Alaleeli Mouza M, Kaimala Suneesh, Adeghate Ernest, Mohsin Sahar
Department of Anatomy, College of Medicine and Health Sciences, United Arab Emirates University, Al-Ain P.O. Box 15551, United Arab Emirates.
Int J Mol Sci. 2025 Aug 22;26(17):8159. doi: 10.3390/ijms26178159.
Type 2 diabetes mellitus (T2DM) is known to increase the risk of fragility fractures; however, the underlying mechanism is still elusive. Reduced miR-155 and elevated are known to drive bone resorption, but their role in T2DM remains unclear. This study investigates bone remodeling imbalances in T2DM through miR-155 and expression profiling. Three-month-old female Wistar rats were fed a high-calorie diet for 3 weeks, followed by intraperitoneal injections of two lower doses of streptozotocin at weekly intervals to induce T2DM. Bone analysis from diabetic rats tested using qRT-PCR showed significantly reduced miR-155 levels and elevated Histological analysis showed a 12.65% increase in Tb.Sp, 10.07% decrease in Tb.Th, and significant increase ( < 0.05) in apoptotic osteocytes. The bone turnover marker CTx-1 level was increased by 20.84%, and RANKL levels were significantly increased in T2DM. IL-1β and TNF-α were increased in T2DM. Bone resorption is more likely to occur in T2DM as both IL-1β and TNF-α work synergistically to promote osteoclastogenesis. MiR-155 could be an important modulator of bone remodeling in T2DM and a potential therapeutic target for diabetic osteopathy.
2型糖尿病（T2DM）已知会增加脆性骨折的风险；然而，其潜在机制仍不清楚。已知miR-155减少和[此处原文缺失相关内容]升高会驱动骨吸收，但其在T2DM中的作用仍不明确。本研究通过miR-155和[此处原文缺失相关内容]表达谱研究T2DM中的骨重塑失衡。对3个月大的雌性Wistar大鼠喂食高热量饮食3周，随后每周腹腔注射两剂较低剂量的链脲佐菌素以诱导T2DM。使用qRT-PCR对糖尿病大鼠进行的骨分析显示miR-155水平显著降低，[此处原文缺失相关内容]升高。组织学分析显示骨小梁间距（Tb.Sp）增加12.65%，骨小梁厚度（Tb.Th）降低10.07%，凋亡骨细胞显著增加（P<0.05）。骨转换标志物I型胶原交联C末端肽（CTx-1）水平增加20.84%，T2DM中核因子κB受体活化因子配体（RANKL）水平显著升高。T2DM中白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）增加。由于IL-1β和TNF-α协同作用促进破骨细胞生成，T2DM中更易发生骨吸收。MiR-155可能是T2DM中骨重塑的重要调节因子及糖尿病性骨病的潜在治疗靶点。
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