Cord Blood-Derived Exosomal CNTN2 and BDNF: Potential Molecular Markers for Brain Health of Neonates at Risk for Iron Deficiency.

Maternal iron deficiency anemia, obesity, and diabetes are prevalent during pregnancy. All are associated with neonatal brain iron deficiency (ID) and neurodevelopmental impairment. Exosomes are extracellular vesicles involved in cell-cell communication.

Alcohol's Dysregulation of Maternal-Fetal IL-6 and p-STAT3 Is a Function of Maternal Iron Status.

Background: Prenatal alcohol exposure (PAE) causes long-term growth and neurodevelopmental deficits that are worsened by maternal iron deficiency (ID). In our preclinical rat model, PAE causes fetal anemia, brain ID, and elevated hepatic iron via increased maternal and fetal hepcidin synthesis. These changes are normalized by a prenatal iron-fortified (IF) diet.

Maternal Perceived Stress during Pregnancy Increases Risk for Low Neonatal Iron at Delivery and Depletion of Storage Iron at One Year.

Objective: To investigate the impact of maternal stress during pregnancy on newborn iron and stage 1 iron deficiency at 1 year of age.

Study Design: In total, 245 mothers and their newborn infants (52% male; 72% white) were recruited at the Meriter Hospital Birthing Center on the basis of known risk factors for iron deficiency. Umbilical cord blood hemoglobin and zinc protoporphyrin/heme (ZnPP/H) were determined to evaluate erythrocyte iron and plasma ferritin was determined to reflect storage iron.

The impact of erythropoietin and iron status on brain myelination in the newborn rat.

Erythropoietin (Epo) drives iron (Fe) utilization for erythropoiesis, but the potentially resultant tissue iron deficiency (ID) can also impede brain development. Conversely, Epo binds to Epo receptors (EpoR) on immature brain oligodendrocytes and neurons, promoting growth and differentiation. The objective of the study was to examine the interaction between Epo and Fe on myelination in brain development during daily Epo treatment.

Dietary Iron Fortification Normalizes Fetal Hematology, Hepcidin, and Iron Distribution in a Rat Model of Prenatal Alcohol Exposure.

Background: Prenatal alcohol exposure (PAE) causes neurodevelopmental disability. Clinical and animal studies show gestational iron deficiency (ID) exacerbates PAE's behavioral and growth deficits. In rat, PAE manifests an inability to establish iron homeostasis, increasing hepcidin (maternal and fetal), and fetal liver iron while decreasing brain iron and promoting anemia.

Impact of the ovarian cycle and pregnancy on plasma chemistry values in ewes.

Normative data for plasma chemistry values in pregnant and non-pregnant reproductive age ewes are scant. Availability of data would aid monitoring of ewe health for both research and veterinary medicine. We determined specific plasma chemistry 95% confidence reference intervals (RIs) in non-pregnant and pregnant ewes.

Ovine uterine space restriction causes dysregulation of the renin-angiotensin system in fetal kidneys.

Unlabelled: In ovine pregnancy, uterine space restriction (USR) resulting from decreased space for placental attachment caused intrauterine growth restriction and impaired nephrogenesis. The fetal kidney renin-angiotensin system (RAS) is involved in nephrogenesis, fluid balance, and iron deposition. Angiotensin II exerts its effects via multiple receptors: angiotensin II 1-8 receptor type 1 (AT 1 R) and type 2 (AT 2 R), and angiotensin II 1-7 Mas receptor (MASR).

Increasing fetal ovine number per gestation alters fetal plasma clinical chemistry values.

Intrauterine growth restriction (IUGR) is interconnected with developmental programming of lifelong pathophysiology. IUGR is seen in human multifetal pregnancies, with stepwise rises in fetal numbers interfering with placental nutrient delivery. It remains unknown whether fetal blood analyses would reflect fetal nutrition, liver, and excretory function in the last trimester of human or ovine IUGR In an ovine model, we hypothesized that fetal plasma biochemical values would reflect progressive placental, fetal liver, and fetal kidney dysfunction as the number of fetuses per gestation rose.

Prenatal Alcohol Exposure Alters Fetal Iron Distribution and Elevates Hepatic Hepcidin in a Rat Model of Fetal Alcohol Spectrum Disorders.

Background: Prenatal alcohol exposure (PAE) causes neurodevelopmental disabilities, and gestational iron deficiency (ID) selectively worsens learning and neuroanatomical and growth impairments in PAE. It is unknown why ID worsens outcomes in alcohol-exposed offspring.

Objective: We hypothesized that PAE alters maternal-fetal iron distribution or its regulation.

Impact of Growth Restriction and Other Prenatal Risk Factors on Cord Blood Iron Status in Prematurity.

Objective: To determine whether prenatal risk factors (RFs) that predict cord blood iron status in term newborns also predict iron status of premature newborns.

Study Design: Cord blood iron indices from 80 preterm newborns were compared with historical and demographic RFs for developing iron deficiency if born at term.

Result: The presence of multiple RFs did not incrementally interfere with cord iron status in preterm newborns.

Dietary-induced gestational iron deficiency inhibits postnatal tissue iron delivery and postpones the cessation of active nephrogenesis in rats.

Gestational iron deficiency (ID) can alter developmental programming through impaired nephron endowment, leading to adult hypertension, but nephrogenesis is unstudied. Iron status and renal development during dietary-induced gestational ID (<6 mg Fe kg-1 diet from Gestational Day 2 to Postnatal Day (PND) 7) were compared with control rats (198 mg Fe kg-1 diet). On PND2-PND10, PND15, PND30 and PND45, blood and tissue iron status were assessed.

Ovine uterine space restriction alters placental transferrin receptor and fetal iron status during late pregnancy.

Background: Fetal growth restriction is reported to be associated with impaired placental iron transport. Transferrin receptor (TfR) is a major placental iron transporter in humans but has not been studied in sheep. TfR is regulated by both iron and nitric oxide (NO), the molecule produced by endothelial nitric oxide synthase (eNOS).

Impact of multiple prenatal risk factors on newborn iron status at delivery.

Background: Maternal anemia and several complications of pregnancy can affect fetal iron acquisition.

Aim: Because it is unknown whether the effects of demographic and maternal risk factors (RF) are summative, we examined cord iron status in newborns with multiple RF for acquiring iron deficiency.

Methods: Cord blood indices from healthy control newborns with and without RF for newborn or infant iron deficiency were studied.

Iron deficiency and renal development in the newborn rat.

Iron is essential for fetal organ development, but the effect of isolated iron deficiency on nephrogenesis is unknown. Human premature infants are at risk for disrupted nephrogenesis because glomerular development is incomplete until 36-wk gestation. We modeled the effects of iron on postnatal glomerulogenesis in four groups of immature rats from P4 to P12: dam fed controls (DF), dam fed with sham gastrostomy surgery (DF + SS), iron-deficiency anemia (IDA), fed iron-deficient formula through gastrostomy apart from the dam, and IDA plus simultaneous enteral iron rescue (IDA+Fe).

Cord blood zinc protoporphyrin/heme ratio in minority neonates at risk for iron deficiency.

We measured cord blood zinc protoporphyrin/heme (ZnPP/H) and plasma ferritin in healthy African-American and Hispanic newborns, matched by gestation with Caucasian newborns. In these at-risk minorities, cord ZnPP/H was higher and plasma ferritin lower, supporting the feasibility of screening newborns at-risk for iron deficiency at birth.

Reticulocyte enrichment of zinc protoporphyrin/heme discriminates impaired iron supply during early development.

In infants and children, elevated whole blood zinc protoporphyrin/heme (ZnPP/H) measures iron-deficient (ID) erythropoiesis. Because immature erythrocytes are less dense than mature erythrocytes, we hypothesized that the sensitivity of ZnPP/H is improved if measured in the least dense cells. Blood was collected from control suckling, mildly and severely ID suckling rats.

Enteral erythropoietin and iron stimulate erythropoiesis in suckling rats.

Objectives: A primary objective was to evaluate whether addition of enteral iron supplementation will facilitate a systemic erythropoietic effect when feeding erythropoietin (Epo) to suckling rats. A secondary objective was to confirm that iron does not alter the previous finding that enteral Epo exerts local trophic effects on the small intestine.

Methods: Four-day-old Sprague-Dawley rats underwent gastrostomy and were fed a cow's milk-based rat milk substitute for 8 days.

Zinc protoporphyrin/heme in large-for-gestation newborns.

Background: Zinc protoporphyrin/heme (ZnPP/H) ratios are indicators of incomplete erythrocyte iron delivery. ZnPP/H is more sensitive than measures of iron stores, such as plasma ferritin, in identifying early pre-anemic iron-deficient erythropoiesis. Cord ZnPP/H ratios are elevated in conditions associated with fetal hypoxia, such as diabetes mellitus during pregnancy.