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1型糖尿病对成骨细胞、骨细胞和破骨细胞的影响。

Effects of Type 1 Diabetes on Osteoblasts, Osteocytes, and Osteoclasts.

作者信息

Kalaitzoglou Evangelia, Popescu Iuliana, Bunn R Clay, Fowlkes John L, Thrailkill Kathryn M

机构信息

UK Barnstable Brown Diabetes Center, University of Kentucky College of Medicine, 830 S. Limestone St., Lexington, KY, 40536, USA.

Department of Pediatrics, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.

出版信息

Curr Osteoporos Rep. 2016 Dec;14(6):310-319. doi: 10.1007/s11914-016-0329-9.


DOI:10.1007/s11914-016-0329-9
PMID:27704393
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5106298/
Abstract

PURPOSE OF REVIEW: To describe the effects of type 1 diabetes on bone cells. RECENT FINDINGS: Type 1 diabetes (T1D) is associated with low bone mineral density, increased risk of fractures, and poor fracture healing. Its effects on the skeleton were primarily attributed to impaired bone formation, but recent data suggests that bone remodeling and resorption are also compromised. The hyperglycemic and inflammatory environment associated with T1D impacts osteoblasts, osteocytes, and osteoclasts. The mechanisms involved are complex; insulinopenia, pro-inflammatory cytokine production, and alterations in gene expression are a few of the contributing factors leading to poor osteoblast activity and survival and, therefore, poor bone formation. In addition, the observed sclerostin level increase accompanied by decreased osteocyte number and enhanced osteoclast activity in T1D results in uncoupling of bone remodeling. T1D negatively impacts osteoblasts and osteocytes, whereas its effects on osteoclasts are not well characterized, although the limited studies available indicate increased osteoclast activity, favoring bone resorption.

摘要

综述目的:描述1型糖尿病对骨细胞的影响。 最新研究结果:1型糖尿病(T1D)与低骨矿物质密度、骨折风险增加及骨折愈合不良相关。其对骨骼的影响主要归因于骨形成受损,但最近的数据表明骨重塑和骨吸收也受到损害。与T1D相关的高血糖和炎症环境会影响成骨细胞、骨细胞和破骨细胞。涉及的机制很复杂;胰岛素缺乏、促炎细胞因子产生以及基因表达改变是导致成骨细胞活性和存活率低下进而导致骨形成不良的一些因素。此外,在T1D中观察到的硬化蛋白水平升高,伴随着骨细胞数量减少和破骨细胞活性增强,导致骨重塑解偶联。T1D对成骨细胞和骨细胞产生负面影响,而其对破骨细胞的影响尚未得到充分表征,尽管现有有限的研究表明破骨细胞活性增加,有利于骨吸收。

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本文引用的文献

[1]
P2X7R-Panx1 Complex Impairs Bone Mechanosignaling under High Glucose Levels Associated with Type-1 Diabetes.

PLoS One. 2016-5-9

[2]
Marrow Adipose Tissue: Trimming the Fat.

Trends Endocrinol Metab. 2016-6

[3]
Low bone turnover and reduced angiogenesis in streptozotocin-induced osteoporotic mice.

Connect Tissue Res. 2016-7

[4]
Bone Structure and Predictors of Fracture in Type 1 and Type 2 Diabetes.

J Clin Endocrinol Metab. 2016-3

[5]
Higher levels of s-RANKL and osteoprotegerin in children and adolescents with type 1 diabetes mellitus may indicate increased osteoclast signaling and predisposition to lower bone mass: a multivariate cross-sectional analysis.

Osteoporos Int. 2016-4

[6]
FGF-23/Vitamin D Axis in Type 1 Diabetes: The Potential Role of Mineral Metabolism in Arterial Stiffness.

PLoS One. 2015-10-13

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IGF-1 Signaling is Essential for Differentiation of Mesenchymal Stem Cells for Peak Bone Mass.

Bone Res. 2013-6-28

[8]
The dependences of osteocyte network on bone compartment, age, and disease.

Bone Res. 2015

[9]
SGLT2 inhibitor therapy improves blood glucose but does not prevent diabetic bone disease in diabetic DBA/2J male mice.

Bone. 2016-1

[10]
Bone's responses to mechanical loading are impaired in type 1 diabetes.

Bone. 2015-12

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