Increased risk of vertebral fracture in patients with diabetes: a meta-analysis of cohort studies

Wang, Jie; You, Wenjun; Jing, Zhaohai; Wang, Robin; Fu, Zhengju; Wang, Yangang

doi:10.1007/s00264-016-3146-y

Cited by 62 publications

(45 citation statements)

References 49 publications

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“…The incidence of osteoporosis is higher in diabetic patients than that in healthy population has been recognized . The causal factors are to be further investigated.…”

Section: Discussionmentioning

confidence: 99%

Micro RNA‐550a interferes with vitamin D metabolism in peripheral B cells of patients with diabetes

Guo

Liu

et al. 2016

Cell Biochemistry & Function

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The pathogenesis of diabetes is to be further investigated. Vitamin D3 (VitD3) can improve diabetes. Micro RNAs (miR) are involved in regulating cell activities. This study tests a hypothesis that miR-550a interferes with the metabolism of VitD3 in peripheral B cells. In this study, blood samples were collected from patients with diabetes and healthy persons. The B cells were isolated from the blood samples to be treated with tumor necrosis factor (TNF)-α. The B cells were then collected and analyzed for the expression of miR-550a and cyp27b1. The results showed that B cells from healthy subjects were capable of converting VitD metabolite calcidiol to calcitriol, which was impaired in B cells collected from diabetic patients. The diabetic patients showed lower bone mineral density than that in healthy subject. The miR-550a was negatively correlated with bone mineral density and the Levels of cyp27b1 in peripheral B cells of patients with diabetes. In vitro study showed that TNF-α increased miR-550a expression and inhibited the expression of cyp27b1 in B cells. miR-550a mediated the effects of TNF-α on inducing chromatin remodeling at the cyp27b1 gene locus. In conclusion, miR-550a mediates the TNF-α-induced suppression of cyp27b1 expression in peripheral B cells of patients with diabetes, which can be blocked by inhibition of miR-550a.

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“…The incidence of osteoporosis is higher in diabetic patients than that in healthy population has been recognized . The causal factors are to be further investigated.…”

Section: Discussionmentioning

confidence: 99%

Micro RNA‐550a interferes with vitamin D metabolism in peripheral B cells of patients with diabetes

Guo

Liu

et al. 2016

Cell Biochemistry & Function

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“…Two logical candidates include diabetes mellitus, and osteoarthritis. Diabetes is recognized to have adverse consequences upon bone and muscle [40,41] and to increase fracture risk above that predicted by FRAX [42]. Similarly, some studies find osteoarthritis to be associated with increased risk for falls and fractures [43,44].…”

Section: оригінальні дослідження / Original Researchesmentioning

confidence: 99%

Синдром Дисмобільності: Зміна Парадигми В Царині Профілактики Переломів

Binkley

Krueger

2021

PJS

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Abstract. Fragility fractures engender major healthcare cost, reduce independence/quality and life and increase mortality risk. Despite availability of multiple therapies to reduce risk for future fracture, few patients are treated even following hip fracture. Clearly, approaches of the past aimed at reducing fragility fracture risk, primarily by diagnosing osteoporosis and initiating bone-active medications, have failed. A di erent approach is required; such a change in focus is proposed here. Brie y, the dysmobility syndrome concept recognizes fragility fracture as the clinical outcome of consequence and appreciates that osteoporosis is only part of the syndrome leading to "osteoporosis-related" fracture. Other components of this syndrome include sarcopenia, obesity, diabetes, osteoarthritis, and potentially multiple other factors that increase risk for falls with attendant increased fracture risk. In summary, the dysmobility syndrome concept moves the eld, and also, importantly, older adults at risk for fragility fracture, beyond a singular focus on bone to more appropriately focus on a holistic approach to fracture risk reduction.

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“…This process is important for bone repair and mineral homeostasis (Raggatt and Partridge 2010). Diabetes can induce osteoporosis and increase the risk of bone fractures (Mai et al 2011;Tsentidis et al 2016;Wang et al 2016). Mesenchymal stem cells (MSCs) possess multiple differentiation abilities and have great therapeutic potentials for bone repair (Doulatov and Daley 2013).…”

Section: Introductionmentioning

confidence: 99%

Metformin Enhances Osteogenesis and Suppresses Adipogenesis of Human Chorionic Villous Mesenchymal Stem Cells

Yang

et al. 2017

Tohoku J. Exp. Med.

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Metformin is the first-line anti-hyperglycemic drugs commonly used to treat type 2 diabetes. Recent studies have shown that metformin can enhance bone formation through induction of endothelial nitric oxide synthase (eNOS). Human chorionic villous mesenchymal stem cells (CV-MSCs) are promising candidates for regenerative medicine. The present study aimed to investigate the effects of metformin on the osteogenic and adipocytic differentiation of human CV-MSCs, and to elucidate the underlying mechanism. CV-MSCs, prepared from human term placentae, were cultured with different concentrations of metformin. Treatment for 72 hours with 0.05 mM metformin had no noticeable effect on the proliferation of CV-MSCs. Consequently, CV-MSCs were cultured for seven or 14 days in the osteogenic medium supplemented with 0.05 mM metformin. Treatment for seven days with metformin increased the expression levels of osteogenic protein mRNAs, including alkaline phosphatase, runt-related transcription factor 2, and osteopontin. Metformin also enhanced the mineralization of CV-MSCs. Furthermore, metformin induced the expression of eNOS in CV-MSCs during osteogenic differentiation. By contrast, when CV-MSCs were cultured for 14 days in the adipogenic medium, 0.05 mM metformin inhibited the expression of adipogenic protein mRNAs, including proliferators-activated receptor-γ and CCAAT/enhancer binding protein-α. The lipid droplet accumulation was also reduced on 28 days after metformin treatment. These findings indicate that metformin can enhance osteogenic differentiation of CV-MSCs and reduce adipocyte formation. The effect of metformin on osteogenic differentiation of CV-MSCs may be associated with eNOS expression. Our findings will highlight the therapeutic potential of metformin in osteoporosis and bone fracture.

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Increased risk of vertebral fracture in patients with diabetes: a meta-analysis of cohort studies

Abstract: Diabetes is an independent risk factor for vertebral fracture, primarily being due to diabetic osteoporosis.

Cited by 62 publications

References 49 publications

Micro RNA‐550a interferes with vitamin D metabolism in peripheral B cells of patients with diabetes

Micro RNA‐550a interferes with vitamin D metabolism in peripheral B cells of patients with diabetes

Синдром Дисмобільності: Зміна Парадигми В Царині Профілактики Переломів

Metformin Enhances Osteogenesis and Suppresses Adipogenesis of Human Chorionic Villous Mesenchymal Stem Cells

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