Kristine Le
Diabetes Mellitus Type 1 The Diabetes Quebec Association states that in the past, "a diagnosis of diabetes meant certain death". This was held true until a Canadian physician, Frederick Banting, discovered the hormone insulin in 1921. He was able to isolate a unknown matter from the pancreas of a dog and inject it into another dogs pancreas 's. This discovery enabled them to save the lives of these diabetic dogs. Through trial and error Banting was able to perfect the purification of insulin in order for it to be injected on a daily basis to compensate for the insulin not being produced by the pancreas to control the blood sugar in hyperglycemic patients. Diabetes mellitus is an inability of the body to catabolize glucose
…show more content…
This disease does not favor one gender over the other, it effects males and females equally. Currently, the origin of diabetes is a conundrum. Although, it is understood that the immune system attacks the beta cells but it is not clear how or why it occurs. It is hypothesized that T1D maybe hereditary and environmental factors contribute to the onset (5). Symptoms prevail in individuals whom have the majority of their beta cells destroyed via a cellular mediated autoimmune response (1). The insulin signaling cascade is initiated when insulin binds to insulin receptors located on the cell 's surface. The insulin receptor has four subunits: two alpha subunits located on the outside of the cell and two transmembrane beta subunits (3 & 4). When insulin binds to the alpha subunit receptors, it transmits a signal across the plasma membrane and activates tyrosine residues that are attached to the beta subunits. The activation of the tyrosine residues causes it to autophosphorolate and then phosphorolate other proteins that also have tyrosine residues attached to them. These phosphorylated proteins then move on to trigger cellular responses such as translocation of GLUT4 vesicule to the cell membrane. The vesicule becomes a transporter to allow glucose to come into the cell so that it can continue on and be stored as glycogen (3). A beta cell-specific autoimmune process is the beginning of the destruction of the beta cells that produce insulin.
Type 1 diabetes is also called insulin-dependent because the pancreas produce little to no insulin due to the destruction of beta cell in pancreas(Bardsley et al, 2004). Therefore, the insulin have to be injected manually for body to function normally. (Seewaldt et.al, 2000) states that in type 1 diabetes, the beta cell located in the islets of Langerhans have antigen that cause the immune system to produce antibodies and kill the insulin producing cells. The autoimmune response is thought to be caused by the autoreactive CD4 and CD8 effector cells that recognise islet self-antigens, as an outcome there is greater than 90% destruction on insulin producing cell BACH (1994). Similarly, (Nakayama et al,2005) and (Kent et al, 2005) supports that insulin in itself is a
Type 1 is characterized by the body’s inability to produce insulin. It is caused by autoimmune-mediated destruction of pancreatic beta cells, which are responsible for producing insulin. There appears to be a hereditary link in people with Type 1 diabetes. Other factors have been known to cause Type 1 diabetes such as viral infections, toxins, and other environmental factors. Type 1 diabetes is the rare form, affecting about 10% of the diabetes population. Its onset usually occurs in people less than the age of 20.
Diabetes type 1 develops when the immune system attacks the only cells that create insulin, the pancreatic beta cells. Due to the cells being destroyed, the person with diabetes type 1 has to be
In 1921, scientist, Frederick Banting, and his lab assistant, Charles Best, found insulin in the pancreatic extracts of dogs. They injected the insulin into a dog and discovered that it lowered high blood sugar levels back to normal. With the aid of James Collip and J.J.R. Macleod, the scientists developed insulin for human treatment. In 1922, Leonard Thompson, a fourteen-year-old boy dying of diabetes, was injected with the first human dose of insulin, saving his life
regulate glucose levels had artificially been altered (“The Discovery of Insulin”). The results were groundbreaking and the diabetic dogs responded well to the injections, marking a major step forward in diabetes research (“The Discovery of Insulin”). Through the help of Professor John Macleod of the University of Toronto, they were able to continue their research (“The Discovery of Insulin”). Finally, in January of 1922, testing Dr. Banting’s developments in diabetes treatment on human beings had finally been completed and the results led to the ultimate development of the insulin treatment that is still used to this day (Simoni, Hill and Vaughan 31).
When I found out that T1D had no cure, I began researching myself. I stumbled upon one of the many trials doctors have been running in an attempt to cure diabetes. This one, however, fascinated me. This trial included beta cells. Beta cells are cells in the pancreas whose main function is to produce and secrete insulin. In people with Type One Diabetes, however, these cells are recognized as enemies and destroyed by the immune system. This bodily attack causes the low number of beta cells within a type one diabetic’s pancreas.
For unknown reasons, the body of a T1D attacks the insulin producing cells, called islets, that are formed in the pancreas and destroys them. This type of attack is known as an autoimmune disorder (Diabetes Research Institute Foundation [DRIF], n.d.). Insulin is the hormone that allows sugar to enter cells, and produce energy. The body now sees islet cells as foreign and eventually the pancreas yields little to no islet cells. Once there are no more islet cells to produce the insulin hormone the sugar levels in the blood become high, called hyperglycemia. This disturbance in homeostasis is not like type 2 diabetes (T2D), where the body becomes insulin resistant. In a T2D, the pancreas still produces islet cells and they are still
Banting graduated from medical school at the University of Toronto in 1916, and served at Granville Hospital in England for thirteen months before being sent to the front line as a battalion medical officer in 1918. Injured during the war, Banting convalesced in Britain, where he became a member of the Royal College of Physicians of London and the Royal College of Surgeons . In 1920, Banting was introduced to the idea of a therapy for diabetes while preparing a lecture on carbohydrate metabolism for his physiology students, he then found and read a relevant article, “The Relation of the Islets of Langerhans to Diabetes with Special Reference to Cases of Pancreatic Lithiasis,” by Moses Barron. He then had an idea that would unlock the dreaded diabetes disorder . Working at the University of Toronto laboratory in the very hot summer of 1921, Fred banting and Charles Best were able to make a pancreatic extract which had anti diabetic characteristics. They were successful in testing their extract on diabetic animals. Within months they put the entire work team to work on the production and purification of
Type 1 diabetes is a chronic autoimmune disorder, in which beta cells in the Islets of Langerhans are destroyed resulting in insulin deficiency and hyperglycemia. “The exact cause of why these normal cells are attacked by the immune system is a combination of genetic predisposition and certain viral infections such as the mumps and coxosackievirus which appear to trigger the destruction of pancreatic beta cells.” (Ignatavicius & Workman, 2013, p 1416) When these cells do not work properly, the body can no longer produce insulin. Insulin is a hormone that allows the body to use glucose that is found in foods for
The type 1 Diabetes that Ava lives with differentiates from type 2 Diabetes in that it is characterized by the complete autoimmune destruction of the pancreatic Beta (B) cells that produce and secrete Insulin in the Islet’s of Langerhans (Craft & Gordon, 2015, pg253). By contrast, type 2 Diabetes is a combination of B cell destruction, B cell dysfunction, and insulin resistance (Turner & Wass, 2009, pg803). The Beta cells of a non-Diabetic person would rapidly respond to glucose, however in type 1 Diabetes antibodies are produced against the body’s own B cells and consequently all the Islets are destroyed (Montague, 1983, pg50 and Craft & Gordon, 2015, pg253). This results in the failure of negative feedback loops in maintaining the body’s
About 10 to 20 percent of people with diabetes mellitus have Type 1, which occurs most often in children and young adults. The disease usually bags suddenly and symptoms can be severe (Goodheart 35). Type 1 diabetes in children is associated with the appearance of islet autoantibodies early in life, which is influenced by environmental factors. Once islet autoantibodies have developed, the progression to diabetes in antibody positive individuals is determined by the age of antibody appearance and by the magnitude of the autoimmunity in turn related to the age of the person. Characteristics that describe the magnitude of the autoimmunity can stage progression to Type 1 diabetes in islet autoantibody positive subjects regardless of genetic background or age (Achenbach et al.). There are very different incidences of Type 1 diabetes between countries that have similar prevalences of autoimmunity that suggests environment can influence the progression of Type 1 diabetes, but these studies suffer from relatively small numbers of people with islet autoantibodies (Achenbach et al.). Viruses and toxins can induce islet autoimmunity and it damages the body’s immune system. The body's immune system plays an essential role in Type 1 because it helps protect against
Beta cells of the endocrine pancreas constantly monitor glucose levels circulating in the blood and respond accordingly by releasing insulin. Glucose is the primary physiological stimulus of insulin secretion. When blood glucose concentration is elevated, glucose is transported across the beta cell plasma membrane by passive diffusion through glucose transporters (GLUT-1
Type I or insulin dependent diabetes mellitus (IDDM) is caused by the autoimmune destruction of the insulin producing β cells in the pancreas. Without insulin, the body does not metabolize glucose and this causes hyperglycemia. Type I can occur and develop quickly. Typically, type I diabetes affects people younger than 30 and is sometimes called juvenile-onset diabetes, but it can happen at any age. Type I can occurs when the body’s immune system is triggered to attack the β cells in the islets of the Langerhans of the pancreas. The β cells are destroyed or damaged to the point that they cannot create insulin. There is an ongoing search for the triggering factors of this process; so far it is believed that genetics and viral infections are a cause (Van Belle 2011).
In type 1 diabetes, the cause is an absolute deficiency of insulin secretion. Individuals at increased risk of developing this type of diabetes can often be identified by serological evidence of an autoimmune pathologic process occurring in the pancreatic islets and by genetic markers (8). In the other, much more prevalent
In type 1 diabetes, the immune system of a person’s body attacks and damages the cells that produce insulin.