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Transient Intermittent Hypoxia Exposure Disrupts Neonatal Bone Strength
Gyuyoup Kim1, Omar Elnabawi1, Daehwan Shin2
1Department of Orthodontics and Pediatric Dentistry, School of Dentistry, University of Maryland , Baltimore, MD , USA.
Frontiers in Pediatrics
|March 26, 2016
Summary
Intermittent hypoxia (IH) after birth impairs bone strength by disrupting zinc homeostasis in bone cells. Supplementing with zinc can restore bone health and strength.
Area of Science:
- Bone biology and mineral metabolism
- Neonatal physiology
- Nutritional science
Background:
- Intermittent hypoxia (IH) after birth is linked to pancreatic islet dysfunction and zinc deficiency.
- The impact of IH on bone health and zinc homeostasis remains largely unexplored.
Purpose of the Study:
- To investigate the effects of neonatal IH exposure on bone quality and zinc homeostasis in osteoblasts.
- To determine if IH-induced bone fragility is associated with altered zinc transport and bone formation markers.
Main Methods:
- Neonatal rats and human osteoblasts (HObs) were exposed to IH.
- Bone hardness, elasticity, alkaline phosphatase, and mineralization were quantified.
- Expression of zinc transporter ZIP8, bone formation markers (Runx2, Collagen-1, osteocalcin), and zinc content were analyzed.
- In vitro experiments manipulated zinc levels in HOb cultures.
Main Results:
- IH exposure significantly reduced bone hardness and elasticity in rats.
- IH decreased alkaline phosphatase, mineralization, and zinc content in bones and osteoblasts.
- Expression of ZIP8, Runx2, Collagen-1, and osteocalcin was reduced by IH.
- Zinc supplementation or ZIP8 over-expression in vitro restored mineralization and marker expression.
Conclusions:
- Neonatal intermittent hypoxia disrupts zinc homeostasis in bone, leading to reduced bone strength.
- Altered zinc transport (ZIP8) and impaired bone formation pathways contribute to IH-induced bone fragility.
- Zinc supplementation offers a potential therapeutic strategy to recover bone health after IH exposure.
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