Type II Diabetes Mellitus Clinical Trial
Official title:
Effect of Pioglitazone on Mitochondrial Function in Muscle and Adipose Tissue in Humans
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.
n/a
Observational Model: Cohort, Time Perspective: Prospective
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