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Departments of Clinical Research (M.-P.C., F.-M.C., D.-M.C., J.C.-R.T., Y.-J.L.) and Clinical Laboratory (H.-F.H.), Pingtung Christian Hospital, Pingtung, 90000 Taiwan; and Graduate Institute of Medicine (S.-J.S.), Kaohsiung Medical University, Kaohsiung 80307, Taiwan
Address all correspondence and requests for reprints to: Dr. Yau-Jiunn Lee, Department of Clinical Research, Pingtung Christian Hospital, No. 60 Da-Lien Road, Pingtung 90000, Taiwan. E-mail: t3275{at}ms25.hinet.net.
Context: Visfatin (also known as pre-B cell colony-enhancing factor or PBEF) is a cytokine that is highly expressed in visceral fat and whose blood levels correlate with obesity. Originally isolated as a secreted factor that promotes the growth of B cell precursors and recently found to act as an insulin analog on the insulin receptor, its pathophysiological role in humans remains largely unknown.
Objectives: In this study we investigated whether plasma visfatin level is altered in patients with type 2 diabetes mellitus (T2DM).
Design and Patients: Plasma visfatin as well as adiponectin and resistin concentrations were measured through ELISA in type 2 diabetic and nondiabetic subjects.
Results: A total of 61 patients with T2DM and 59 sex- and age-matched nondiabetic subjects were studied. Plasma visfatin was found to be elevated in patients with T2DM (31.9 ± 31.7 vs. 15.8 ± 16.7 ng/ml, P = 0.002). In contrast, adiponectin was decreased (4.3 ± 2.5 vs. 30.8 ± 10.3 µg/ml, P < 0.001), whereas plasma resistin level did not differ between the groups. Increasing concentrations of visfatin were independently and significantly associated with T2DM. Multiple logistic regression analysis revealed visfatin as an independent association factor for T2DM, even after full adjustment of known biomarkers. The association between adiponectin and T2DM was no longer significant after adjustments for body mass index or waist to hip ratio. In a multiple linear regression analysis, only waist to hip ratio was independently associated with plasma visfatin level.
Conclusion: Our results indicate that visfatin may play a role in the pathogenesis of T2DM.
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