Calcium-Sensing Receptor and Bone Turnover in Neonates
Author Information
Author(s): Shu Lei, Ji Ji, Zhu Qi, Cao Guofan, Karaplis Andrew, Pollak Martin R, Brown Edward, Goltzman David, Miao Dengshun
Primary Institution: Nanjing Medical University
Hypothesis
Does the calcium-sensing receptor mediate the effects of dietary calcium on bone turnover and modulate parathyroid hormone-induced bone turnover in neonates?
Conclusion
The calcium-sensing receptor is essential for mediating changes in bone turnover in response to dietary calcium and parathyroid hormone in neonates.
Supporting Evidence
- The calcium-sensing receptor is expressed in various bone cells and modulates their function.
- High dietary calcium increases bone formation parameters in wild-type and Pth–/– pups.
- PTH treatment enhances bone growth and mineralization in pups, but less so in Pth–/–CaR–/– pups.
- Deletion of both Pth and CaR leads to more severe skeletal defects than deletion of Pth alone.
- Calcium-sensing receptor deficiency abolishes dietary calcium-induced bone formation.
- Calcium levels in milk are influenced by the dietary calcium intake of lactating mothers.
Takeaway
This study shows that a special receptor helps baby mice grow strong bones by using calcium from their mother's milk and a hormone called parathyroid hormone.
Methodology
The study involved examining wild-type and genetically modified pups nursed on different calcium diets and treated with parathyroid hormone, assessing bone growth and turnover.
Limitations
The study primarily focuses on neonates, and results may not directly apply to adults or other developmental stages.
Participant Demographics
Neonatal mice of various genotypes (wild-type, Pth–/–, and Pth–/–CaR–/–).
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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