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Sponsored by: |
Mayo Clinic |
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Information provided by: | Mayo Clinic |
ClinicalTrials.gov Identifier: | NCT00588172 |
Type 2 diabetes its microvascular and macrovascular complications have become a major global health problem. Metformin is often used as first-line therapy for this disorder given that it is cheap, may cause weight loss and does not have significant side-effects in healthy patients. On the other hand, as many as one third of all patients with type 2 diabetes initially treated with metformin never achieve a meaningful response to this intervention. Recently, genetic variation in the organic cation transporter 1 (Oct1) gene which encodes a protein, OCT1, mediating metformin uptake by the liver, its primary site of action, has been shown alter metformin action. In Oct1-deficient mice the glucose-lowering effects of metformin are completely abolished. Moreover a polymorphism with a 20% minor allele frequency in Caucasians also alters the effect of metformin on glucose tolerance (the net result of glucose uptake and glucose release) after ingestion of 75g of glucose. However, it is unknown if this polymorphism affects suppression of endogenous glucose production or stimulation of peripheral glucose uptake by metformin, or both, and to what degree. We propose to utilize established methodology to measure glucose turnover in response to a mixed meal to determine how common genetic variation in OCT1 alters response to metformin in healthy volunteers. This will clarify the effect of these variants on response to metformin in humans. The knowledge gained from this study will help to design future studies examining the role of OCT1 genotype in determining initial therapy for type 2 diabetes.
Condition | Intervention | Phase |
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Type 2 Diabetes |
Drug: Metformin |
Phase IV |
Study Type: | Interventional |
Study Design: | Basic Science, Non-Randomized, Open Label, Parallel Assignment, Efficacy Study |
Official Title: | Genetic Variation in OCT1 and Response to Metformin |
Estimated Enrollment: | 32 |
Study Start Date: | May 2008 |
Estimated Study Completion Date: | December 2009 |
Estimated Primary Completion Date: | December 2009 (Final data collection date for primary outcome measure) |
Arms | Assigned Interventions |
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1: Sham Comparator
Individuals with no nsSNPs or mutations known to alter oct1 function
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Drug: Metformin
1000mg bid for 1 week
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2: Active Comparator
Individuals with nsSNPs or mutations known to alter oct1 function
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Drug: Metformin
1000mg bid for 1 week
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Ages Eligible for Study: | 18 Years to 70 Years |
Genders Eligible for Study: | Both |
Accepts Healthy Volunteers: | Yes |
Inclusion criteria: -
Exclusion criteria: -
Contact: Paula D Giesler, RN | 507-255-8345 | giesler.paula@mayo.edu |
United States, Minnesota | |
Mayo Clinic | |
Rochester, Minnesota, United States, 55905 |
Principal Investigator: | Adrian Vella, MD | Mayo Clinic |
Responsible Party: | Mayo Clinic ( Adrian Vella MD ) |
Study ID Numbers: | 07-004310, OCT1 and metformin |
Study First Received: | December 22, 2007 |
Last Updated: | December 22, 2007 |
ClinicalTrials.gov Identifier: | NCT00588172 History of Changes |
Health Authority: | United States: Food and Drug Administration |
Metformin Type 2 diabetes Oct1 |
Hypoglycemic Agents Metabolic Diseases Metformin Diabetes Mellitus, Type 2 Diabetes Mellitus |
Endocrine System Diseases Endocrinopathy Glucose Metabolism Disorders Metabolic Disorder |
Hypoglycemic Agents Metabolic Diseases Physiological Effects of Drugs Metformin Diabetes Mellitus, Type 2 |
Diabetes Mellitus Endocrine System Diseases Glucose Metabolism Disorders Pharmacologic Actions |