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Published on: May 10, 2022
Iron deficiency during pregnancy affects postnatal blood pressure in the rat
Lorraine Gambling1, Susan Dunford, Donna I Wallace
1Rowett Research Institute, Aberdeen AB21 9SB, UK.
Insights
Maternal iron deficiency during pregnancy increases offspring
Area of Science:
- Perinatal nutrition and developmental origins of health and disease
Background:
- Maternal iron deficiency during pregnancy is linked to adverse perinatal outcomes.
- It is a significant risk factor for later-life disease in offspring.
Purpose of the Study:
- To establish a rat model investigating maternal iron deficiency's impact on postnatal growth and blood pressure.
- To determine the critical role of prenatal nutrition in offspring development.
Main Methods:
- Weanling rats were fed control or iron-deficient diets throughout pregnancy.
- Offspring were cross-fostered to control-fed dams and weaned onto a control diet.
- Offspring growth, organ weights, haematocrit, iron levels, and blood pressure were monitored.
Main Results:
- Prenatal iron deficiency resulted in higher pup mortality, smaller size, reduced haematocrit, and altered organ weights at birth.
- Despite normal growth, offspring exhibited altered blood pressure and haematocrit levels postnatally.
- Increased duodenal iron uptake was observed in deficient mothers and newborn offspring.
Conclusions:
- Prenatal nutrition is critical for normal postnatal development and physiological function.
- Maternal iron deficiency has lasting effects on offspring cardiovascular health.
- Cross-fostering confirmed the impact of prenatal nutrition, independent of lactation effects.
Abstract:
Iron (Fe) deficiency anaemia during pregnancy results in an increased risk of perinatal mortality and morbidity and is a significant factor for increased risk of disease in later life. Consequently we have developed a rat model to study the relationship between maternal Fe deficiency and postnatal growth and blood pressure in the offspring. Weanlings were fed a control or Fe-deficient diet prior to and throughout pregnancy. At term, all pups were cross-fostered to control fed dams and weaned onto control diet. At birth, pups from deficient dams had a greater mortality rate, were smaller and had reduced haematocrit and liver Fe levels. They also had larger hearts, smaller kidneys and spleens and unchanged livers (relative organ weight). The pups grew normally. At 6 weeks, male pups from deficient dams had a higher and females a lower blood pressure than their normal counterparts. At 10 and 16 weeks, blood pressure in the males from deficient dams was still raised and in the females was now greater than controls. The haematocrit was lower in males throughout the 16 weeks and in females until 10 weeks of age. There was no significant difference in the offsprings' liver Fe stores at 6, 10 or 16 weeks. Duodenal Fe uptake in both the Fe-deficient mother and newborn offspring was significantly increased. By cross-fostering, we have eliminated confounding factors, such as maternal anaemia during lactation and show, unequivocally, that prenatal nutrition is critical for the development of normal postnatal function.
