Diabetogenic Animal Model

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

Insulin resistance is the first physiological change occurring in type two diabetes. In these type two diabetic patients, insulin is unable to move glucose into liver, kidney and muscle cells although insulin is able to attach properly to the cell surface receptors. In order to rectify this, most patients with type two diabetes start secreting normal to very high levels of insulin, which can initially overcome this resistance. After a while, the pancreas cannot keep up with this high insulin production and the cells become resistant to glucose intake. Persistent hyperglycemia or high blood glucose levels are not desirable since this causes damage to the beta cells of the pancreas that produces the insulin hormone. This damage to beta cells further hampers insulin synthesis and patients at this stage are categorized as full-blown diabetic. Such patients consistently show a hyperglycemia state even after hours of fasting ( Hinkle & Cheever,

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.

Diabetes is a disorder that is formed by high blood glucose. Diabetes is the seventh leading cause for death in the United States. It occurs most often in adults, but it’s one of the most chronic disorders in children. Individuals suffering from hyperglycemia have low production of insulin. American Diabetes Association is trying to prevent and cure diabetes and improve the lives of all people affected by diabetes.

During the study, 20 islets were studied from each case, and the focus was to measure B-cell volume, frequency, replication, and the ability for the endocrine ducts to produce new islet (Butler, et al. 2003). Based on the findings, there was an increase of B-cell in the obese population. “Obese humans with IFG and type 2 diabetes had a 40% (P < 0.05) and 63% (P < 0.01) deficit and lean cases of type 2 diabetes had a 41% deficit (P < 0.05) in relative β-cell volume compared with nondiabetic obese and lean cases, respectively” (Butler, et al. 2003).

A beta cell-specific autoimmune process is the beginning of the destruction of the beta cells that produce insulin.

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

The development of diabetes mellitus has several processes. These processes include autoimmune destruction of β-cells of the pancreas which consequently causes

Type 2 Diabetes, unlike people with Type 1 Diabetes are able to make insulin. To enhance our understanding of Type 2 Diabetes, knowing what Diabetes is crucial. When a person has diabetes; the body either does not make enough insulin or cannot use his or her own insulin properly, causing glucose (sugar) to build up in the body. It is the seventh leading cause of death in United States in 2010. In this paper, I provide an overview of the function of pancreas in controlling the sugar level in the human body and the function of insulin and glucagon hormones in the pancreatic process. I also present an anatomy of the human pancreas. Finally, I review the signs and symptoms, causes, treatments,

Destruction of beta cells > Beta cells decline> insulin secretion decreases until insulin is no longer available to maintain normal blood glucose levels.>Beta cells

Diabetes is one the most critical medical issues of our time. According to the Center of Disease Control and Prevention nearly 26 million Americans (approximately 8% of all Americans) have diabetes and an estimated of 79 million adults are pre-diabetes. Approximately $200 billion per year is lost due to diabetes because of medical treatments and lost wages. Insulin resistance and the dysfunction of beta cells are the two pathogenic hallmarks of the development and progression of T2DM. Studies have shown that pancreatic beta cell functional mass is affected in T2DM (1, 2). Secretion of insulin stimulated by glucose is lower in human islets of Langerhans isolated from patients with T2DM than from normal individuals (1, 3). Knowledge of the molecular mechanism underlying defects in beta cell function found in humans and animal models of T2DM is incomplete. Without a more complete understanding of the mechanisms that regulate beta cell insulin secretion we will be unable to develop new approaches to prevent and treat diabetes.

In type 1 diabetes the immune system attacks and destroys the insulin producing beta cells in the islets of Langerhans. The body is believed to do this because of some unfortunate genetic coding.

Diabetes Mellites(DM), is a deficiency of insulin action causing hyperglycemia. The majority of DM have a decreased secretion of the cells, insulin resistance, or counterregulatory hormones( McPhee & Hammer, 2010). Insulin is synthesized from the beta cells from the pancreases. Composed from A peptide and B peptide connected to C peptide and disulfide bonds. Insulin is a hormone that aids in metabolism. encourages glucose uptake and the synthesis works mainly in the liver, muscle, and adipose tissue

Alexandra E. Butler et al focuses on the increased B cell apoptosis in type 2 diabetes. He noted that the decreased mass of pancreatic beta cell results from increasing apoptosis rather than decrease. The mass of the beta cell is balanced by apoptosis and beta cell replication . Disruption of this pathway leads to reduction of beta cell mass thereby decreasing the capacity to produce insulin . He further addresses that there is 10-fold increase in the frequency of apoptosis in non obese type 2 diabetic mice when compared to the control(non diabetic mice) and about a 3- fold increase in obese diabetic mice when also compared with the control . The pancreatic islet has deposits of peptide, Islet amyloid polypeptide( IAPP) also known as amylin

The results of OGTT revealed, HAEAD treated dextrose loaded normal rats showed reduction in AUC glucose (0 -150 min) which might be due to activation of pancreatic insulin release. The low doses of alloxan induced diabetes through destroying pancreatic β-cells partially, surviving and regeneration of beta cells is possible (Kalia et al., 2008). The hyperglycaemia in diabetes is primarily due to excessive glycogenolysis,