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Visfatin is a recently described new adipokine that is considered to bind to the insulin receptor and induce insulin action via signal transduction pathways distinct from those of insulin. This study investigated whether circulating plasma visfatin levels may be influenced by PPARγ activation, as shown for adiponectin and other adipokines. Samples from a prospective single-blinded placebo-controlled three-month intervention study with rosiglitazone were retrospectively analysed.
The samples were derived from 39 patients with type 2 diabetes mellitus suffering from coronary artery disease as confirmed by angiography (rosiglitazone arm: 18 men, 1 woman, age (mean ± STD): 65 ± 9 years, disease duration: 4.8 ± 4.0 years, HbA1c: 7.3 ± 1.3%; Placebo: 19 men, 1 woman, age: 64 ± 10 years, disease duration: 5.1 ± 6.5 years, HbA1c: 7.5 ± 1.5%). Laboratory measurements for lipids, adiponectin, and visfatin were performed with validated tests. The baseline values were comparable for all observation markers. After three months, a significant increase in the adiponectin concentrations could be observed only in the rosiglitazone group (from: 6.9 ± 0.9 mg/l to 16.5 ± 1.5 mg/l, (p<0.001) vs placebo: 7.8 ± 6.3 mg/l to 8.0 ± 0.8 mg/l, (n.s.), p<0.001 between the groups at endpoint).
No changes were seen in both treatment arms for the other observation parameters. In particular, no influence of rosiglitazone was seen on the visfatin concentrations (25.9 ± 2.3 ng/ml to 25.8 ± 1.9 ng/ml; Placbo: 26.9 ± 5.4 ng/ml to 27.2 ± 4.9 ng/ml, n.s.). Our investigation demonstrates that rosiglitazone has different effects on circulating concentrations of adiponectin and visfatin. Visfatin secretion is not regulated by PPARγ and further research is required to investigate its role in insulin resistance.
DOI: Clin. Lab. 2008;54:237-241
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