Incretins in Impaired Fasting Glucose
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|ClinicalTrials.gov Identifier: NCT00364377|
Recruitment Status : Completed
First Posted : August 15, 2006
Results First Posted : December 6, 2011
Last Update Posted : December 6, 2011
|Condition or disease||Intervention/treatment||Phase|
|Pre-diabetes||Drug: Sitagliptin Other: Placebo||Phase 4|
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.
|Study Type :||Interventional (Clinical Trial)|
|Actual Enrollment :||22 participants|
|Intervention Model:||Parallel Assignment|
|Masking:||Double (Participant, Investigator)|
|Official Title:||The Role of Incretins in the Pathogenesis of Fasting and Postprandial Glucose Metabolism in People With Impaired Fasting Glucose|
|Study Start Date :||August 2006|
|Actual Primary Completion Date :||December 2008|
|Actual Study Completion Date :||December 2008|
Active Comparator: Sitagliptin
People with impaired fasting glucose randomized to treatment with sitagliptin 100 mg once daily.
100 mg once daily
Other Name: Januvia
Placebo Comparator: Placebo
People with impaired fasting glucose randomized to treatment with placebo once daily.
once daily for duration of the study
- Lowering of Fasting Glucose [ Time Frame: 8 weeks ]fasting glucose taken as the mean of blood glucose measured at -30, -20, -10 and 0 minutes prior to each inpatient meal study
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00364377
|United States, Minnesota|
|Rochester, Minnesota, United States, 55905|
|Principal Investigator:||Adrian Vella, M.D.||Mayo Clinic|