on patients over age 18, and with tantalizing successes amidst with nearly universal failure.
Part 4:
A cure~
Diabetes type 1 is caused by the non-existence of a sufficient number of beta cells in the body; these cells, which are found in the Langerhans islets in the pancreas, produce and secrete insulin, the single hormone responsible for allowing glucose to enter from the blood into cells. Hence, the phrase "curing diabetes type 1" means "causing a maintenance or restoration of the endogenous ability of the body to produce insulin in response to the level of blood glucose". This section does not deal with approaches other than that (for instance, closed-loop integrated glucometer/insulin pump products), which may also greatly increase quality of life for those who have diabetes type 1, and may by some be termed "artificial pancreas". Instead, it only deals with such approaches for thoroughly curing the underlying condition of diabetes type 1, by enabling the body to endogenously, in vivo, produce insulin in response to the level of blood glucose.
Several ideas are placed below
Encapsulation approach
Technology for gene therapy is advancing rapidly such that there are multiple pathways possible to support endocrine function, with potential to practically cure diabetes.
Gene therapy can be used to manufacture insulin directly: an oral medication, consisting of viral vectors containing the insulin sequence, is digested and delivers its genes to the upper intestines. Those intestinal cells will then behave like any viral infected cell, and will reproduce the insulin protein. The virus can be controlled to infect only the cells which respond to the presence of glucose, such that insulin is produced only in the presence of high glucose levels. Due to the limited numbers of vectors delivered, very few intestinal cells would actually be impacted and would die off naturally in a few days. Therefore by varying the amount of oral medication used, the amount of insulin created by gene therapy can be increased or decreased as needed. As the insulin producing intestinal cells die off, they are boosted by additional oral medications.
Gene therapy might eventually be used to cure the cause of beta cell destruction, thereby curing the new diabetes patient before the beta cell destruction is complete and irreversible.
Gene therapy can be used to turn duodenum cells and duodenum adult stem cells into beta cells which produce insulin and amylin naturally. By delivering beta cell DNA to the intestine cells in the duodenum, a few intestine cells will turn into beta cells, and subsequently adult stem cells will develop into beta cells. This makes the supply of beta cells in the duodenum self replenishing, and the beta cells will produce insulin in proportional response to carbohydrates consumed.
Nanotechnology approach
Under the nanotechnological approach to curing diabetes type 1, many "nanobots" would be injected into the patient's bloodstream. These nanobots would be able to synthesize insulin, and to secrete it according to the level of glucose they would sense
Other:
Scientists in the South Korean university of Yonsei have, in 2000, succeeded in reversing diabetes in mice and rats. Using a viral vector, a DNA encoding the production of an insulin analog was injected to the animals, which remained non-diabetic for at least the eight months duration of the study.