Beta cells pancreas

Diabetes mellitus is a complicated, chronic disorder characterized by either insufficient insulin production by the beta cells of die pancreas or by cellular resistance to insulin. Insulin insufficiency results in elevated blood glucose levels, or hyperglycemia As a result of the disease, individuals with diabetes are at greater risk for a number of disorders, including myocardial infarction, cerebrovascular accident (stroke), blindness, kidney disease, and lower limb amputations. 

Insulin is a hormone manufactured by the beta cells of the pancreas. It is the principal hormone required for the proper use of glucose (carbohydrate) by the body. Insulin also controls the storage and utilization of amino acids and fatty acids. Insulin lowers blood glucose levels by inhibiting glucose production by the liver. 

The sulfonylureas appear to lower blood glucose by stimulating the beta cells of the pancreas to release insulin. The sulfonylureas are not effective if the beta cells of the pancreas are unable to release a sufficient amount of insulin to meet the individual s needs. The first generation sulfonylureas (eg, chlorpropamide, tolazamide, and tolbutamide) are not commonly used today because they have a long duration of action and a higher incidence of adverse... 

Like the sulfonylureas, the meglitinides act to lower blood glucose levels by stimulating the release of insulin from the pancreas. This action is dependent on the abilily of the beta cell in the pancreas to produce some insulin. However, the action of die meglitinides is more rapid than that of the sulfonylureas and their... 

Coskun O, Kanter M, Korkmaz A, Oter S. (2005) Quercetin, a flavonoid antioxidant, prevents and protects streptozotocin-induced oxidative stress and beta-cell damage in rat pancreas. Pharmacol Res 51 117-123. 

Pharmacology Nateglinide lowers blood glucose levels by stimulating insulin secretion from the pancreas. This action is dependent upon functioning beta-cells in the pancreatic islets. 

Mechanism of Action Afirst-generation sulfonylurea that promotes release of insulin from beta cells of pancreas. Therapeutic Effect Lowers blood glucose concentration. Pharmacokinetics Rapidly absorbed from the gastrointestinal (Gl) tract. Protein binding 60%-90%. Extensively metabolized in liver. Excreted primarily in urine. Removed by hemodialysis. Half-life 30-42 hr. 

Mechanism of Action An antihyperglycemic that stimulates release of insulin from beta cells of the pancreas by depolarizing beta cells, leading to an opening of calcium channels. Resulting calcium influx induces insulin secretion. TiicrapcuticEffect Lowers blood glucose concentration. 

Mechanism of Action A first-generation sulfonylurea thatpromotesthereleaseof insulin from beta cells of pancreas. T herapeutic Effect Lowers blood glucose concentra-... 

In their report the researchers describe a culturing technique that can turn mouse embryonic stem cells into cell clusters that resemble pancreatic islets. The clusters inner cells produced insulin, while outer cells produced glucagon and somatostatin, two other proteins typically synthesized by pancreatic cells. Most important, the embryonic stem cell-derived pancreas cells produce insulin in response to glucose, the fundamental role of beta cells that regulate insulin secretion. The major shortcoming of the system at this time is the low levels of insulin production. Refinements in culture technique or drug manipulation may be needed to achieve therapeutic levels. 

Diazoxide inhibits insulin release from the pancreas (probably by opening potassium channels in the beta cell membrane) and is used to treat hypoglycemia secondary to insulinoma. Occasionally, hyperglycemia complicates diazoxide use, particularly in persons with renal insufficiency. 

GLUT 2 Beta cells of pancreas liver, kidney gut 15-20 Regulation of insulin release, other aspects of glucose homeostasis... 

Insulin-dependent diabetes mellitus (IDDM) is an example of a metabolic disease under active consideration for inducible gene therapy strategies. In this disorder, inflammatory cytokines have been shown to activate apoptosis in pancreatic beta cells. Experimental studies indicate that expression of insulinlike growth factor-1 (IGF-1) can prevent the cytokine-mediated destruction of beta cells of the pancreas (Giannoukakis et al., 2001). Regulated expression of IGF-1 in human pancreatic islets, to preserve beta cell function, may be a useful approach in the treatment of certain types of diabetes (Demeterco and Levine, 2001). 

An important interaction between insulin and glucagon may also take place directly within the pancreas, and insulin appears to be the dominant hormone controlling this interaction.29,53 When the beta cells sense an increase in blood glucose, they release insulin, which in turn inhibits glucagon release from the alpha... 

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