Vol 66, No 2 (2015)
Original paper
Published online: 2015-05-01

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Visfatin concentrations in obese patients in relation to the presence of newly diagnosed glucose metabolism disorders

Anna Kamińska, Ewa Kopczyńska, Maciej Bieliński, Alina Borkowska, Roman Junik
DOI: 10.5603/EP.2015.0016
Pubmed: 25931039
Endokrynol Pol 2015;66(2):108-113.


Introduction: Visfatin, protein secreted by visceral adipose tissue, exerts insulin-mimetic actions. Visfatin concentration increases in patients with longer-standing diabetes type 2 with progressive b-cell dysfunction. Data about the role of visfatin in newly diagnosed glucose metabolism abnormalities are limited. Evaluation of visfatin concentration in patients with obesity, in relation to the presence of newly diagnosed glucose metabolism disorders.
Material and methods: The study included 68 subjects with obesity, without a previous diagnosis of abnormal glucose metabolism. In all subjects we performed an oral glucose tolerance test, and according to the results the group was divided into the subgroups: A (n = 31), with glucose metabolism disorders (impaired fasting glucose, impaired glucose tolerance and type 2 diabetes); and B (n = 37), without abnormalities. In all subjects serum lipids, uric acid, C-peptide, glycated haemoglobin (HbA1c), creatinine, and serum visfatin concentrations were measured. The control group comprised 30 lean, healthy individuals with normal glucose tolerance.
Results: We found elevated visfatin levels in obese individuals versus the control group (50.0 ± 48 vs. 26.7 ± 22.1 ng/mL; p = 0.01). Visfatin concentrations in both subgroups, A and B, did not differ (40.86 ± 27.84 vs. 57.7 ± 59.79 ng/mL; p = 0.19). In subgroup A visfatin concentration correlated significantly with triglycerides (r = 0.37, p = 0.038), HbA1c (r = –0.43, p = 0.02), C-peptide (r = –0.38,p = 0.048), and waist-hip ratio (r = –0.41, p = 0.036).
Conclusions: The presence of newly diagnosed glucose metabolism abnormalities in obese subjects had no influence on the visfatin level, probably due to preserved endogenous insulin secretion and relatively short exposure to hyperglycaemia in patients with prediabetes or at early stage of type 2 diabetes. (Endokrynol Pol 2015; 66 (2): 108–113)