Molecular mechanisms of action of glyburide on the beta cell

Article Abstract:

Non-insulin-dependent diabetes mellitus (NIDDM) is a disorder of glucose metabolism occurring mainly in obese adults and characterized by hyperglycemia, or increased blood glucose levels, and glycosuria, glucose in the urine. This disorder of glucose metabolism results from the decreased production or utilization of the protein hormone insulin by the tissues. Insulin is produced and released by the pancreas and functions to increase the consumption of glucose by the cells for the production of energy. The drug glyburide used to treat NIDDM stimulates the pancreas to produce more insulin. The mechanism whereby glyburide and similar antidiabetic agents activates insulin release is discussed. Glyburide and other antidiabetic drugs bind very strongly to a site on the beta cell of the pancreas called the sulfonylurea receptor. This glyburide receptor interacts with a channel or passage in the cell membrane that specifically prevents potassium from leaving the cell. The prevention of potassium movement out of the cell results in changes in the electrical properties of the cell membrane that lead to increased calcium movement into the cell. An increase in calcium within the beta cells causes them to release insulin. Several drug companies are in the process of purifying the receptor that binds glyburide and the gene that controls the production of the receptor. This research will contribute to the development of new approaches to treating NIDDM and further elucidate the causes of NIDDM. (Consumer Summary produced by Reliance Medical Information, Inc.)

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Effect of glyburide on beta cell responsiveness to glucose in non-insulin-dependent diabetes mellitus

Article Abstract:

Non-insulin-dependent diabetes mellitus (NIDDM) is a disorder of glucose metabolism that develops most often in obese adults. It is characterized by hyperglycemia, or increased blood levels of glucose, and glycosuria, the presence of glucose in the urine, which result from the decreased utilization of glucose by tissues of the body. In NIDDM, the body's cells become resistant or less responsive to the actions of the protein hormone insulin, which controls the consumption of glucose by tissue for the production of energy. Agents such as glyburide can compensate for the decreased tissue responsiveness to insulin by increasing the production of insulin by the beta cells of the pancreas. Recent studies show that short- and long-term treatment with glyburide increases the levels of C-peptide, a factor released with insulin and a measure of insulin secretion, in both normal subjects and diabetic patients. Glyburide did not affect resting insulin levels, but did increase the total amount of insulin released over a 24-hour period. This increase was due to a greater secretion of insulin occurring after lunch and dinner, but this effect was not as dramatic in the morning. These findings suggest that the primary effect of glyburide is to increase the beta cell's responsiveness to glucose, the levels of which are highest after a meal. Further research is needed to identify the mechanism of action of glyburide effects on beta cells. (Consumer Summary produced by Reliance Medical Information, Inc.)

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Glyburide: New insights into its effects on the beta cell and beyond - introduction

Article Abstract:

Non-insulin-dependent diabetes mellitus (NIDDM) is a disorder of glucose metabolism that develops mainly in adults. It is characterized by hyperglycemia, or high blood glucose, and glycosuria, glucose in the urine, resulting from the decreased production or utilization of insulin by tissues. Insulin, a protein hormone produced and released by the pancreas, allows glucose to be used by the cells of the body for energy. This chronic disease affects approximately seven percent of the population and its prevalence is expected to increase in the coming decades. Recent research has shown that people who are generally susceptible to developing the disease become resistant to insulin in the early stages of the disease. Diabetes does not occur in these individuals as long as the pancreas can compensate by making more insulin. NIDDM is more frequently seen in obese people, a condition strongly associated with insulin resistance. Therapy initially involves diet modification along with regular exercise. This may be supplemented by treatment with drugs such as glyburide, which are given once a day to increase the pancreatic secretion of insulin and exert other actions to regulate glucose levels in the blood. A recent symposium has examined some of the more recent research on glyburide and its effects in NIDDM. The proceedings of the symposium are published in a special supplement to the American Journal of Medicine. (Consumer Summary produced by Reliance Medical Information, Inc.)

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