Lisa Tussing-Humphreys1, Bazil LaBomascus2, Kimberly O'Brien3, Elizabeta Nemeth4, Veena Sangkhae4, Alana D Steffen5, Karla Castellanos1, Victoria DeMartelly6, Rungnapa Ruchob7, Lauren Welke8, Nefertiti OjiNjideka Hemphill1, Lacey Pezley1, Andrew McLeod1, Bruni Hirsch9, Gloria Elam10, Carol Estwing Ferrans5, Mary Dawn Koenig11. 1. Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL, USA. 2. Northwestern Feinberg School of Medicine, Chicago, IL, USA. 3. Division of Nutritional Sciences, Cornell University, Ithaca, NY, USA. 4. Center for Iron Disorders, Department of Medicine, University of California, Los Angeles, Los Angeles, CA, USA. 5. Department of Biobehavioral Nursing Science, University of Illinois at Chicago, Chicago, IL, USA. 6. Department of Obstetrics and Gynecology, University of Chicago, Chicago, IL, USA. 7. Mahidol University, Bangkok, Thailand. 8. Abbvie, Chicago, IL, USA. 9. Saint Anthony Hospital, Chicago, IL, USA. 10. Department of Obstetrics and Gynecology, University of Illinois at Chicago, Chicago, IL, USA. 11. Department of Human Development Nursing Sciences, University of Illinois at Chicago, Chicago, IL, USA.
Abstract
BACKGROUND: Iron is critical for fetal development. Neonates of obese women may be at risk for poor iron status at birth as a result of maternal inflammation-driven overexpression of hepcidin. OBJECTIVES: The objective of this study was to determine differences in placental transfer of oral iron (57Fe) and expression of placental transferrin receptor 1 (TFR1) and ferroportin (FPN) mRNA and protein and their association with maternal and neonatal iron-related parameters, including maternal hepcidin, among women with and without prepregnancy (PP) obesity. METHODS: 57Fe ingested during the third trimester of pregnancy was recovered in venous umbilical cord blood among 20 PP obese [BMI (in kg/m2): 30.5-43.9] and 22 nonobese (BMI: 18.5-29.0) women aged 17-39 y. Placental TFR1 and FPN mRNA and protein expression were quantified via qPCR and Western blot. Maternal and neonatal markers of iron status and regulation, as well as inflammation, were measured. Descriptive and inferential statistical tests (e.g., Student t test, Pearson correlation) were used for data analysis. RESULTS: There was no difference in cord blood enrichment of 57Fe or placental mRNA or protein expression of TFR1 or FPN among the women with and without PP obesity. Maternal hepcidin was not correlated with cord blood enrichment of 57Fe or placental FPN mRNA or protein expression. Maternal log ferritin (corrected for inflammation) was inversely correlated with log percent enrichment of 57Fe in cord blood (partial r = -0.50; P < 0.01, controlled for marital status) and protein expression of TFR1 (r = -0.43; P = 0.01). CONCLUSIONS: Placental iron trafficking did not differ among women with and without PP obesity. Findings reinforce the importance of maternal iron stores in regulating placental iron trafficking.
BACKGROUND: Iron is critical for fetal development. Neonates of obese women may be at risk for poor iron status at birth as a result of maternal inflammation-driven overexpression of hepcidin. OBJECTIVES: The objective of this study was to determine differences in placental transfer of oral iron (57Fe) and expression of placental transferrin receptor 1 (TFR1) and ferroportin (FPN) mRNA and protein and their association with maternal and neonatal iron-related parameters, including maternal hepcidin, among women with and without prepregnancy (PP) obesity. METHODS: 57Fe ingested during the third trimester of pregnancy was recovered in venous umbilical cord blood among 20 PP obese [BMI (in kg/m2): 30.5-43.9] and 22 nonobese (BMI: 18.5-29.0) women aged 17-39 y. Placental TFR1 and FPN mRNA and protein expression were quantified via qPCR and Western blot. Maternal and neonatal markers of iron status and regulation, as well as inflammation, were measured. Descriptive and inferential statistical tests (e.g., Student t test, Pearson correlation) were used for data analysis. RESULTS: There was no difference in cord blood enrichment of 57Fe or placental mRNA or protein expression of TFR1 or FPN among the women with and without PP obesity. Maternal hepcidin was not correlated with cord blood enrichment of 57Fe or placental FPN mRNA or protein expression. Maternal log ferritin (corrected for inflammation) was inversely correlated with log percent enrichment of 57Fe in cord blood (partial r = -0.50; P < 0.01, controlled for marital status) and protein expression of TFR1 (r = -0.43; P = 0.01). CONCLUSIONS: Placental iron trafficking did not differ among women with and without PP obesity. Findings reinforce the importance of maternal iron stores in regulating placental iron trafficking.
Authors: Katherine M Delaney; Chang Cao; Ronnie Guillet; Eva K Pressman; Kimberly O O'Brien Journal: Am J Clin Nutr Date: 2022-04-01 Impact factor: 8.472