High serum pentosidine but not esRAGE is associated with prevalent fractures in type 1 diabetes independent of bone mineral density and glycaemic control

Neumann, Thomas; Lodes, S.; Kästner, B.; Franke, Sybille; Kiehntopf, Michael; Lehmann, Thomas; Müller, Ulrich A.; Wolf, Günter; Sämann, A.

doi:10.1007/s00198-014-2631-7

Cited by 99 publications

(63 citation statements)

References 33 publications

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“…We were only able to measure CML, a non-cross-linking type of AGEs, which may not be as strongly involved in the deterioration of cartilage integrity as is pentosidine. A similar discrepancy has been shown for CML in diabetes-induced osteoporosis [21]. Based on our results, we can only speculate about the underlying mediators of the therapeutic effect of fasting in patients with OA.…”

Section: Discussioncontrasting

confidence: 42%

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AGE-RAGE Interaction Does Not Explain the Clinical Improvements after Therapeutic Fasting in Osteoarthritis

et al. 2017

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Background: Therapeutic fasting improves joint pain in patients with osteoarthritis (OA), but the underlying mechanisms are unknown. Interactions of advanced glycation end products (AGEs) and their receptors (RAGE) play a role in OA pathogenesis. This study aimed to investigate whether the benefits of fasting in OA can be explained by changes in AGEs or RAGE. Patients and Methods: 37 patients with OA underwent fasting for 8 days. Serum levels of an AGE (N-ε-(carboxymethyl)-lysine; CML) and the soluble RAGE (sRAGE) as well as clinical outcome parameters such pain characteristics (measured by visual analogue scale; VAS), joint function (determined by the Western Ontario and McMaster Universities Arthritis Index; WOMAC), and quality of life (via the 36-Item Short-Form Health Survey (SF-36) questionnaire) were assessed. The variables were measured at baseline, the end of fasting, and at follow-up at 4 weeks. Results: The CML levels did not significantly change from baseline to the end of intervention (Δ = -25.6 ± 92.2 ng/ml; p = 0.10). In contrast, the sRAGE levels (Δ = -182.7 ± 171.4 ng/ml; p < 0.0001) and the sRAGE/CML ratio (Δ = -0.4 ± 0.6; p < 0.001) significantly decreased, but they returned to baseline levels 4 weeks after the end of fasting. The scores for pain, WOMAC, and the physical subscale of the SF-36 significantly improved during fasting. There was no correlation between the clinical outcomes and changes in serum levels of CML, sRAGE, or the sRAGE/CML ratio. Conclusions: Fasting resulted in a significant but non-sustained reduction of sRAGE levels and the sRAGE/CML ratio in OA, while the CML levels did not change. Improvement in clinical endpoints of OA does not correlate with changes in CML or sRAGE.

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Section: Discussioncontrasting

confidence: 42%

“…Increased AGE formation has been described in different diseases, e.g. Alzheimer's disease, cataract, diabetes mellitus, renal insufficiency, rheumatoid arthritis, and osteoporosis [14,15,16,17,18,19,20,21]. AGEs bind and interact with specific receptors (RAGE).…”

Section: Introductionmentioning

confidence: 99%

AGE-RAGE Interaction Does Not Explain the Clinical Improvements after Therapeutic Fasting in Osteoarthritis

et al. 2017

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“…Various AGES and their receptors (RAGES) have been implicated in the development of complications of diabetes, including diabetic bone disease. In a crosssectional study, T1DM people with fracture were having higher serum levels of pentosidine, an AGE product, compared to non-fracture ones, although values largely overlapped with those of non-fractured diabetics (102).…”

Section: Hyperglycaemia and Agesmentioning

confidence: 93%

“…Sclerostin is an osteocyte-derived inhibitor of Wnt signalling pathway, essential for osteoblast differentiation and bone formation (108). In humans, sclerostin levels have been shown to be higher in patients with T1DM compared to controls in a cross-sectional study (102). Catalano et al (109) showed that sclerostin levels are higher in females with T1DM compared to males and that the duration of the disease was associated with higher levels of sclerostin.…”

Section: Osteocyte Functionmentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: Mechanisms and evaluation of bone fragility in type 1 diabetes mellitus

Hough

Pierroz²,

Cooper

et al. 2016

European Journal of Endocrinology

125

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Subjects with type 1 diabetes mellitus (T1DM) have decreased bone mineral density and an up to sixfold increase in fracture risk. Yet bone fragility is not commonly regarded as another unique complication of diabetes. Both animals with experimentally induced insulin deficiency syndromes and patients with T1DM have impaired osteoblastic bone formation, with or without increased bone resorption. Insulin/IGF1 deficiency appears to be a major pathogenetic mechanism involved, along with glucose toxicity, marrow adiposity, inflammation, adipokine and other metabolic alterations that may all play a role on altering bone turnover. In turn, increasing physical activity in children with diabetes as well as good glycaemic control appears to provide some improvement of bone parameters, although robust clinical studies are still lacking. In this context, the role of osteoporosis drugs remains unknown.

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“…Major mechanisms potentially contributing to the increased fracture risk in T1D are the insulin deficiency and the increased accumulation of nonenzymatic cross-links (AGEs) in bone matrix, with consequent impairment of bone strength [3]. Indeed, serum levels of AGEs are associated with prevalent fractures in T1D, independently from BMD values [4].…”

Section: Introductionmentioning

confidence: 99%

Trabecular bone score in type 1 diabetes—a cross-sectional study

et al. 2015

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High serum pentosidine but not esRAGE is associated with prevalent fractures in type 1 diabetes independent of bone mineral density and glycaemic control

Abstract: The pentosidine levels but not BMD are independently associated with prevalent fractures. Impaired bone quality in T1D may result from increased AGE formation.

Cited by 99 publications

References 33 publications

AGE-RAGE Interaction Does Not Explain the Clinical Improvements after Therapeutic Fasting in Osteoarthritis

AGE-RAGE Interaction Does Not Explain the Clinical Improvements after Therapeutic Fasting in Osteoarthritis

MECHANISMS IN ENDOCRINOLOGY: Mechanisms and evaluation of bone fragility in type 1 diabetes mellitus

Trabecular bone score in type 1 diabetes—a cross-sectional study

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