Peroxisome proliferator activated receptor gamma (PPARγ) and osteoprotegerin levels as indicator and diagnostic determinator of endothelial dysfunction

Objective: Hypertension is a major risk factor for cardiovascular disease and endothelial dysfunction plays an important role in the pathogenesis of hypertension. Endothelial dysfunction is an early step in the development of atherosclerosis and its clinical diagnosis is important for the prevention of atherosclerosis and cardiovascular disease. Peroxisome proliferator activated receptor gamma (PPARγ) and osteoprotegerin are known as potential markers in the development of atherosclerosis. The aim of this study is to investigate the association of PPARγ and osteoprotegerin levels with endothelial function in patients with hypertension, and also to investigate the relationship of PPARγ gene Pro12Ala polymorphism, PPARγ and osteoprotegerin levels with hypertension and peripheral arterial disease. Materials and Methods: The study group were consisted of the patients with hypertension (first group) and the patients with the diagnosis of peripheral arterial disease (second group). The healthy volunteers were included in the study as a control group. Samples for routine biochemical parameters were studied on the same day. For other analyses, the venous blood samples were centrifuged and stored at -80°C until the analysis time of the samples. Serum PPARγ and osteopotegerin levels were determined by ELISA method. PPARγ gene Pro12Ala polymorphism was determined by RT-PCR. Flow-mediated dilatation of the brachial artery (FMD) and intima-media thickness of the carotid artery were measured to evaluate endothelial function in the hypertension group. Results: Serum PPARγ levels were significantly lower in patients with peripheral arterial disease than controls (p<0.05). Serum PPARγ levels were significantly lower (p<0.001) and serum osteopotegerin levels were significantly higher in the hypertensive group (p<0.001) compared with controls. PPARγ levels were significantly higher in patients with impaired FMD (% FMD<7) in the hypertension group (p<0.05). According to the results of PPARγ gene Pro12Ala polymorphism, there was a significant difference in genotype distribution between controls and hypertension group (p<0.05). Conclusions: In patients with impaired FMD responses in the hypertension group, high levels of PPARγ suggest that it can be used as a marker of endothelial dysfunction. According to our findings, we suggest that serum PPARγ levels can be used as an important marker for determining of endothelial dysfunction. However, these findings should be supported by further studies.