The impact of maternal obesity on iron status, placental transferrin receptor expression and hepcidin expression in human pregnancy

L Garcia-Valdes, C Campoy, H Hayes, J Florido, I Rusanova, M T Miranda, H J McArdle

Research output: Contribution to journalArticlepeer-review

66 Citations (Scopus)


BACKGROUND: Obesity is associated with decreased iron status, possibly due to a rise in hepcidin, an inflammatory protein known to reduce iron absorption. In animals, we have shown that maternal iron deficiency is minimised in the foetus by increased expression of placental transferrin receptor (pTFR1), resulting in increased iron transfer at the expense of maternal iron stores.

OBJECTIVE: This study examines the effect of obesity during pregnancy on maternal and neonatal iron status in human cohorts and whether the placenta can compensate for decreased maternal iron stores by increasing pTFR1 expression.

SUBJECTS/METHODS: A total of 240 women were included in this study. One hundred and fifty-eight placentas (Normal: 90; Overweight: 37; Obese: 31) were collected at delivery. Maternal iron status was measured by determining serum transferrin receptor (sTFR) and ferritin levels at 24 and 34 weeks and at delivery. Hepcidin in maternal and cord blood was measured by ELISA and pTFR1 in placentas by western blotting and real-time RT-PCR.

RESULTS: Low iron stores were more common in obese women. Hepcidin levels (ng ml(-1)) at the end of the pregnancy were higher in obese than normal women (26.03±12.95 vs 18.00±10.77, P<0.05). Maternal hepcidin levels were correlated with maternal iron status (sTFR r=0.2 P=0.025), but not with neonatal values. mRNA and protein levels of pTFR1 were both inversely related to maternal iron status. For mRNA and all women, sTFR r=0.2 P=0.044. Ferritin mRNA levels correlated only in overweight women r=-0.5 P=0.039 with hepcidin (r=0.1 P=0.349), irrespective of maternal body mass index (BMI).

CONCLUSIONS: The data support the hypothesis that obese pregnant women have a greater risk of iron deficiency and that hepcidin may be a regulatory factor. Further, we show that the placenta responds to decreased maternal iron status by increasing pTFR1 expression.

Original languageEnglish
Pages (from-to)571-578
Number of pages8
JournalInternational Journal of Obesity
Issue number4
Publication statusPublished - Apr 2015

Bibliographical note

We thank the families participating in the study, and clinicians and personnel from the hospital who provided invaluable assistance and support. This work was supported by Spanish Government Innovation, Science and Company Ministry (Excellence project P06-CTS-02341 (PREOBE) and Scottish Government (Rural and Environmental Scientific and Analytical Services (RESAS). Dr Luz Garcia Valdes gratefully acknowledges support from the Alfonso Martin Escudero Foundation.


  • Adult
  • Antigens, CD
  • Antimicrobial Cationic Peptides
  • Biomarkers
  • Body Mass Index
  • Dietary Carbohydrates
  • Dietary Sucrose
  • Female
  • Hepcidins
  • Homeostasis
  • Humans
  • Infant, Newborn
  • Iron
  • Iron, Dietary
  • Male
  • Maternal Nutritional Physiological Phenomena
  • Maternal-Fetal Exchange
  • Mothers
  • Obesity
  • Obesity, Abdominal
  • Placenta
  • Pregnancy
  • Receptors, Transferrin
  • Transferrin
  • Journal Article
  • Research Support, Non-U.S. Gov't


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