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Effect of Pioglitazone on Mitochondrial Function in Muscle and Adipose Tissue in Humans

NCT01165190 · Status: COMPLETED · Type: OBSERVATIONAL · Enrollment: 20

Last updated 2024-08-13

No results posted yet for this study

Summary

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.

Conditions

  • Type II Diabetes Mellitus

Interventions

OTHER

pioglitazone

Sponsors & Collaborators

  • Takeda

    collaborator INDUSTRY

  • Arizona State University

    lead OTHER

Eligibility

Min Age
18 Years
Max Age
65 Years
Sex
ALL
Healthy Volunteers
No

Timeline & Regulatory

Start
2008-05-31
Primary Completion
2010-05-31
Completion
2010-05-31

Countries

  • United States

Study Locations

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Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT01165190 on ClinicalTrials.gov