Effect of Pioglitazone on Mitochondrial Function in Muscle and Adipose Tissue in Humans (PIO)
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.|
|ClinicalTrials.gov Identifier: NCT01165190|
Recruitment Status : Unknown
Verified July 2010 by Arizona State University.
Recruitment status was: Recruiting
First Posted : July 19, 2010
Last Update Posted : July 19, 2010
Mitochondrial dysfunction in skeletal muscle results in decreased muscle fatty acid oxidation, leading to conversion of fatty acids into triglycerides and its accumulation inside the muscle tissue. Moreover, in adipose tissue mitochondrial dysfunction results in decreased fatty acid oxidation and triglyceride synthesis, leading to increased circulating fatty acid concentrations, which in turn also leads to lipid accumulation inside muscle tissue. Lipid accumulation inside muscle tissue interferes with the insulin signaling pathway and causes insulin resistance. Mitochondrial dysfunction in both tissues has therefore been proposed to play an important role in insulin resistance in humans.
Pioglitazone, a thiazolidinedione, is an FDA approved medication for the treatment of type 2 diabetes. It improves muscle insulin sensitivity at least in part by lowering intramuscular lipid concentrations but the mechanism by which this occurs is unclear. In the present study, we shall therefore test the hypothesis that pioglitazone improves mitochondrial function in muscle and adipose tissue in humans who are insulin resistant.
|Condition or disease|
|Type II Diabetes Mellitus|
|Study Type :||Observational|
|Estimated Enrollment :||20 participants|
|Official Title:||Effect of Pioglitazone on Mitochondrial Function in Muscle and Adipose Tissue in Humans|
|Study Start Date :||May 2008|
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): NCT01165190
|Contact: Christian Meyer, MD||(480) 965-2473||Christian.Meyer@asu.edu|
|United States, Arizona|
|Clinical Research Unit||Recruiting|
|550 East Orange Street, Arizona, United States, 85287|
|Contact: Christian Meyer, MD (480) 965-2473 Christian.Meyer@asu.edu|