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Preterm Piglets Born by Cesarean Section as a Suitable Animal Model for the Study of Iron Metabolism in Premature
Xiuying Wang1, Małgorzata Lenartowicz2, Rafał Mazgaj1
1Laboratory of Iron Molecular Biology, Department of Molecular Biology, Institute of Genetics and Animal Biotechnology, Polish Academy of Sciences, 05-552 Jastrzębiec, Poland.
Insights
Preterm infants face high iron deficiency risk. This study developed a prematurity model in piglets, revealing altered iron metabolism and tissue iron accumulation in preterm neonates.
Area of Science:
- Neonatology
- Iron Metabolism
- Animal Models
Background:
- Preterm infants are highly susceptible to iron deficiency.
- Iron homeostasis regulation in preterm infants is poorly understood.
- A validated animal model is crucial for studying preterm infant iron status.
Purpose of the Study:
- To develop and validate a porcine model of human prematurity.
- To assess iron status and metabolism in preterm piglets.
- To investigate the regulation of iron homeostasis in preterm neonates.
Main Methods:
- Cesarean section performed on sows at day 109 of gestation (equivalent to human third trimester).
- Comparative analysis of iron status, red blood cell indices, and iron regulatory markers between preterm and term piglets.
- Quantification of hepatic and splenic non-heme iron, plasma and hepatic ferritin, hepcidin mRNA and protein, and hepcidin regulators.
Main Results:
- Preterm piglets exhibited lower body weight, red blood cell indices, plasma iron, and transferrin saturation.
- Elevated hepatic and splenic non-heme iron and plasma/hepatic ferritin levels were observed in preterm piglets.
- Increased hepatic hepcidin mRNA but not plasma hepcidin-25 levels, alongside altered hepcidin regulators, were noted in preterm piglets.
Conclusions:
- The porcine prematurity model effectively mimics human preterm infant iron status.
- Preterm piglets display a pattern of functional iron deficiency with tissue iron accumulation.
- Dysregulation of iron metabolism and hepcidin in preterm neonates warrants further investigation.
Abstract:
Preterm infants are most at risk of iron deficiency. However, our knowledge of the regulation of iron homeostasis in preterm infants is poor. The main goal of our research was to develop and validate an animal model of human prematurity to assess iron status in preterm infants. We performed a cesarean section on sows on the 109th day of pregnancy, which corresponds to the last trimester of human pregnancy. Preterm piglets showed decreased body weight, red blood cell indices, plasma iron level and transferrin saturation. Interestingly, higher hepatic and splenic non-heme iron content and plasma and hepatic ferritin levels were found in premature piglets compared with term ones. In addition, premature piglets showed higher mRNA levels of iron-regulatory hormone hepcidin in the liver than term animals, which have not been reflected in higher plasma hepcidin-25 levels. We also showed changes in hepcidin regulators, including hepatic bone morphogenetic protein 6, plasma erythroferrone and growth differentiation factor 15 in preterm piglets. Consequently, no difference was observed in iron-exporter ferroportin levels in the spleen and liver. Overall, it seems that premature piglets show a pattern of iron metabolism characteristic of functional iron deficiency and iron accumulation in the tissue.
