Ignite Creation Date:
2024-05-05 @ 5:01 PM
Last Modification Date:
2024-10-26 @ 9:26 AM
Study NCT ID:
NCT00364377
Status:
COMPLETED
Last Update Posted:
2011-12-06
First Post:
2006-08-14
Brief Title:
Incretins in Impaired Fasting Glucose
Sponsor:
Mayo Clinic
Organization:
Mayo Clinic
Study Overview
Official Title:
The Role of Incretins in the Pathogenesis of Fasting and Postprandial Glucose Metabolism in People With Impaired Fasting Glucose
Status:
COMPLETED
Status Verified Date:
2011-11
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
People with high fasting glucose can develop type 2 diabetes with the passage of time This study is being done to determine the effect of a novel medication in people with this elevated fasting glucose Sitagliptin is a substance that raises levels of a hormone normally found in the blood This hormone called glucagon-like peptide-1 GLP-1 is normally released by the intestine in response to the presence of food This hormone acts like a messenger between the intestine and the pancreas to raise insulin levels and therefore lower blood sugars Sitagliptin is effective in people with diabetes however this study is being done to determine if Sitagliptin is effective in people with high fasting glucose who do not yet have diabetes
Detailed Description:
Impaired fasting glucose IFG confers a high risk of progression to diabetes Its pathogenesis has been an area of active investigation with defects in insulin and glucagon secretion as well as insulin action likely to play a role Several studies have suggested that the prediabetic and diabetic state are associated with alterations in circulating incretin concentrations More recently a large study of non-diabetic individuals demonstrated decreased GLP-1 concentrations after a glucose challenge in individuals with prediabetes but concluded that defects in GLP-1 secretion were unrelated to insulin secretion In impaired glucose tolerance IGT defects in incretin-induced insulin secretion coexist with defects in glucose induced insulin secretion
Worsening degrees of glucose tolerance are associated with decreased insulin secretion for the prevailing insulin action Moreover early glucagon suppression is impaired in IGT Since GLP-1 is an insulin secretagogue and suppresses glucagon it is conceivable that defects in GLP-1 secretion could contribute to the pathogenesis of pre-diabetes Inhibition of Dipeptidyl Peptidase-4 DPP-4 an enzyme which rapidly degrades the incretin hormones has been shown to be a useful therapeutic strategy in type 2 diabetes DPP-4 inhibitors increase model-calculated insulin secretion and decrease glucagon concentrations resulting in a lowering of fasting and postprandial glucose concentrations in people with type 2 diabetes Their effects in people with IFG are less certain However DPP-4 inhibitors provide an opportunity to directly examine the contribution of abnormal incretin concentrations to the pathogenesis of IFG by raising concentrations of endogenous incretin hormones
The current experiments tested this hypothesis by measuring insulin secretion and action and fasting and postprandial glucose turnover before and after 8 weeks of therapy with a DPP-4 inhibitor
Worsening degrees of glucose tolerance are associated with decreased insulin secretion for the prevailing insulin action Moreover early glucagon suppression is impaired in IGT Since GLP-1 is an insulin secretagogue and suppresses glucagon it is conceivable that defects in GLP-1 secretion could contribute to the pathogenesis of pre-diabetes Inhibition of Dipeptidyl Peptidase-4 DPP-4 an enzyme which rapidly degrades the incretin hormones has been shown to be a useful therapeutic strategy in type 2 diabetes DPP-4 inhibitors increase model-calculated insulin secretion and decrease glucagon concentrations resulting in a lowering of fasting and postprandial glucose concentrations in people with type 2 diabetes Their effects in people with IFG are less certain However DPP-4 inhibitors provide an opportunity to directly examine the contribution of abnormal incretin concentrations to the pathogenesis of IFG by raising concentrations of endogenous incretin hormones
The current experiments tested this hypothesis by measuring insulin secretion and action and fasting and postprandial glucose turnover before and after 8 weeks of therapy with a DPP-4 inhibitor
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None