Objective:

To ascertain the effect of obesity-related inflammation on maternal and fetal iron status. We hypothesized that obese (Ob) pregnant women would have increased inflammation, hepcidin levels, and that their infants would have impaired iron status compared with lean (Lc) controls.

Study Design:

Fifteen Ob and fifteen Lc women were recruited in their second trimester of pregnancy. Markers of iron status, inflammation and hepcidin were measured in maternal and cord blood. Student's t-test was used to compare Ob and Lc groups, and Pearson's correlation coefficients were determined between maternal and cord blood values.

Result:

Maternal C-reactive protein (P< 0.01) and hepcidin (P< 0.01) were higher, and cord blood iron (P< 0.01) was lower in the Ob group. Maternal body mass index (P< 0.01) and hepcidin (P< 0.05) were negatively correlated with cord blood iron status.

Conclusion:

Maternal obesity is associated with impaired maternal-fetal iron transfer, potentially through hepcidin upregulation.

Introduction

Over half of all reproductive age women in industrialized nations are overweight or obese and this burden is growing rapidly in developing nations as well. 1, 2, 3 Epidemiologic data has shown that infants and children born to obese women are more likely to develop chronic health conditions such as asthma and diabetes, but there have been no studies describing the effect of maternal obesity on infant iron status. Hepcidin, a regulator of iron homeostasis, has been shown to be overexpressed in obesity and to correlate with low iron status in the obese. 4, 5, 6, 7, 8 Iron reaches the fetus through active transport in the placenta, and hepcidin is known to be one regulator of this process. 9