Plasma Osteoprotegerin Concentrations in Type 2 Diabetic Patients and its Association with Neuropathy

Terekeci, Hakan; Şenol, Mehmet Güney; Top, Cihan; Sahan, Betul; Çeli̇k, Sefa; Sayán, Oscar Alejandro Castillo; Küçükardalı, Yaşar; Ipcioglu, OM; Çağıltay, Eylem; Öktenli, Çağatay; Özata, Metịn

doi:10.1055/s-0028-1085425

Cited by 32 publications

(31 citation statements)

References 17 publications

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“…In the following years, several authors confirmed the association between serum OPG and both types of diabetes [24,35,36,41,42,[49][50][51][52][53][54][55][56][57][58][59]. Galluzzi et al [41] showed that plasma OPG levels are significantly higher in prepubertal children with type 1 diabetes mellitus than in controls, and evidenced a correlation between OPG serum concentrations and glycated haemoglobin (HbA1c).…”

Section: Opg and Diabetesmentioning

confidence: 82%

“…In concordance with these data, it has been shown that OPG was also significantly elevated both in a subgroup of recently diagnosed diabetic patients (within 2 years) [36] and in newly diagnosed type 1 patients [51,52] in which OPG levels decreased markedly after 6 month of insulin treatment and, in which a relation of OPG with HbA1c was, once more, evidenced. In another recent research, Terekeci et al [35] confirmed in type 2 diabetic patients that plasma OPG levels correlated significantly with diabetes duration and HbA1c levels. Rasmussen et al [42] made a similar observation in patients with type 1 diabetes.…”

Section: Opg and Diabetesmentioning

confidence: 87%

“…In vitro studies have, moreover, shown that OPG is expressed in vascular smooth muscle cells [27,34] and that it can act as a survival factor for endothelial cells [28]. It has been observed in vitro that human vascular smooth muscle cells produce by far more OPG than human umbilical vascular endothelial cells, and that the production of OPG by vascular smooth muscle cells is regulated not only by TNFbut also by insulin [24,35]. Nevertheless, TNF-also stimulates OPG production in endothelial cells [36], which may indicate that OPG is secreted by several type of cells.…”

Section: Biological Functions Of Opgmentioning

confidence: 97%

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Osteoprotegerin and Diabetes-Associated Pathologies

Blázquez‐Medela

Jm²,

Martı́nez-Salgado³

2011

CMM

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Osteoprotegerin (OPG) is a member of the tumour necrosis factor receptor superfamily of cytokines which, in spite of being initially described as a strong anti-resorptive factor, has lately been considered as a possible link between bone and vascular disease. In the last few years, several studies have evidenced its close relationship with the development of diabetes. In this review, we analyse the role of OPG in diabetic patients and its links with the most relevant associated diseases such as atherosclerosis, hypertension, endothelial dysfunction and diabetic nephropathy, as well as its connection with related pathologies as fibrosis, obesity and metabolic syndrome.

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Section: Opg and Diabetesmentioning

confidence: 82%

Section: Opg and Diabetesmentioning

confidence: 87%

Section: Biological Functions Of Opgmentioning

confidence: 97%

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Osteoprotegerin and Diabetes-Associated Pathologies

Blázquez‐Medela

Jm²,

Martı́nez-Salgado³

2011

CMM

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“…2b). OPG expression and production are regulated by inflammatory cytokines, and elevated plasma OPG levels have been recorded in T1DM and T2DM patients [39,[87][88][89][90]. Lower RANKL to OPG ratios have also been found in T1DM [91].…”

Section: Inflammatory Signals Prolong Osteoclast Lifementioning

confidence: 96%

Inflammation as death or life signal in diabetic fracture healing

Röszer

2010

Inflamm. Res.

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Increased apoptosis of chondrocytes and osteoblasts and prolonged survival of osteoclasts lead to early destruction of callus tissue and impair bone remodeling in fracture healing of diabetic patients. Diabetes is accompanied by an increased inflammatory state, reactive oxgen species (ROS) generation and accumulation of advanced glycation end products (AGEs), a heterogenous group of toxic metabolites that can induce inflammation. Prolonged hyperglycemia and insulin resistance correlate with increased apoptosis rate and, accordingly, the proapoptotic role of several inflammatory mediators, ROS and AGEs has been also documented. In this review we summarize the most recent reports supporting the idea that inflammatory signaling increases chondrocyte and osteoblast death and prolongs osteoclast survival, resulting in impaired bone regeneration in diabetes. Antagonising inflammatory signal pathways and solution of inflammation may deserve greater attention in the management of diabetic fracture healing.

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“…24 Furthermore, OPG is associated with atherosclerosis and diabetic complications, such as neuropathy, nephropathy, or retinopathy. 17,21, 25 However, studies have yet to determine whether OPG is causally related to atherosclerotic disease progression or is implicated as a modulatory response to subclinical CVD. In endothelial cells, OPG acts as a survival and antiapoptotic factor.…”

Section: Discussionmentioning

confidence: 99%

Effects of Salt Loading on Plasma Osteoprotegerin Levels and Protective Role of Potassium Supplement in Normotensive Subjects

Liu

Zhang

et al. 2017

Circ J

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Osteoprotegerin (OPG), a soluble member of the tumor necrosis factor (TNF) receptor superfamily, acts as a decoy receptor of the receptor activator of nuclear factor κ-B ligand (RANKL) and the TNF-related apoptosis-inducing ligand (TRAIL); RANKL and TRAIL are 2 cytokines of the TNF family mainly involved in bone metabolism; they are also found in other tissues, such as vascular smooth muscle cells. 13 OPG has been implicated in various inflammatory reactions and endothelial dysfunctions, which are also associated with diabetes mellitus and atherosclerosis. 14-16 Increased plasma OPG concentrations are also related to coronary artery disease frequently accompanied by atherosclerosis, stroke, diabetes mellitus, vascular death, and overall cardiovascular morbidity and mortality. [17][18][19][20] Data are still scarce in the literature with regard to the link between salt intake and OPG. Our study was designed to examine the effects of salt intake and potassium supple-E xcess dietary salt induces adverse cardiovascular and renal effects, as demonstrated in numerous epidemiological, interventional, and experimental studies. 1-3 Hypertension prevention studies have provided supporting evidence that modest reductions in salt intake promote 25% long-term reduction in the risk of cardiovascular events; thus, salt intake is implicated in cardiovascular function. 4 Several mechanisms, including endothelial dysfunction, oxidative stress, inflammation, insulin resistance, and neurogenically mediated increase in peripheral resistance, contribute to the harmful effects of dietary salt. 5-9 Potassium likely elicits favorable effects on cardiovascular morbidity and mortality. 10-12 Dietary potassium supplementation may prevent the salt loading-induced elevation of blood pressure (BP) by inhibiting the sympathetic nerve excitability, salt-induced insulin resistance, and oxygen-reactive free radical generation. Background: Excess dietary salt is strongly correlated with cardiovascular disease, morbidity, and mortality. Conversely, potassium likely elicits favorable effects on cardiovascular disorders. In epidemiological studies, increased plasma osteoprotegerin (OPG) concentrations are associated with atherosclerosis and vascular deaths. Our study was designed to examine the effects of salt intake and potassium supplementation on plasma OPG levels in normotensive subjects.

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Plasma Osteoprotegerin Concentrations in Type 2 Diabetic Patients and its Association with Neuropathy

Cited by 32 publications

References 17 publications

Osteoprotegerin and Diabetes-Associated Pathologies

Osteoprotegerin and Diabetes-Associated Pathologies

Inflammation as death or life signal in diabetic fracture healing

Effects of Salt Loading on Plasma Osteoprotegerin Levels and Protective Role of Potassium Supplement in Normotensive Subjects

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