Glycemic Control and Bone in Diabetes.

Glycemic Control and Bone in Diabetes.
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DOI:
10.1007/s11914-022-00747-6
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发表时间:
2022-12
影响因子:
4.3
通讯作者:
--
中科院分区:
医学2区
文献类型:
--
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本文综述了血糖控制和糖尿病对骨骼健康影响的最新进展。我们讨论了糖尿病和血糖控制受损影响骨生物学的基本细胞机制,以及这些过程如何导致糖尿病患者的骨脆性。葡萄糖对成骨细胞分化和成熟成骨细胞的能量消耗是重要的。胰岛素的作用尚不清楚,但小鼠成骨细胞中胰岛素受体的缺失会减少骨形成。流行病学上,1型(T1D)和2型糖尿病(T2D)与骨折风险增加有关,这在T1D患者中更高。皮质骨微孔的积累、微血管并发症和AGEs可能导致糖尿病相关的骨脆性。青年发病的T2D对达到峰值骨量和随后的骨骼脆性的影响特别值得关注。需要进一步的研究来了解高血糖症在整个生命周期中对骨骼健康的影响,包括炎症和微血管损伤的相关因素。
This review summarizes recent developments on the effects of glycemic control and diabetes on bone health. We discuss the foundational cellular mechanisms through which diabetes and impaired glucose control impact bone biology, and how these processes contribute to bone fragility in diabetes. Glucose is important for osteoblast differentiation and energy consumption of mature osteoblasts. The role of insulin is less clear, but insulin receptor deletion in mouse osteoblasts reduces bone formation. Epidemiologically, type 1 (T1D) and type 2 diabetes (T2D) associate with increased fracture risk, which is greater among people with T1D. Accumulation of cortical bone micro-pores, micro-vascular complications, and AGEs likely contribute to diabetes-related bone fragility. The effects of youth-onset T2D on peak bone mass attainment and subsequent skeletal fragility are of particular concern. Further research is needed to understand the effects of hyperglycemia on skeletal health through the lifecycle, including the related factors of inflammation and microvascular damage.
DOI: 10.1016/j.cell.2010.06.003
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影响因子: 3.5
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