Plasma concentrations of osteoprotegerin during normo‐ and hyperglycaemic clamping

Knudsen, S. T.; Jeppesen, Peter; Poulsen, P; Andersen, Niels Holmark; Bek, Toke; Schmitz, O.; Ce, Mogensen; Rasmussen, Lars Melholt

doi:10.1080/00365510600987728

Cited by 19 publications

(15 citation statements)

References 16 publications

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“…In a previous study of acute effects of hyperglycemia, we found no effects on plasma OPG in a set-up very similar to the present, also using the same OPG assay (38). Thus, no variations seem to occur in plasma OPG during the time of the day, where these experiments are performed.…”

Section: Discussionsupporting

confidence: 84%

Acute hyperinsulinemia decreases plasma osteoprotegerin with diminished effect in type 2 diabetes and obesity

Jörgensen

Vind²,

Nybo³

et al. 2009

European Journal of Endocrinology

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Objective: Osteoprotegerin (OPG) is a soluble tumour necrosis factor-receptor-like molecule present in connective tissues, especially bone and vasculature. It is known to accumulate in the arterial wall in diabetes. As its synthesis in vascular cells is decreased by insulin, we wanted to elucidate the acute effects of insulin on plasma OPG concentrations in individuals with type 2 diabetes and obese individuals compared with lean controls. Design: The study population consisted of ten type 2 diabetic, ten obese subjects, and ten lean subjects with no family history of diabetes. Methods: All subjects underwent a 4-h euglycemic-hyperinsulinemic clamp. Plasma OPG, insulin, lactate, HbA1c, cholesterol, triglycerides, free fatty acids (FFA), and glucose disposal rate were measured before and at the end of the clamp. Results: Baseline OPG concentrations did not differ significantly between groups. Insulin infusion decreased plasma OPG concentrations in all groups (P!0.01); however, the fall in OPG was 50% less in obese and type 2 diabetic individuals (PZ0.007). Baseline OPG correlated with fasting insulin, baseline lactate, and low density lipoprotein cholesterol in the diabetic group, and with baseline FFA in the lean group. The relative change of OPG in response to insulin correlated inversely with HbA1c and baseline FFA in the lean group. Conclusions: Acute hyperinsulinemia decreases plasma OPG, but with diminished effect in individuals with type 2 diabetes and obesity. Increased levels of OPG in arteries and plasma in diabetes together with the capability of plasma OPG as a cardiovascular risk predictor may be related to the described effects of insulin.European Journal of Endocrinology 161 95-101

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Section: Discussionsupporting

confidence: 84%

Acute hyperinsulinemia decreases plasma osteoprotegerin with diminished effect in type 2 diabetes and obesity

Jörgensen

Vind²,

Nybo³

et al. 2009

European Journal of Endocrinology

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“…Rasmussen et al [42] made a similar observation in patients with type 1 diabetes. Knudsen et al [53] have suggested that the elevated plasma levels of OPG observed in diabetic subjects with poor metabolic control cannot be ascribed to hyperglycaemia per se, a fact confirmed by other authors [36,60]. Oral glucose intake causes decreases in serum OPG levels in postmenopausal women, and this effect is attenuated in women with type 2 diabetes [57].…”

Section: Opg and Diabetesmentioning

confidence: 84%

“…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: 90%

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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“…During a hyperglycemic clamp study Knudsen et al showed that decreasing levels of OPG were negatively correlated with changes in insulin levels but not with changes in glucose concentrations, indicating that hyperinsulinemia may suppress OPG synthesis and/or release (33). Two recent in vitro studies have partly supported this theory, and have shown insulinsuppressed OPG synthesis in adipocytes and vascular smooth muscle cells (34,35).…”

Section: Opg Levels Declined After the Oral Glucose Loadmentioning

confidence: 99%

Inflammatory mediators in morbidly obese subjects: associations with glucose abnormalities and changes after oral glucose

Hofsø

Ueland²,

Hager³

et al. 2009

European Journal of Endocrinology

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Objective: To explore inflammatory mediators in morbidly obese (MO) subjects with various categories of glucose tolerance and to study the changes in these mediators after an oral glucose load. Design: Cross-sectional and experimental study. Methods: A total of 144 MO subjects were classified into three categories: normal glucose tolerance (NGT); pre-diabetes; and new onset diabetes mellitus (NODM) were included, as were 27 normal weight normoglycemic controls. Serum osteoprotegerin (OPG), visfatin, leptin, adiponectin, interleukin-1 receptor antagonist (IL-1Ra), and C-reactive protein (CRP) were analyzed during an oral glucose tolerance test (OGTT). Results: Fasting levels of leptin and IL-1Ra were consistently higher in obese persons (P!0.001 and P!0.05). MO subjects with NGT had higher CRP levels (P!0.001) and lower adiponectin levels (P!0.05) compared to controls. Yet when compared with MO subjects with NODM, those with NGT had lower CRP levels and higher adiponectin levels (both P!0.05). Baseline OPG and visfatin levels did not differ between the groups (PZ0. 326 and PZ0.198). During OGTT, OPG levels decreased (P!0.001) and visfatin levels increased transiently (PZ0.018). The response in OPG and visfatin did not differ between the groups (PZ0.690 and PZ0.170). There were minor changes in adiponectin and leptin levels. Conclusions: Morbid obesity and glucose intolerance were associated with lower adiponectin levels and higher CRP levels, thus supporting a relationship between obesity, glucose homeostasis, and inflammation. Oral glucose suppressed OPG levels and transiently enhanced visfatin levels independent of obesity and glucose tolerance status, indicating that glucose may be involved in the acute regulation of these proteins.

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Plasma concentrations of osteoprotegerin during normo‐ and hyperglycaemic clamping

Cited by 19 publications

References 16 publications

Acute hyperinsulinemia decreases plasma osteoprotegerin with diminished effect in type 2 diabetes and obesity

Acute hyperinsulinemia decreases plasma osteoprotegerin with diminished effect in type 2 diabetes and obesity

Osteoprotegerin and Diabetes-Associated Pathologies

Inflammatory mediators in morbidly obese subjects: associations with glucose abnormalities and changes after oral glucose

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