Imbalances between bone formation and bone resorption, which can occur due to aging or sex hormone deprivation, result in decreased bone mass and an increased risk of fracture. Previous studies have suggested that the β-galactoside binding lectin, galectin-3, is involved in bone remodeling. We compared bone parameters of mice having null alleles of the galectin-3 gene (Lgals3-KO) with those of their wild-type littermates. Lgals3 deficiency increased cortical bone expansion at 36 weeks (wk) and preserved or enhanced bone mass in both male and female mutant mice. In addition, female Lgals3-KO mice were protected from age-related loss of trabecular bone. Histomorphometry and ex vivo primary cell differentiation assays showed increased osteoblastogenesis with little-to-no effect on osteoclastogenesis, suggesting the increased bone mass phenotype is primarily due to increased anabolism. Our study identifies galectin-3 as a negative regulator of bone formation and suggests that disruption of galectin-3 may be useful in preventing bone loss during aging.

骨形成和骨吸收之间的失衡可能是由于衰老或性激素缺乏引起的，导致骨量减少和骨折的风险增加。先前的研究表明，β-半乳糖苷结合凝集素（galectin-3）参与骨骼重塑。我们比较了具有galectin-3基因无效等位基因（Lgals3 - KO）的小鼠的骨参数与其野生型同窝仔的骨参数。Lgals3缺乏症在36周（周）时增加了皮质骨的膨胀，并且在雄性和雌性突变小鼠中均保留或增强了骨量。此外，女性Lgals3保护-KO小鼠免受年龄相关的小梁骨丢失的影响。组织形态计量学和离体原代细胞分化试验显示成骨细胞增多，对破骨细胞形成几乎没有影响，表明增加的骨量表型主要是由于合成代谢增加。我们的研究确定了半乳糖凝集素3作为骨形成的负调节剂，并表明破坏半乳糖凝集素3可能有助于防止衰老期间的骨质流失。