Glimepiride Induced Insulin Secretion Will be Inhibited by Hypoglycemia
|Study Design:||Allocation: Randomized
Intervention Model: Factorial Assignment
Masking: Single Blind (Subject)
|Official Title:||Glimepiride Induced Insulin Secretion Will be Inhibited by Hypoglycemia|
- catecholamines [ Time Frame: 1 day ]
|Study Start Date:||August 2002|
|Study Completion Date:||December 2010|
|Primary Completion Date:||September 2004 (Final data collection date for primary outcome measure)|
Glimepiride (Amaryl) 4 mg oral dose during protocol, given once during each protocol.
Other Name: Amaryl
Glyburide (Dia-Beta) 10 mg oral dose during protocol, given once during each protocol.
Other Name: Dia-Beta
Other: glucose clamp
Hyperinsulinemic euglycemic glucose clamp procedure-120 minutes
Other: glucose clamp
hypoglycemic glucose clamp procedure -120 minutes
In patients with type 2 diabetes, sulfonylurea drugs are a mainstay for effective glucose control. These agents produce their hypoglycemic effects via stimulation of endogenous insulin secretion. Oversecretion of insulin, per se, or a continued relative increase of the hormone even when plasma glucose is normal will result in hypoglycemia. This latter situation commonly occurs if a patient decides to omit, delay, or reduce the size of a meal. An important defense against hypoglycemia in the above situations is glucose dependent regulation of insulin secretion. In other words, a low ambient glucose concentration could regulate the magnitude of the amount of insulin released in response to a sulfonylurea. Thus during hypoglycemic conditions, the sulfonylurea would result in little or no insulin secretion, whereas its effects during hyperglycemia would be amplified. Glimepiride and glyburide are both second-generation sulfonlyurea drugs used commonly for treatment of type 2 diabetes. This study will compare the two and ask the following question:
Is Glimepiride insulin secretion dependent upon glucose concentration in-vivo?
Please refer to this study by its ClinicalTrials.gov identifier: NCT00608179
|Principal Investigator:||Stephen N. Davis, MD||Vanderbilt University|