AI Article Synopsis
- The study examined the impact of PPAR-gamma agonists, specifically pioglitazone and rosiglitazone, on endothelial dysfunction and angiogenesis markers in type-2 diabetes patients.
- Pioglitazone was found to significantly improve lipid profiles, lowering total cholesterol and increasing HDL cholesterol compared to rosiglitazone, while both drugs lowered CRP levels and TNF-alpha.
- Pioglitazone also showed increased levels of angiogenesis markers like VEGF compared to rosiglitazone, suggesting potential benefits for complications like diabetic nephropathy and retinopathy, while it outperformed rosiglitazone in reducing inflammatory markers and cholesterol levels.
Article Abstract
The purpose of this study was to assess the effects of PPAR-gamma agonists (pioglitazone and rosiglitazone) on mediators of endothelial dysfunction and markers of angiogenesis in patients with type-2 diabetes. Pioglitazone group showed favorable reductions in serum total cholesterol, triglycerides, LDL cholesterol, VLDL cholesterol and increase in HDL cholesterol as compared to rosiglitazone group, after 16 weeks of treatment and also with control group. There was significant reduction of CRP level in pioglitazone and rosiglitazone group. The level of serum TNF-alpha decreased significantly in pioglitazone and mildly decreased in rosiglitazone group. The level of VEGF, IL-8 and Angiogenin were increased in pioglitazone than rosiglitazone group. There were no significant changes observed in the serum angiogenin and IL-8 levels in the control group. Pioglitazone and rosiglitazone therapy in type-2 diabetes subjects have additional benefits of reducing mediators of endothelial dysfunction. Increase in angiogenesis markers in patients receiving pioglitazone could have variable effects in diabetic nephropathy and retinopathy as there may be increased vascular neogenesis. Pioglitazone has advantage over rosiglitazone in lowering lipid and proinflammatory cytokines.
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| http://dx.doi.org/10.1007/s00592-008-0054-7 | DOI Listing |
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