Hyperinsulinemia Research Paper

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Hyperinsulinemia develops due to an increased tissue demand. As tissue response to insulin is decreased, the beta cells in the pancreas must produce more. Over time the pancreas must produce more and more until the beta cells cannot keep up with tissue demand. Beta cell dysfunction develops and leads to type 2 diabetes. This dysfunction can be due to a relative decrease in mass of beta cells (beta cell death), abnormal secretion in insulin by beta cells, or a combination of the two. Because beta cells are especially sensitive to elevated glucose levels and free fatty acids, beta cells will undergo programmed cell death when confronted with these conditions. Other conditions associated with obesity also contribute to apoptosis of beta cells; …show more content…

Glucagon is a hormone that works to increase blood glucose levels by stimulating the breakdown of glycogen to glucose, and the production of glucose from none carbohydrate pathways. Glucagon is an antagonist to insulin by making more glucose and keeping it available in the blood stream, whereas insulin works to transport glucose from the blood stream into tissue cells. Amylin is another hormone produce by beta cells. It is co-secreted with insulin and works to inhibit glucagon. Typically and dysfunction of insulin production is associated with a dysfunction in amylin production. Incretins are peptides found in the gastrointestinal tract. They are peptide hormones that are released in response to the intake of food. Incretins are responsible for the sensitivity of beta cells to blood glucose levels, and help improve insulin response to meals. These peptides bind to the beta cells and stimulate the production and release of insulin (McCance, 2010). A combination of multiple factors dysfunction is responsible for type 2 diabetes. When treating the disease, the number one priority to control glucose intake and decrease weight of the patient. A reduction in weight will result in a decrease in insulin need. Medications like metformin, pioglitazone, and glimepiride can also help to control blood glucose by working with …show more content…

It works by lowering blood glucose and increasing glucose tolerance. Metformin works in three ways to achieve this. First, it decreases the production of glucose in the liver. Second, metformin reduces the absorption of glucose in the stomach (Burchum, 2015). These to mechanisms decrease the overall availability of glucose in the blood stream. However, metformin also increases sensitivity of receptors to insulin in tissues such as fat and skeletal muscle. This causes an increase of glucose uptake by cells and further decreases serum glucose levels. These mechanisms cause and overall decrease in free glucose circulating in the blood. However, the third mechanism is dependent on the availability of insulin. Without insulin, metformin cannot work to increase cellular uptake of glucose. Metformin does not stimulate the release of insulin from the pancreas, it simply works with it to lower blood glucose. Because of this, there is no danger of hypoglycemia while using metformin alone. Metformin should not be used in patients with impaired kidney function. It is not metabolized, and is excreted by the kidneys completely unaltered. This creates a problem in patients with kidney impairment or failure. The potential for metformin to cause toxicity is present (Burchum,

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