Pancreatic Beta Cells Research Paper

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.

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).

Insulin is a hormone produced by the pancreas. It is a large gland that is located in the abdomen behind the stomach. Insulin is produced by special cells called pancreatic islets (or islets of Langerhans), which exist as small isolated clumps of cells within the pancreas. Insulin is produced by the beta cells of the pancreatic islets and is released when we have just eaten a meal and the level of glucose in our bloodstream is high. Insulin works by stimulating the cells within our body to take up the glucose in our blood, either for immediate energy, or for storing as glycogen in the liver or muscles cells.

Islets of Langerhans contain beta cells and are located within the pancreas. Beta cells produce insulin which is needed to metabolize glucose within the body.

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

Very few cases of Metabolic Syndrome can be fully attributed to hereditary causes. Rather, over-time, an individual’s lack of proper lifestyle habits, including diet, physical activity, environmental health, stress, and interrupted sleep patterns, can lead to the formation of insulin resistance and the five conditions, eventually leading to Metabolic Syndrome. This is brought about by the invasion of white adipose tissue. Mononuclear cells release cytokines, which then create insulin resistance in various tissues including muscle and the liver. In fact, the American Heart Association states, “skeletal muscle is the primary tissue that accounts for glucose disposal.” (AHA) As a result of insulin resistance, glucose uptake and fat mass increase substantially. The reason for the uptake in glucose is due to the suppression of gluconeogenesis and glycogenolysis, which results in a decrease in glucose output from the liver. When these areas are lacking or have been neglected, the body physiologically responds by producing inflammation, which is the first line of immune defense of the innate immune

Brenda´s pancreas possesses cellular clusters which are designated islets. The function of the islets in Brenda’s pancreas is to produce insulin and liberate the insulin into the bloodstream. In the event that the beta cells do not develop sufficient insulin or if Brenda’s body is unable to respond to the insulin that is in her bloodstream, the glucose accumulates in the blood instead of being subjected to absorption by the cells in Brenda´s body. This can lead to the manifestation of pre-diabetes. Pre-diabetes is a situation which causes the indexes of the blood glucose to be more elevated than normal. The blood glucose in pre-diabetes is not sufficient to warrant a diagnosis of diabetes. In diabetes type 1 and 2, the cells are deprived of glucose notwithstanding the high glucose levels that Brenda may be demonstrating (National Institute of Diabetes and Digestive and Kidney Diseases 2014).

Each islet is composed of alpha, beta, and delta cells. Alpha cells release the hormone glucogon (Ali, 2011, pp. 9-10). Glucogon changes the stored glycogen to glucose that is within the liver (Venes, 2013, p. 1031). Beta cells release insulin (Ali, 2011, pp. 9-10). Insulin is secreted when the glucose levels are elevated. It will stimulate cells to take up glucose, promote the storage of glucose in the liver and muscles and promote the storage of fat (Irland, 2011). Delta cells produce somatostatin which functions as a hormone inhibitor (Venes, 2013, p.

(Hermanns-Le, Scheen, & Pierard, 2014, p. 200) As our cells fail to respond to insulin, the beta cells of the pancreas produce more insulin and trigger the liver to produce more glucose to restore glycemic control. This compensational mechanism will eventually be unable to keep up with the body’s demands leading to elevated glucose levels in circulation. Eventually, the high demand of pancreatic beta cells to produce insulin will not be able to keep up and insulin production will become insufficient, lessening the uptake of glucose. This now opens the path to Type II Diabetes Mellitus. (Thoenes, 2012, p. 621)

Produced by beta cells in the pancreas, insulin is vital to humans’ existence. By regulating the cellular intake of glucose from the blood stream, insulin regulates the levels of sugar in the blood. It seems a very nominal process; however, disrupting the body’s production or response to insulin can have very dire consequences. Type 1 diabetes is when the body no longer produces insulin, and if left untreated, glucose, from food, and kentones, from fat degradation, will build up in the individual’s bloodstream. If left untreated, the condition is fatal. Type 2 diabetes is when the body’s cells are no longer responsive, or have a lessoned response, to insulin. Such a condition can cause poor circulation, resulting in amputations, and ailments such as blindness. Type 2 diabetes can also be fatal. Thus, even though synthetic insulin and corrective diets are available for diabetics, more research is needed to find ways to regenerate beta cells for individuals with type 1 diabetes. On a personal note, this subject matter appeals to me, because my younger brother had type 1 diabetes, and if enough people put hard work into researching this disease, maybe one day they will have a cure.

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

The pancreas is the gland that’s involved in this form of diabetes. When the body has too much glucose levels in the blood, there isn’t a moderate amount of the insulin hormone that is being released by the pancreas. Therefore, the body’s blood control is corrupted and so the body dosen’t work efficiently.

Insulin is a significant hormone which regulates glucose homeostasis by respond to target cells such as muscle cell, adipose tissue or liver. Insulin is entirely secreted by the β-cells of the islets of Langerhans (identified by Paul Langerhans in 1869) which are the areas in pancreas stored some endocrine cells. Most of the islet mass are β-cells, and there are the pancreatic islets contain α-cells that secret glucagon, δ-cells that secret somatostatin as well, and all of these located in the islet periphery cells where produce pancreatic polypeptide. The molecular mechanisms illuminated by which these cell types are created constitutes a topic of intense study and has important implications for our understanding of the etiopathological processes

In the pancreas, there are specialized cells that form small islands of cells, called "islets of Langerhans," that are alpha cells and beta cells. In these endocrine cells, they release pancreatic hormones, such as insulin and glucagon that diffuse into the bloodstream to regulate glucose levels. Beta cells secretes insulin, which regulates carbohydrate, protein, fat metabolism and storage. On the other hand, alpha cells secrete glucagon, in which it breaks down stored sugar (glycogenolysis). Without enough production of insulin, glucose remains in the blood that generates an increase levels of sugar in the blood.