|Dao, Maria Carlota|
Submitted to: Journal of Perinatology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/17/2012
Publication Date: 2/21/2013
Citation: Dao, M., Sen, S., Iyer, C., Klebenov, D., Meydani, S.N. 2013. Obesity during pregnancy impairs fetal iron status: is hepcidin the link?. Journal of Perinatology. 33:177-181. Interpretive Summary: The obesity epidemic is expanding worldwide, affecting women of reproductive age. Previous evidence has shown that obese individuals are more likely to be iron deficient. This occurs because chronic inflammation of obesity causes an increase in the levels of hepcidin, a hormone that lowers iron levels in circulation. Proper iron status during pregnancy is crucial for fetal development. Obesity during pregnancy has negative consequences on infant health. We are the first to report the effect of obesity during pregnancy on fetal iron status. We conducted a prospective case control study in which we measured iron status, inflammation, and hepcidin levels in 15 lean and 15 obese pregnant women, as well as their cord blood upon birth. We found that obese pregnant women had significantly higher inflammation and hepcidin levels than lean pregnant women, and that cord blood from the obese group had significantly lower iron status than the lean group. These results suggest that iron transfer from the mother to the fetus can be hindered by obesity, and that this likely happens through the action of hepcidin. Given the growing numbers of obese reproductive age women worldwide and the negative impact of dysregulated iron transfer from the mother to the fetus, our findings require urgent recognition from those who care for pregnant women and their children.
Technical Abstract: Over half of reproductive age women in the developed world are overweight or obese. Obesity during pregnancy has serious consequences for maternal and child health which we are just beginning to understand. Obesity is characterized by chronic inflammation, which upregulates hepcidin, a peptide hormone that controls cellular iron export, and results in iron insufficiency. However, the effect of this pro-inflammatory environment on fetal iron status, a critical factor in infant neurodevelopment, is not known. We sought to determine, for the first time, the effect of maternal obesity on maternal-fetal iron transfer. Fifteen obese and 15 lean women were recruited in their second trimester of pregnancy. Markers of iron status and inflammation as well as levels of hepcidin were measured in maternal and cord blood. We found that pre-pregnancy obesity increases maternal inflammation and hepcidin and is associated with impaired maternal-fetal iron transfer. Maternal obesity creates a pro-inflammatory environment for the developing fetus. Our findings suggest that this inflammation increases hepcidin, which impairs maternal-fetal iron transfer. As obesity reaches epidemic proportions worldwide, it is critical to recognize its ramifications on current and future generations in order to devise targeted prevention and treatment strategies.