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Effects of rosiglitazone and metformin on inflammatory markers and adipokines: decrease in interleukin-18 is an independent factor for the improvement of homeostasis model assessment-beta in type 2 diabetes mellitus
Summary
Objective We examined the individual pharmacological effects of the addition of rosiglitazone and metformin to glimepiride on inflammatory markers and adipokines in patients with type 2 diabetes mellitus. We analysed the relationships between these variables, the measurements of insulin sensitivity and β‐cell function in patients treated with rosiglitazone plus glimepiride.
Design and patients One hundred twenty (120) patients with type 2 diabetes mellitus were randomized and treated with glimepiride plus rosiglitazone or glimepiride plus metformin for 12 weeks. The plasma concentrations of the inflammatory markers and adipokines were measured at baseline and after 12 weeks.
Measurements Markers of insulin sensitivity and β‐cell function were determined by the quantitative insulin sensitivity check index (QUICKI) and the homeostasis model assessment of β‐cell function (HOMA‐β), respectively. Plasma concentrations of adiponectin were measured by radioimmunoassay. Plasma concentrations of resistin, tumour necrosis factor‐α (TNF‐α), interleukin‐6 (IL‐6) and interleukin‐18 (IL‐18) were measured using ELISA.
Results Improvements in fasting insulin level, QUICKI and HOMA‐β were noted in the rosiglitazone‐treated group. Only the QUICKI value improved in the metformin‐treated group. Adiponectin concentrations significantly increased in the rosiglitazone‐treated group after 12 weeks. Significant decreases in resistin, C‐reactive protein, TNF‐α, IL‐6 and IL‐18 were seen in the rosiglitazone‐treated patients but not in the metformin‐treated patients. The independent risk factor for the HOMA‐β change according to stepwise multivariate regression analysis was a change in IL‐18.
Conclusions Rosiglitazone, but not metformin, improved the plasma concentrations of inflammatory markers and adipokines in patients with type 2 diabetes mellitus. A decrease in IL‐18 is an independent factor for the improvement of HOMA‐β in type 2 diabetes mellitus.