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Serum hepcidin at mid‐gestation is not associated with neonatal hepcidin or maternal obesity among pregnant adolescents
Author(s) -
O'Brien Kimberly O,
Cao Chang,
Young Melissa F,
McNanley Thomas J,
Cooper Elizabeth M,
Pressman Eva K,
McIntyre Allison W,
Westerman Mark,
Guillet Ronnie
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.238.4
Subject(s) - hepcidin , medicine , gestation , ferritin , pregnancy , cord blood , fetus , endocrinology , soluble transferrin receptor , iron deficiency , physiology , anemia , iron status , biology , genetics
Hepcidin is a systemic regulator of iron (Fe) homeostasis whose synthesis is increased in inflammatory conditions such as obesity. To assess determinants of hepcidin in pregnant adolescents, maternal and cord blood were obtained from a group of 93 pregnant teens (17.1 ± 1.1 y with prepregnancy BMI from 17.0 – 41.5 kg/m 2 ). Serum ferritin (SF), transferrin receptor (sTfR) and hepcidin concentrations (by C‐ELISA) were measured at mid‐gestation (26.3 ± 3.5 wks) and in cord blood at delivery (39.8 ± 1.3 wks). Maternal weight gain across pregnancy averaged 17.4 ± 7.3 kg and ranged from −2.2 – 39.5 kg. Maternal hepcidin was significantly lower than neonatal hepcidin (32.1 ± 28.3 vs.132 ± 95.9 ng/mL, p<0.0001) but the two were not significantly correlated. Maternal hepcidin was significantly lower in adolescents with tissue Fe depletion (sTfR >8.5 mg/dL; p=0.009, n=78) and depleted Fe stores (ferritin < 20 ug/L; p=0.01, n=77) at mid‐gestation. Unlike observations among non‐pregnant women, no significant relationship was evident between maternal hepcidin and prepregnancy BMI or between those with a BMI < 30 vs.> 30 kg/m 2 at term. The high iron demands of the pregnant adolescent and her developing fetus may override the effect of inflammation on hepcidin during pregnancy. USDA: 2005–35200 & 2008–0857