OBJECTIVE: Statins are extensively used for lowering LDL-cholesterol and reducing cardiovascular events. Recent studies have shown that statins have beneficial anti-inflammatory effects. We aimed to determine whether and how adipokines are regulated during statin treatment in type 2 diabetic patients. METHOD: In this study,we investigated the changes of CRP and inflammation-related adipokines (SAA,IL-6,TNFalpha and adiponectin) in 23 type 2 diabetic patients with atherosclerosis who received statin therapy, and 20 diabetic patients with atherosclerosis and 14 diabetic patients without atherosclerosis who did not receive statin therapy for a period of three months. RESULTS: By the end of the simvastatin treatment (40 mg, daily), LDL-cholesterol was decreased by 16.7% and HDL-cholesterol was increased by 31.9%. SAA, CRP, TNFalpha and IL-6 levels were decreased by 31.8%, 66.2%, 53.9% and 14%, respectively and adiponectin was increased by 59.6%, compared with the baseline levels. Interestingly, the decrease of SAA was positively correlated with that of LDL-cholesterol but negatively with HDL-cholesterol during statin treatment. Among the adipokines, the decrease of SAA was positively correlated with TNFalpha (r = 0.50, p = 0.016). CONCLUSION: The results suggest that adipokines may be differentially regulated and independent of cholesterol changes and that adipokines may be a mediator, and the adipose tissue may be a target of statins' anti-inflammatory effect.
RCT Entities:
OBJECTIVE: Statins are extensively used for lowering LDL-cholesterol and reducing cardiovascular events. Recent studies have shown that statins have beneficial anti-inflammatory effects. We aimed to determine whether and how adipokines are regulated during statin treatment in type 2 diabeticpatients. METHOD: In this study,we investigated the changes of CRP and inflammation-related adipokines (SAA,IL-6,TNFalpha and adiponectin) in 23 type 2 diabeticpatients with atherosclerosis who received statin therapy, and 20 diabeticpatients with atherosclerosis and 14 diabeticpatients without atherosclerosis who did not receive statin therapy for a period of three months. RESULTS: By the end of the simvastatin treatment (40 mg, daily), LDL-cholesterol was decreased by 16.7% and HDL-cholesterol was increased by 31.9%. SAA, CRP, TNFalpha and IL-6 levels were decreased by 31.8%, 66.2%, 53.9% and 14%, respectively and adiponectin was increased by 59.6%, compared with the baseline levels. Interestingly, the decrease of SAA was positively correlated with that of LDL-cholesterol but negatively with HDL-cholesterol during statin treatment. Among the adipokines, the decrease of SAA was positively correlated with TNFalpha (r = 0.50, p = 0.016). CONCLUSION: The results suggest that adipokines may be differentially regulated and independent of cholesterol changes and that adipokines may be a mediator, and the adipose tissue may be a target of statins' anti-inflammatory effect.
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