AlArab Hanine, Zenno Anna, Pierce Melinda
Department of Pediatrics, University of Washington, 4800 Sand Point Way NE, M/S OC.7.820, PO Box 5371, Seattle, WA, 98145, USA.
Curr Osteoporos Rep. 2025 Jul 25;23(1):33. doi: 10.1007/s11914-025-00925-2.
This paper will discuss the impact of type 2 diabetes (T2D) on skeletal health in youth. We will review the myriad physiology and pathophysiology of diabetic bone fragility with a focus on several new findings in the past five years.
T2D is associated with increased fracture risk despite normal or high bone mineral density. Evidence suggests T2D may adversely affect bone density acquisition during peak bone mass development. The pathophysiology involves low bone turnover, reduced unmineralized bone matrix, and increased collagen glycation, contributing to compromised bone strength. Recent findings from mouse models, Mendelian randomization, and human studies highlight the interplay between metabolic imbalances, genetic influences, cellular dysfunction, and treatment strategies. Bone fragility is a frequently underdiagnosed complication in youth with T2D. Early intervention in youth is crucial to prevent the progression of metabolic and osteopathic disturbances associated with diabetes that can impact long-term skeletal health.
本文将讨论2型糖尿病（T2D）对青少年骨骼健康的影响。我们将回顾糖尿病性骨脆性的众多生理和病理生理机制，并重点关注过去五年中的一些新发现。
尽管骨矿物质密度正常或较高，但T2D仍与骨折风险增加相关。有证据表明，T2D可能会对骨量峰值发育期间的骨密度获取产生不利影响。其病理生理机制包括骨转换率降低、未矿化骨基质减少以及胶原糖基化增加，从而导致骨强度受损。小鼠模型、孟德尔随机化研究和人体研究的最新发现凸显了代谢失衡、遗传影响、细胞功能障碍和治疗策略之间的相互作用。骨脆性是青少年T2D中一种经常被漏诊的并发症。对青少年进行早期干预对于预防与糖尿病相关的代谢和骨病紊乱的进展至关重要，这些紊乱会影响长期骨骼健康。
