INTRODUCTION Osteoprotegerin (OPG) is a secreted member of the TNF receptor superfamily that negatively regulates osteoclastogenesis (Fig. 1). It has recently been demonstrated that OPG is produced by a variety of tissues, including heart, arteries, veins, lung, kidney, immune tissues, and bone; in particular circulating OPG levels have been associated to cardiovascular risks in diabetes mellitus, metabolic syndrome and obesity. AIM OF THE STUDY To investigate the association between OPG blood levels and cardiovascular risk factors in a population of obese fertile women. MATERIAL AND METHODS We enrolled 42 consecutive obese patients (BMI 32.5±3) and 40 healthy women of the same age. Exclusion criteria were: cardiovascular events, hypertension, diabetes mellitus, hyperglycemia (triglycerides > 150 mg/dl), smoke, any type treatment. Cardiovascular risk was evaluated by measuring number of endothelial progenitor cells (EPC), apolipoprotein CIII (ApoCIII), HDL cholesterol and Forearm flow blood ratio (FBFr), assessed by venous occlusion plethysmography. All tests have been conducted between the 1st and the 7th day of the menstrual cycle. RESULTS Circulating levels of OPG were significantly higher in obese women (96 ± 25 ng / L vs. 78 ± 13ng / L, P <0.0005) (Fig. 2). The OPG values correlated positively with BMI and age and negatively with endothelial dysfunction (FBFr) (Fig. 3) and HDL cholesterol. No correlation was found with the circulating levels of ApoCIII and with the number of circulating EPCs. Multivariate analysis of the data showed that the levels of OPG are an independent risk factor for endothelial dysfunction:R square 0.57,p<0.00001 (Table 1). CONCLUSIONS Our study reinforces the evidence of OPG involvement in endothelial dysfunction, although we need further studies in order to define the pathophysiological mechanism of OPG

Osteoprotegerin levels are related to endothelial dysfunction in obese women / Tozzi, R.; Rossi, Fm.; Bertone, C.; Anzuini, A.; Gangitano, E.; Basciani, S.; Mariani, S.; Lenzi, A.; Gnessi, L.; Lubrano, Carla. - (2017). (Intervento presentato al convegno 39° Congresso Nazionale della Società Italiana di Endocrinologia tenutosi a Rome; Italy).

Osteoprotegerin levels are related to endothelial dysfunction in obese women

Tozzi R.
;
Bertone C.;Gangitano E.;Basciani S.;Mariani S.;Lenzi A.;Gnessi L.;Lubrano
2017

Abstract

INTRODUCTION Osteoprotegerin (OPG) is a secreted member of the TNF receptor superfamily that negatively regulates osteoclastogenesis (Fig. 1). It has recently been demonstrated that OPG is produced by a variety of tissues, including heart, arteries, veins, lung, kidney, immune tissues, and bone; in particular circulating OPG levels have been associated to cardiovascular risks in diabetes mellitus, metabolic syndrome and obesity. AIM OF THE STUDY To investigate the association between OPG blood levels and cardiovascular risk factors in a population of obese fertile women. MATERIAL AND METHODS We enrolled 42 consecutive obese patients (BMI 32.5±3) and 40 healthy women of the same age. Exclusion criteria were: cardiovascular events, hypertension, diabetes mellitus, hyperglycemia (triglycerides > 150 mg/dl), smoke, any type treatment. Cardiovascular risk was evaluated by measuring number of endothelial progenitor cells (EPC), apolipoprotein CIII (ApoCIII), HDL cholesterol and Forearm flow blood ratio (FBFr), assessed by venous occlusion plethysmography. All tests have been conducted between the 1st and the 7th day of the menstrual cycle. RESULTS Circulating levels of OPG were significantly higher in obese women (96 ± 25 ng / L vs. 78 ± 13ng / L, P <0.0005) (Fig. 2). The OPG values correlated positively with BMI and age and negatively with endothelial dysfunction (FBFr) (Fig. 3) and HDL cholesterol. No correlation was found with the circulating levels of ApoCIII and with the number of circulating EPCs. Multivariate analysis of the data showed that the levels of OPG are an independent risk factor for endothelial dysfunction:R square 0.57,p<0.00001 (Table 1). CONCLUSIONS Our study reinforces the evidence of OPG involvement in endothelial dysfunction, although we need further studies in order to define the pathophysiological mechanism of OPG
2017
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1560446
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