ECE2009 Poster Presentations Diabetes and Cardiovascular (103 abstracts)
Hacettepe University Faculty of Medicine, Ankara, Turkey.
While well defined for their roles in new bone formation, osteoprotegerin and RANK-ligand (RANKL) are also being questioned for their possible association with the atherosclerotic process since the similarity between the pathogenic process of atherosclerotic plaque calcification and new bone formation is recently under observation. In our study we aimed to find whether there is an association between OPG and RANKL levels and carotid intima media thickness (taken as a measure of atheroslerosis) in diabetic and prediabetic subjects.
We evaluated 78 subjects (17 male). Twenty of them were type 2 diabetic, 16 had impaired glucose tolerance (IGT), 19 had impaired fasting glucose (IFG) and 23 were healthy controls. None of the subjects had a known cardiovascular or cerebrovascular disease neither suffered micro- macrovascular complications of diabetes. Anthropometric measurements are taken in all subjects, serum OPG and RANKL levels are measured as well as serum lipids and lipoprotein a, C reactive protein, homocysteine and insulin. Carotid intima media thickness is measured by ultrasonography.
Overall, RANKL and OPG levels did not differ between groups. There was a positive correlation between OPG and mean carotid intima media thickness in IFG group only (P<0.05; r=0.47). OPG is positively correlated with insulin levels in type 2 diabetic patients (P<0.05; r=0.51). RANKL levels were positively correlated with triglyceride levels in healthy controls (P<0.05; r=0.42) In multivariate analysis, we failed to find an independent parameter related to carotid intima media thickness in each group.
OPG level is positively correlated with mean carotid intima media thickness in subjects with IFG. This effect disappears when confounding factors are taken into account. We believe that the relationship between OPG and RANKL levels and atherosclerosis needs to be studied in larger populations with or without conventional risk factors for atherosclerosis.