Am J Perinatol 2019; 36(05): 511-516 DOI: 10.1055/s-0038-1669444
Original Article
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
Cord Blood Erythropoietin and Hepcidin Reflect Lower Newborn Iron Stores due to Maternal Obesity during Pregnancy
Colin Korlesky
1
Department of Pediatrics, University of Wisconsin-Madison, Madison, Wisconsin
2
Department of Pediatrics, UnityPoint Health-Meriter, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin
,
Pamela J. Kling
1
Department of Pediatrics, University of Wisconsin-Madison, Madison, Wisconsin
2
Department of Pediatrics, UnityPoint Health-Meriter, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin
,
Daphne Q. D. Pham
3
Department of Biological Sciences, University of Wisconsin-Parkside, Kenosha, Wisconsin
,
Albina A. Ovasapyan
3
Department of Biological Sciences, University of Wisconsin-Parkside, Kenosha, Wisconsin
4
North Central Health Care, Medical College of Wisconsin, Milwaukee, Wisconsin
,
Cheryl E. G. Leyns
3
Department of Biological Sciences, University of Wisconsin-Parkside, Kenosha, Wisconsin
5
Department of Neurology, Washington University School of Medicine, Saint Louis, Missouri
,
Morgan B. Weber
2
Department of Pediatrics, UnityPoint Health-Meriter, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin
6
Department of Orthopedics, Case Western Reserve, Cleveland, Ohio
,
Christopher L. Coe
7
Department of Psychology, Harlow Center for Biological Psychology, University of Wisconsin-Madison, Madison, Wisconsin
› Author AffiliationsFunding This work was supported by Meriter Foundation, National Institutes of Health (NIH 1 ULRR026011 UW CTSA Program and NIH T32 DK077586 Pediatric Endocrinology Scholar), UW Education & Research Committee-Wisconsin Partnership Program, and Thrasher Research Fund.
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
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