NCT01028846|TerminatedPhase 4ResultsFDA Drug
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IRB approval expired 6/13/2023. Primary Completion Date and Study Completion Date updated after definitions were explained to PI/study team. Study never reached intended enrollment and will be categorized as terminated.
Sponsor study identifier
Secondary identifiers
NIH
interventional
10
1 country
1
Study Start
November 2, 2006
Actual (reported)Primary Completion
December 5, 2007
Actual (reported)Study Completion
December 5, 2007
Actual (reported)Type 2 diabetes is a chronic condition that affects the ability of the body to regulate glucose (sugar). When glucose levels are low, the liver can make glucose to increase levels in the body. This important process is called endogenous glucose production (EGP). Previous studies suggest that the central nervous system (CNS), including the brain, helps to coordinate this process by communicating with the liver through potassium channels. Control of EGP can be impaired in people with type 2 diabetes, which may contribute to the high levels of glucose seen in these individuals. The purpose of this study is to understand how activating these potassium channels in the control centers of the brain with a medication called diazoxide might inhibit the amount of glucose made by the liver. This is particularly important for people with diabetes who have very high production of glucose, which in turn causes hyperglycemia (high levels of sugar in the blood) that leads to diabetes complications.
Registry-reported information. Elapsed time and enrollment totals alone do not measure study progress or recruitment pace.
December 5, 2007
Actual (reported)Click on a node to explore related trials.
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Dates and qualifiers reported by the registry. Estimated dates do not confirm that a milestone has occurred.
November 2, 2006
Actual (reported)December 5, 2007
Actual (reported)December 5, 2007
Actual (reported)December 7, 2009
Actual (reported)December 9, 2009
Actual (reported)March 14, 2025
Actual (reported)Rate of Endogenous Glucose Production (EGP)
Rate of EGP (a measure of the body's production of sugar) was measured using analysis of blood samples taken throughout the pancreatic clamp procedure under various treatment conditions (e.g., diazoxide or placebo) by monitoring changes in the level of a non-radioactive, naturally occurring form of glucose (sugar). Rates were summarized by treatment (Diazoxide or Placebo) in mg/kg/min sing basic descriptive statistics.
Final 60 minutes (t=180-240 minutes) of the pancreatic clamp, 6-7 hours after dosing
4 mg/kg body weight total dosage administered orally during pancreatic clamp study
Saline administered orally during pancreatic clamp study
4 mg/kg body weight total dosage administered orally
Oral saline
Registry-reported names are shown in full. Names without a link have not yet been matched to a Syfrah profile.
Albert Einstein College of Medicine
The Bronx, New York, 10461, United States
Kishore P, Boucai L, Zhang K, Li W, Koppaka S, Kehlenbrink S, Schiwek A, Esterson YB, Mehta D, Bursheh S, Su Y, Gutierrez-Juarez R, Muzumdar R, Schwartz GJ, Hawkins M. Activation of K(ATP) channels suppresses glucose production in humans. J Clin Invest. 2011 Dec;121(12):4916-20. doi: 10.1172/JCI58035. Epub 2011 Nov 7.
Meredith Hawkins, M.D., M.S.
Albert Einstein College of Medicine
10 participants (actual enrollment reported by the registry).
First Submitted
December 7, 2009
First Posted
December 9, 2009
Study Start
November 2, 2006
Continuous Glucose Monitoring in Patients With Type 2 Diabetes
Contact the study team to confirm eligibility.
Primary Completion
December 5, 2007
Actual (reported)Study Completion
December 5, 2007
Actual (reported)Last Updated
May 16, 2025
Results First Posted
March 14, 2025
Record last verified: 2025-05
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Source: ClinicalTrials.gov.
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