Abstract
Objective Obesity during pregnancy impedes fetal iron endowment. In adults, both iron depletion
and hypoxia stimulate erythropoietin (Epo) production, while hepcidin, the primary
iron regulator, is inhibited by Epo and stimulated by obesity. To understand this
relationship in fetuses, we investigated obesity, inflammation, and fetal iron status
on fetal Epo and hepcidin levels.
Study Design Epo, hepcidin, C-reactive protein (CRP), and ferritin levels were measured in 201
newborns of 35 to 40 weeks' gestation with historical risk factors for a low fetal
iron endowment, including half with maternal obesity.
Results Epo was unrelated to fetal size, but Epo was directly related to maternal body mass
index (BMI; kg/m2) (p < 0.03) and CRP (p < 0.0005) at delivery. Epo levels were twice as likely to be elevated (≥50 IU/L)
while comparing the lowest quartile of ferritin with the upper three quartiles (p < 0.01). Hepcidin was directly related to ferritin (p < 0.001) and indirectly related to maternal BMI (p < 0.015), but BMI became nonsignificant when undergoing multivariate analysis. Hepcidin
was unrelated to Epo.
Conclusion Although some of the fetal responses involving Epo were similar to adults, we did
not find a hepcidin–Epo relationship like that of adults, where fetal liver is the
site of both hepcidin and Epo production.
Keywords
erythropoietin - iron - maternal obesity - hepcidin - ferritin - C-reactive protein
- large for gestational age
