Effect of Bezafibrate on Monocyte Cytokine Release and Systemic Inflammation in Patients With Impaired Fasting Glucose

This study assessed the effect of bezafibrate on monocyte secretory function and systemic inflammation in patients with impaired fasting glucose (IFG), comparing this effect with that produced by bezafibrate in mixed dyslipidemic subjects. The study included 28 patients with IFG, 29 individuals with mixed dyslipidemia, and 24 age-, sex- and weight-matched control subjects without lipid and glucose metabolism abnormalities. Compared with the control group, in both IFG and mixed dyslipidemic subjects, monocyte release of monocyte chemoattractant protein-1 (MCP-1), interleukin-6, tumor necrosis factor-α (TNF-α), and interleukin-1β was increased, which was accompanied by higher plasma levels of high-sensitivity C-reactive protein (hsCRP). Despite affecting plasma lipids in both treatment groups, bezafibrate administration (200 mg twice daily for 90 days) reduced fasting plasma glucose levels, the homeostasis model assessment index, and glycated hemoglobin only in IFG subjects. Bezafibrate treatment normalized monocyte release of MCP-1, interleukin-6, TNF-α, and interleukin-1β and also normalized plasma hsCRP levels in mixed dyslipidemic subjects, whereas in IFG individuals the drug reduced only MCP-1 and interleukin-6 release. This study shows that IFG is associated with the presence of systemic inflammation and abnormal monocyte secretory function. Compared with patients with mixed dyslipidemia, IFG patients who are administered bezafibrate experience a stronger effect on glucose metabolism and weaker anti-inflammatory and monocyte-suppressing actions.