Background, subjects & methods: Dexamethasone increases visfatin synthesis in vitro, but it is not clear, whether it is reflected in the changes of serum levels of this cytokine. We have therefore assessed fasting serum concentrations of visfatin, glucose, insulin and cortisol in 20 subjects (4 males, 5 subjects with type 2 diabetes) age (mean±S.D.) 42.1±17.2 years, BMI 36,7±8.38 kg/m2 before and after 48 hours of administration of dexamethasone during screening for Cushings disease/syndrome. Dexamethasone was administered at the dose of 0.5 mg every 6 hours for 48 hours. Insulin resistance was assessed according to the HOMA method in non-diabetic individuals.
Results: In all subjects we achieved suppression of cortisol concentrations below 50 nmo/l. Dexamethasone administration resulted in an increase in fasting insulin (from 11.5±6.9 to 16.9±7.6 microU/ml, P=0.011), an increase in HOMA (from 2.73±1.74 to 4.02±2.27, P=0.015), however, without a significant change in serum visfatin concentrations (61.1±19.8 versus 68.3±19,4 ng/ml, P=ns). There was a negative association between serum visfatin and fasting insulin before dexamethasone administration (r=−0.49, P=0.046). There was no significant correlation between serum visfatin and age, BMI or HOMA.
Conclusions: Dexamethasone administration (4 mg/48 hours) induces an increase in insulin resistance, however, without a significant change in serum visfatin concentrations. This implies that, in contrast to the in vitro data, short term glucocorticoid administration does not result in appreciable changes in serum levels of this adipocytokine.