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

Abstract

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.

Prevalence of anemia and associations between neonatal iron status, hepcidin, and maternal iron status among neonates born to pregnant adolescents

“…The median cord SF in our study (124.1 µg/l) was approximately 27% lower than median values reported from both China (170 µg/l) (2) and Norway (169 µg/l) (25), and approximately 7.4% lower than US data reported in term newborns (134 µg/l, n = 308) (26). In addition, the mean cord SF of neonates born to mothers with low iron stores at delivery (SF < 12 µg/l) in our study (91 µg/l) was approximately 43% lower than the mean value reported in recent neonatal data from Spain (160 µg/l) (12). The combined Hb and ferritin data in this group of neonates are indicative of insufficient iron stores at birth when compared to other neonatal populations.…”

“…Hepcidin is the master regulator of iron homeostasis, and the production of this hormone is known to be regulated by iron stores, inflammation, hypoxia, and erythropoietic activity (9). Despite its crucial role in regulation of iron homeostasis, currently, little is known about fetal hepcidin production and its regulatory function, and few normative hepcidin data are available in maternal-neonatal pairs at birth (10)(11)(12).…”

The placenta: the forgotten essential organ of iron transport

“…104,105 This is likely accomplished by upregulation of intestinal and placental iron transporters. Elevated placental TFR1 expression has been consistently observed in human and animal models of gestational iron deficiency 97,103,106,107 and is perhaps the best-known compensatory change in maternal deficiency. The mechanisms underlying this regulation is not well characterized and may involve placental iron regulatory protein 1 and intracellular iron.…”

“…102 Thus, available evidence suggests that TFR1-mediated iron uptake may be the primary target of hepcidin action in the placenta, although it cannot be ruled out that hepcidin also affects iron efflux by regulating subcellular localization of FPN1. 102 Interestingly, recent human studies failed to find significant relationships between cord hepcidin levels and either placental TFR1 expression 103 or placental transfer of maternal dietary iron, 104 suggesting differences between humans and rodents in hepcidin regulation of placental iron transfer. More research is needed to clarify the role of hepcidin in regulating iron homeostasis during the prenatal period and to identify other fetal factors regulating placental iron transport, such as those related to growth and development.…”

A Higher Rate of Iron Deficiency in Obese Pregnant Sudanese Women

“…Comparable studies among obese pregnant women are limited and mostly based on small sample size [19]. Likewise, studies assessing the impact of obesity on iron status during pregnancy did not consider the potential effect of the expected ID on erythropoiesis [10]. …”