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Submitted on June 23, 2005
Accepted on December 21, 2005
The Lundberg Laboratory for Diabetes Research, Department of Internal Medicine, The Sahlgrenska Academy at Göteborg University, Göteborg, Sweden; Department of Medicine, University of Kuopio, Finland
* To whom correspondence should be addressed. E-mail: ann.hammarstedt{at}medic.gu.se.
Context: Visfatin was recently reported to be expressed in human adipose tissue and to exert insulin-mimicking effects.
Objective: To examine if visfatin is a true adipokine and expressed in isolated fat cells. We also examined if visfatin is regulated by thiazolidinediones and, thus, can contribute to the ability of these agents to improve insulin sensitivity.
Design: Open labeled drug therapy trial.
Setting: University Hospital.
Patients: Seven newly diagnosed and previously untreated Type 2 diabetic patients and 6 healthy individuals with reduced insulin sensitivity participated in the study.
Intervention: Pioglitazone therapy, 30-45 mg per day for 3-4 weeks.
Main outcome measures: Serum and adipose tissue mRNA levels of visfatin and adiponectin.
Results: Visfatin mRNA is expressed in both adipose tissue and isolated adipocytes. Treatment with thiazolidinediones for 3-4 weeks did not alter the gene expression or circulating levels of visfatin in either the non-diabetic or the diabetic individuals, while adiponectin increased significantly.
Conclusion: The present study shows that visfatin is a true adipokine but it is not regulated by TZD and, thus, is unlikely to contribute to the insulin-sensitizing actions of these drugs.
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