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<p>The effects of vanadyl acetylacetonate (VAC) were evaluated on femur intramedullary osteoclasts in a rat model of type 1 diabetes (T1D) associated bone remodeling. In this study, BB Wistar rats were administered intramedullary injections consisting of either VAC at a dose of 1.5&#xa0;mg/kg or a control saline solution. These injections were administered at least 12&#xa0;weeks after the onset of T1D (i.e., treatment began ≥ 12&#xa0;weeks after diabetes onset) to allow for the establishment of diabetic bone changes. At 4&#xa0;weeks following treatment, the femurs treated with VAC exhibited a significant increase in trabecular thickness, specifically a 19.03% increase (p &lt; 0.05). Osteoclasts, which were identified using TRAP staining, were found to be reduced in number at both 6 and 8&#xa0;weeks in the femurs that received VAC treatment (p &lt; 0.05). Likewise, when VAC was added to culture media, it resulted in a substantial decrease in osteoclast formation in vitro (8.1 ± 16.8 vs. 91.6 ± 16.0 cells, p &lt; 0.001). In addition, expression of Dcstamp was significantly decreased in VAC-treated femurs compared to those treated with saline (p &lt; 0.05). Taken together, this study demonstrates that intramedullary VAC delivery appears to inhibit T1D-related bone loss by impairing the process of osteoclastogenesis.</p>

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Vanadium salt inhibits osteoclast formation and preserves bone integrity in a rat model of type-1 diabetes associated bone loss

  • 期刊论文

  • 发表日期：

    2026年4月3日

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  • Joshua Greendyk,
  • James Thornton,
  • Darian Napoleon,
  • Michael Greenberg,
  • Anthony Lin,
  • Mike Levidy,
  • Jonathan R. Lopez,
  • Maximilian Muñoz,
  • Kevin Innella,
  • Yazan Kadkoy,
  • Maya Deza Culbertson,
  • Jessica A. Cottrell,
  • J. Patrick O’Connor,
  • Joseph Benevenia,
  • David N. Paglia,
  • Sheldon S. Lin

摘要

The effects of vanadyl acetylacetonate (VAC) were evaluated on femur intramedullary osteoclasts in a rat model of type 1 diabetes (T1D) associated bone remodeling. In this study, BB Wistar rats were administered intramedullary injections consisting of either VAC at a dose of 1.5 mg/kg or a control saline solution. These injections were administered at least 12 weeks after the onset of T1D (i.e., treatment began ≥ 12 weeks after diabetes onset) to allow for the establishment of diabetic bone changes. At 4 weeks following treatment, the femurs treated with VAC exhibited a significant increase in trabecular thickness, specifically a 19.03% increase (p < 0.05). Osteoclasts, which were identified using TRAP staining, were found to be reduced in number at both 6 and 8 weeks in the femurs that received VAC treatment (p < 0.05). Likewise, when VAC was added to culture media, it resulted in a substantial decrease in osteoclast formation in vitro (8.1 ± 16.8 vs. 91.6 ± 16.0 cells, p < 0.001). In addition, expression of Dcstamp was significantly decreased in VAC-treated femurs compared to those treated with saline (p < 0.05). Taken together, this study demonstrates that intramedullary VAC delivery appears to inhibit T1D-related bone loss by impairing the process of osteoclastogenesis.