Phosphate Metabolism in the High Bone Mass (HBM) Mouse Model
Abstract
X-linked hypophosphatemia (XLH) is the disorder of renal phosphate wasting, and the most common form of heritable rickets (Carpenter, 2011). XLH is characterized by imperfect calcification, softening, and distortion of the bones, usually resulting in bowed legs. Previous research has indicated that XLH patients have increased levels of FGF23 and elevated levels of sclerostin which suppresses bone formation by antagonizing the Wnt-signaling pathway. Wnt signaling is an important mediator of bone mass, and in the High Bone Mass (HBM) mouse model, the G171V mutation activates the Wnt signaling. Since previous research suggests a link between Wnt signaling and FGF23 production with respect to phosphate metabolism. This project utilizes the HBM mouse model to understand how the mutation leads to increased bone mass, how the mutation leads to increased technical function, and the mutation’s relation to phosphate metabolism. The HBM genotype was associated with lower Ultimate stress, Pre-yield strain, and Modulus of Toughness. Additionally, Yield stress and Young’s Modulus was increased in the HBM mice. The data collected indicates increased toughness and stronger and stiffer material properties of bones in the HBM mice in comparison to the Wild-type mice.
Phosphate Metabolism in the High Bone Mass (HBM) Mouse Model
X-linked hypophosphatemia (XLH) is the disorder of renal phosphate wasting, and the most common form of heritable rickets (Carpenter, 2011). XLH is characterized by imperfect calcification, softening, and distortion of the bones, usually resulting in bowed legs. Previous research has indicated that XLH patients have increased levels of FGF23 and elevated levels of sclerostin which suppresses bone formation by antagonizing the Wnt-signaling pathway. Wnt signaling is an important mediator of bone mass, and in the High Bone Mass (HBM) mouse model, the G171V mutation activates the Wnt signaling. Since previous research suggests a link between Wnt signaling and FGF23 production with respect to phosphate metabolism. This project utilizes the HBM mouse model to understand how the mutation leads to increased bone mass, how the mutation leads to increased technical function, and the mutation’s relation to phosphate metabolism. The HBM genotype was associated with lower Ultimate stress, Pre-yield strain, and Modulus of Toughness. Additionally, Yield stress and Young’s Modulus was increased in the HBM mice. The data collected indicates increased toughness and stronger and stiffer material properties of bones in the HBM mice in comparison to the Wild-type mice.