Plasma concentration of visfatin is a new surrogate marker of systemic inflammation in type 2 diabetic patients

It is not clear whether plasma visfatin level is related with systemic inflammation or diabetic nephropathy in diabetic patients. In this study, we investigated the relationship between plasma visfatin levels and systemic inflammation or diabetic nephropathy in type 2 diabetic patients. In addition, we examined the physiological action of visfatin in cultured adipocytes in diabetic condition. Plasma visfatin concentrations were significantly higher in the diabetic groups than in the controls. Plasma visfatin levels were positively correlated with systolic blood pressure, body weight, fasting blood glucose, plasma levels of MCP-1, urinary albumin excretion (UAE), and carotid intima-media thickness (IMT), and were inversely correlated with plasma adiponectin, and creatinine clearance. However, plasma visfatin concentrations did not show a significant relationship with HbA1C, BMI or HOMA-IR. Regression analysis showed that plasma levels of MCP-1 and UAE were only independent determinants of plasma visfatin concentration. In cultured adipocytes, high glucose and angiotensin II stimuli markedly increased visfatin synthesis. Exogenous visfatin treatment significantly decreased differentiation of adipocytes and increased NF-kappaB transcriptional activity and pro-inflammatory molecules in adipocytes. These findings suggest that visfatin synthesis is activated from adipose tissue in a diabetic environment, induces NF-kappaB activation and leads to activation of pro-inflammatory cytokines and systemic inflammation.