Association of serum osteoprotegerin with vascular calcification in patients with type 2 diabetes

Abstract

BackgroundOsteoprotegerin is a member of the tumor necrosis factor-related family and inhibits RANK stimulation of osteoclast formation as a soluble decoy receptor. The goal of this study was to determine the relationship of serum osteoprotegerin with vascular calcification in patients with type 2 diabetes.MethodsThe subjects were 124 patients with type 2 diabetes mellitus, including 88 males and 36 females with a mean (± SD) age of 65.6 ± 8.2 years old. Serum levels of osteoprotegerin, osteocalcin, fibroblast growth factor 23 (FGF23), 25-hydroxyvitamin D3 and adiponectin were measured by ELISA. Vascular calcification in the cervical artery was examined by ultrasound sonography. The subjects were divided into 4 quartiles depending on serum osteoprotegerin levels.ResultsVascular calcification was significantly higher in the 4th quartile and significantly lower in the 1st quartile of serum osteoprotegerin levels, compared to other quartiles. There were no differences in serum osteoprotegerin and vascular calcification among patients with different stages of diabetic nephropathy, but serum FGF23 levels were elevated in those with stage 4 diabetic nephropathy. Simple regression analysis showed that serum osteoprotegerin levels had significant positive correlations with age, systolic blood pressure and serum adiponectin levels, and significant negative correlations with BMI and serum 25-hydroxyvitamin D3.ConclusionsThese findings suggest that elevated serum osteoprotegerin may be involved in vascular calcification independently of progression of diabetic nephropathy in patients with type 2 diabetes.

Osteoprotegerin is a Better Serum Biomarker of Coronary Artery Calcification than Osteocalcin in Type 2 Diabetes

“…Our results support the results of an earlier study (8) in which increased serum OPG levels were associated with elevated CAC scores in asymptomatic individuals with type 2 diabetes. Our results are in agreement with several other studies that have shown an increase in serum OPG in association with vascular injury assessed by various methods in patients with and without type 2 diabetes (7, 26–28). The mechanisms for the increased serum OPG levels are, however, not clear.…”

Associations of fetuin-A and osteoprotegerin with arterial stiffness and early atherosclerosis in chronic hemodialysis patients

“…OPG is produced by osteoblasts as well as by endothelial cells and VSMCs [9]. Its anti-osteoclastic properties argue for a potential role in bone-vascular crosstalk affecting vascular calcification [16] although the exact underlying mechanisms remain largely unknown.…”

“…OPG concentrations in serum from CKD patients were found to be independently associated with the serum potential to induce calcification of smooth muscle cells in vitro [39]. Moreover, serum OPG levels have been independently associated with cervical artery calcification in non-dialysis CKD patients [9] and with moderate coronary artery calcification in patients with type 2 diabetes, with and without diabetic nephropathy [40]. Studies in HD patients demonstrated higher serum OPG levels compared with control subjects [17] and a positive association of OPG with arterial medial calcification assessed by plain film radiography of the pelvis [18], with coronary artery calcification score assessed by CT scan both at baseline and after 1 year [41], as well as with mortality [11].…”

“…Osteoprotegerin (OPG) is a soluble member of the tumor necrosis factor (TNF) receptor superfamily, produced by osteoblasts and vascular endothelial and smooth muscle cells [9]. It has an anti-osteoclastic effect being a soluble decoy receptor for the osteoclast activator RANKL (receptor activator of nuclear factor-κB ligand).…”

Cardiovascular Calcification in Chronic Hemodialysis Patients: Contributors Interplay

“…Osteoprotegerin (OPG) is a soluble member of the tumor necrosis factor (TNF) receptor superfamily, produced by osteoblasts and vascular endothelial and smooth muscle cells [27]. It has an anti-osteoclastic effect being a soluble decoy receptor for the osteoclast activator RANKL (receptor activator of nuclear factor-κB ligand).…”