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 journalArticle

25 Citations (Scopus)

Abstract

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
Volume39
Issue number4
DOIs
Publication statusPublished - Apr 2015

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Hepcidins
Transferrin Receptors
Iron
Obesity
Mothers
Pregnancy
Placenta
Ferritins
Messenger RNA
Serum
Fetal Blood

Keywords

  • 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

Cite this

The impact of maternal obesity on iron status, placental transferrin receptor expression and hepcidin expression in human pregnancy. / Garcia-Valdes, L; Campoy, C; Hayes, H; Florido, J; Rusanova, I; Miranda, M T; McArdle, H J.

In: International Journal of Obesity, Vol. 39, No. 4, 04.2015, p. 571-578.

Research output: Contribution to journalArticle

Garcia-Valdes, L ; Campoy, C ; Hayes, H ; Florido, J ; Rusanova, I ; Miranda, M T ; McArdle, H J. / The impact of maternal obesity on iron status, placental transferrin receptor expression and hepcidin expression in human pregnancy. In: International Journal of Obesity. 2015 ; Vol. 39, No. 4. pp. 571-578.
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abstract = "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.",
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author = "L Garcia-Valdes and C Campoy and H Hayes and J Florido and I Rusanova and Miranda, {M T} and McArdle, {H J}",
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.",
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TY - JOUR

T1 - The impact of maternal obesity on iron status, placental transferrin receptor expression and hepcidin expression in human pregnancy

AU - Garcia-Valdes, L

AU - Campoy, C

AU - Hayes, H

AU - Florido, J

AU - Rusanova, I

AU - Miranda, M T

AU - McArdle, H J

N1 - 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.

PY - 2015/4

Y1 - 2015/4

N2 - 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.

AB - 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.

KW - Adult

KW - Antigens, CD

KW - Antimicrobial Cationic Peptides

KW - Biomarkers

KW - Body Mass Index

KW - Dietary Carbohydrates

KW - Dietary Sucrose

KW - Female

KW - Hepcidins

KW - Homeostasis

KW - Humans

KW - Infant, Newborn

KW - Iron

KW - Iron, Dietary

KW - Male

KW - Maternal Nutritional Physiological Phenomena

KW - Maternal-Fetal Exchange

KW - Mothers

KW - Obesity

KW - Obesity, Abdominal

KW - Placenta

KW - Pregnancy

KW - Receptors, Transferrin

KW - Transferrin

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1038/ijo.2015.3

DO - 10.1038/ijo.2015.3

M3 - Article

VL - 39

SP - 571

EP - 578

JO - International Journal of Obesity

JF - International Journal of Obesity

SN - 0307-0565

IS - 4

ER -