Effect of Pioglitazone on Mitochondrial Function in Muscle and Adipose Tissue in Humans (PIO)
Recruitment status was: Recruiting
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.
Type II Diabetes Mellitus
|Study Design:||Observational Model: Cohort
Time Perspective: Prospective
|Official Title:||Effect of Pioglitazone on Mitochondrial Function in Muscle and Adipose Tissue in Humans|
|Study Start Date:||May 2008|
Please refer to this study by its ClinicalTrials.gov identifier: NCT01165190
|United States, Arizona|
|Clinical Research Unit|
|550 East Orange Street, Arizona, United States, 85287|