scholarly journals Effect of Oral Supplementation of Healthy Pregnant Sows with Sucrosomial Ferric Pyrophosphate on Maternal Iron Status and Hepatic Iron Stores in Newborn Piglets

Animals ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 1113
Author(s):  
Rafał Mazgaj ◽  
Mateusz Szudzik ◽  
Paweł Lipiński ◽  
Aneta Jończy ◽  
Ewa Smuda ◽  
...  
Keyword(s):  
Animal Model ◽  
Pregnancy Outcome ◽  
Iron Supplementation ◽  
Iron Status ◽  
Heme Iron ◽  
Oral Iron ◽  
Ferric Pyrophosphate ◽  
Non Heme Iron ◽  
Nutritional Studies ◽  
Maternal Iron

Background: The similarities between swine and humans in physiological and genomic patterns, as well as significant correlation in size and anatomy, make pigs an useful animal model in nutritional studies during pregnancy. In humans and pigs iron needs exponentially increase during the last trimester of pregnancy, mainly due to increased red blood cell mass. Insufficient iron supply during gestation may be responsible for the occurrence of maternal iron deficiency anemia and decreased iron status in neonates. On the other hand, preventive iron supplementation of non-anemic mothers may be of potential risk due to iron toxicity. Several different regimens of iron supplementation have been applied during pregnancy. The majority of oral iron supplementations routinely applied to pregnant sows provide inorganic, non-heme iron compounds, which exhibit low bioavailability and intestinal side effects. The aim of this study was to check, using pig as an animal model, the effect of sucrosomial ferric pyrophosphate (SFP), a new non-heme iron formulation on maternal and neonate iron and hematological status, placental transport and pregnancy outcome; Methods: Fifteen non-anemic pregnant sows were recruited to the experiment at day 80 of pregnancy and randomized into the non-supplemented group (control; n = 5) and two groups receiving oral iron supplementation—sows given sucrosomial ferric pyrophosphate, 60 mg Fe/day (SFP; n = 5) (SiderAL®, Pisa, Italy) and sows given ferrous sulfate 60 mg Fe/day (Gambit, Kutno, Poland) (FeSO4; n = 5) up to delivery (around day 117). Biological samples were collected from maternal and piglet blood, placenta and piglet tissues. In addition, data on pregnancy outcome were recorded.; Results: Results of our study show that both iron supplements do not alter neither systemic iron homeostasis in pregnant sows nor their hematological status at the end of pregnancy. Moreover, we did not detect any changes of iron content in the milk and colostrum of iron supplemented sows in comparison to controls. Neonatal iron status of piglets from iron supplemented sows was not improved compared with the progeny of control females. No statistically significant differences were found in average piglets weight and number of piglets per litter between animals from experimental groups. The placental expression of iron transporters varied depending on the iron supplement.

scholarly journals Exploratory Study: Excessive Iron Supplementation Reduces Zinc Content in Pork without Affecting Iron and Copper

Animals ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 776
Author(s):  
Maureen Middleton ◽  
Manuel Olivares ◽  
Alejandra Espinoza ◽  
Miguel Arredondo ◽  
Fernando Pizarro ◽  
...  
Keyword(s):  
Iron Supplementation ◽  
Iron Status ◽  
Zinc Content ◽  
Serum Levels ◽  
Serum Copper ◽  
Heme Iron ◽  
Control Group ◽  
Non Heme Iron ◽  
High Concentrations ◽  
Iron Heme

The aim of this work was to determine in an exploratory manner the effect of excessive iron supplementation on iron, zinc, and copper contents in pork and pork offal. Pigs averaging 50 days in age and 15 ± 1.3 kg body weight were allocated to a control group (500 ppm dietary Fe) and a supplemental group (3000 ppm dietary Fe). After an iron supplementation period of 60 days, blood samples were analyzed to determine iron biomarkers, serum copper, and zinc contents. Animals were slaughtered to assess total iron, non-heme iron, heme iron, zinc, and copper contents in samples of nine meat cuts and some offal. Iron supplementation improved the iron status in pigs with increased hemoglobin and hematocrit, but did not affect serum levels of iron, zinc, and copper. Iron supplementation did not affect the heme and non-heme iron contents of the different meat cuts. Zinc contents decreased by 32–55% in meat cuts, where iron content increased in the liver, spleen, kidneys, and pancreas. No differences of zinc and copper were observed in offal samples. High concentrations of iron supplementation reduce zinc content in pork.

scholarly journals SUN-359 Antenatal Oral Iron Supplementation, FGF23 and Bone Metabolism in Kenyan Women and Their Offspring: A Randomised Controlled Trial

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Vickie S Braithwaite ◽  
Ayse Y Demir ◽  
Martin N Mwangi ◽  
Kerry S Jones ◽  
Ann Prentice ◽  
...  
Keyword(s):  
Vitamin D ◽  
Iron Supplementation ◽  
Iron Status ◽  
Controlled Trial ◽  
Oral Iron ◽  
Vitamin D Metabolism ◽  
Fgf23 Concentration ◽  
Kenyan Women ◽  
Randomised Controlled ◽  
Maternal Iron

Abstract Objectives: FGF23 decreases reabsorption and increases phosphate excretion in the kidney and regulates vitamin D metabolism. Maternal iron deficiency may be implicated in the pathogenesis of hypophosphataemia-driven rickets in offspring through perturbed FGF23 expression. We aimed to determine the effect of antenatal oral iron supplementation on maternal and neonatal markers of bone mineral regulation. Methods: 470 rural Kenyan women with singleton pregnancies and haemoglobin concentrations ≥90g/L were randomly allocated to daily, supervised supplementation iron (60mg as ferrous fumarate) or placebo from 13–23 weeks gestational age until 1 month postpartum. We analysed maternal and neonatal plasma samples collected at birth, with primary outcomes being concentrations of FGF23 in its intact form (I-FGF23, the phosphate- and vitamin D-regulating hormone) and its C-terminal fragment (C-FGF23). Results: In mothers and neonates, antenatal iron supplementation reduced C-FGF23 concentration by 62.6% (95%CI: -70.3% to -53.0%) and 15.2% (-28.4% to 0.3%), respectively; increased neonatal I-FGF23 concentration by 21.6% (1.2% to 46.1%); increased maternal hepcidin concentration by 136%, (86% to 200%); and decreased maternal 25-hydroxyvitamin D concentrations by 6.1nmol/L (1.2 to 11.0nmol/L). We found no effect on markers of bone turnover in either mothers or neonates. The magnitude of the effect of antenatal iron supplementation on concentrations of C-FGF23, I-FGF23 and phosphate, and on estimated glomerular filtration rate (a measure of kidney glomerular function) depended on maternal iron status at baseline Conclusions: Antenatal iron supplementation may provide health benefits to pregnant women and their offspring beyond increasing iron status. Whether iron supplementation reduces present and future infant risk of rickets remains unclear.

scholarly journals Baseline iron status and presence of anaemia determine the course of systemic Salmonella infection following oral iron supplementation in mice

EBioMedicine ◽  
2021 ◽  
Vol 71 ◽  
pp. 103568 ◽  
Author(s):  
Alexander Hoffmann ◽  
David Haschka ◽  
Lara Valente de Souza ◽  
Piotr Tymoszuk ◽  
Markus Seifert ◽  
...  
Keyword(s):  
Iron Supplementation ◽  
Iron Status ◽  
Oral Iron ◽  
Salmonella Infection

scholarly journals Assessment of Gastrointestinal Symptoms and Non-transferrin Bound Iron After Oral Ferrous Sulfate and Iron-enriched Aspergillus Oryzae Supplementation in Women (P24-039-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Amanda Bries ◽  
Chong Wang ◽  
Brian Wels ◽  
Isaac Agbemafle ◽  
Olivia Meier ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Side Effects ◽  
Ferrous Sulfate ◽  
Serum Iron ◽  
Iron Supplementation ◽  
Iron Status ◽  
Transferrin Saturation ◽  
Oral Iron ◽  
Deficiency Anemia ◽  
Iron Supplements

Abstract Objectives Iron deficiency anemia (IDA) is a widespread nutritional deficiency. Iron supplementation with ferrous sulfate (FeSO4) is the most common strategy to treat IDA; however, the compliance with daily FeSO4 administration is poor, due to contraindicating side effects. Previously, we have reported that A. oryzae (Ultimine®; ULT) is a novel iron source. Therefore, the objective of this study was to determine the biochemical assessment, non-transferrin bound iron (NTBI) and commonly related gastrointestinal side effects to assess the safety of A. oryzae compared to FeSO4. Methods Female participants (n = 16) with serum ferritin concentrations 40 µg/L were randomized to a double-blind, 9-wk cross-over study with a 3-wk placebo washout period between treatments. Oral iron supplements (65 mg Fe), FeSO4 and ULT were administered for 21 consecutive days for each subject. Side effect questionnaires were collected 3d/wk over the 9-wk study period. Side effects and biochemical markers (nausea, heartburn, abdominal pain, fatigue, headache, diarrhea, constipation, oxidative stress and liver and kidney function) from iron supplementation were evaluated, along with serum iron, % transferrin saturation (TS) and NBTI 8 h curves. Results Serum iron, TS, and NTBI were all markedly higher with FeSO4 at each time-point from 2–8 hours (P < 0.001) compared to ULT, whereas NTBI was undetected. Among treatments, FeSO4 resulted in higher inflammation, though not statistically significant. Compliance based on returned pills was higher with ULT (97.3%) than placebo and FeSO4 (95.2% and 93.2%, respectively). Subjects taking FeSO4 reported abdominal discomfort 2% more than ULT, which was not significantly different. FeSO4 caused marginally higher incidence of combined nauseation, constipation and diarrhea when subjects were taking FeSO4 (P < 0.07). Iron status was maintained similarly by both oral iron supplements. Oxidative stress, inflammation, kidney and liver function markers were not elevated with ULT supplementation, suggesting safety of its consumption. Conclusions Better compliance and less gastrointestinal related side effects were reported with ULT compared to FeSO4, while maintaining normal iron status. Our data suggests ULT is a safe oral iron supplement for treatment of IDA. Funding Sources Cura Global Health, Inc.

Effects of Iron Status and Iron Supplementation on Salmonella Typhimurium and Plasmodium Yoelii Infection In Mice

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2052-2052
Author(s):  
Eldad A. Hod ◽  
Eric H. Ekland ◽  
Shruti Sharma ◽  
Boguslaw S. Wojczyk ◽  
David A. Fidock ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Salmonella Typhimurium ◽  
Median Survival ◽  
Iron Supplementation ◽  
Iron Status ◽  
Plasmodium Yoelii ◽  
Oral Iron ◽  
Deficiency Anemia ◽  
Iron Deficient ◽  
Deficient Mice

Abstract Abstract 2052 To clarify the interactions between iron status, oral iron supplementation, and bacterial and malarial infections, we examined iron-replete mice and mice with dietary iron deficiency infected with Salmonella typhimurium, Plasmodium yoelii, or both, with and without oral iron administration. These studies were designed to identify potential mechanisms underlying the increased risk of severe illness and death in children in a malaria-endemic region who received routine iron and folic acid supplementation during a randomized, controlled trial in Pemba, Tanzania (Sazawal et al. Lancet 2006;367:133-43). To this end, weanling C57BL/6 female mice were fed an iron-replete or an iron-deficient diet, the latter of which resulted in severe iron deficiency anemia. Groups of mice were then infected by intraperitoneal injection of Salmonella typhimurium strain LT2, Plasmodium yoelii strain 17X parasites, or both. With Salmonella infection alone, iron-deficient mice had a median survival (7.5 days, N=8) approximately half that of iron-replete mice (13 days, N=10, p<0.0001). At death, the mean level of bacteremia was significantly higher in infected iron-deficient mice. In blood cultures performed at death, all iron-deficient mice were bacteremic, but bacteria were detected in only 4 of 10 iron-replete mice. Both iron-deficient and iron-replete Salmonella-infected mice had gross hepatosplenomegaly with hepatitis, distorted hepatic and splenic architecture, massive expansion of the splenic red pulp with inflammatory cells, and Gram-negative bacilli by tissue Gram stain. With P. yoelii infection alone, iron-deficient and iron-replete mice cleared the infection at similar rates (by ~13 days following infection, N=5 in each group) and no deaths due to parasitemia occurred. With Salmonella and P. yoelii co-infection, death was earlier than with Salmonella alone in iron-replete mice (median survival of 10 vs. 13 days; N=10 in each group; p=0.005), but not in iron-deficient mice (median survival of 7 vs. 7.5 days; N=10 and 8, respectively; p=0.8). To examine the effect of short-term oral iron supplementation with Salmonella infection alone, mice received daily iron (ferrous sulfate, 1 mg/kg) by gavage for 4 days before infection with Salmonella, and supplementation continued for a total of 10 days. After gavage, plasma non-transferrin-bound iron (NTBI) appeared at 1–2 hours with a mean peak level of approximately 5 μM. In iron-deficient mice, short-term oral iron supplementation did not fully correct the iron deficiency anemia or replenish iron stores. Oral iron supplementation reduced the median survival of both iron-deficient and iron-replete Salmonella-infected mice by approximately 1 day; the difference was significant only in the iron-replete group (N=5, p<0.05). In summary, these results indicate that iron deficiency decreases the survival of Salmonella-infected mice; the median survival of iron-deficient mice was approximately half that of those that were iron replete. These observations are similar to those in the Pemba sub-study in which iron-deficient children given placebo had a 200% increase in the risk of adverse events relative to iron-replete children. Iron deficiency had no apparent effect on the course of infection with P. yoelii but further studies with more virulent Plasmodium species are needed. Co-infection with Salmonella and Plasmodium significantly increased mortality as compared to single infections, but only in iron-replete mice. Oral iron supplementation of Salmonella-infected mice significantly decreased the median survival, but only of iron-replete animals; however, our study may have had insufficient power to detect an effect on iron-deficient mice. Systematic examination in mice of the effect of iron supplements on the severity of malarial and bacterial infection in iron-replete and iron-deficient states may ultimately help guide the safe and effective use of iron interventions in humans in areas with endemic malaria. Disclosures: No relevant conflicts of interest to declare.

Alternative pathways for absorption of iron from foods

2010 ◽  
Vol 82 (2) ◽  
pp. 429-436 ◽  
Author(s):  
Bo Lönnerdal
Keyword(s):  
Iron Absorption ◽  
Iron Status ◽  
Age Groups ◽  
Heme Iron ◽  
Dietary Factors ◽  
Iron Binding ◽  
Alternative Pathways ◽  
Non Heme Iron ◽  
Lactoferrin Receptor ◽  
Iron Binding Proteins

Iron is known to be absorbed from foods in two major forms, heme iron and non-heme iron. Iron status as well as dietary factors known to affect iron absorption has limited effect on heme iron absorption, whereas inhibitors and enhancers of iron absorption have pronounced effects on non-heme iron absorption. The enterocyte transporter for non-heme iron, DMT1, is strongly up-regulated during iron deficiency and down-regulated during iron overload. A transporter for heme iron, HCP1, was recently characterized and is present on the apical membrane of enterocytes. Two other pathways for iron absorption have been discovered and may serve to facilitate uptake of iron from two unique iron-binding proteins, lactoferrin and ferritin. Lactoferrin is an iron-binding protein in human milk and known to survive proteolytic digestion. It mediates iron uptake in breast-fed infants through endocytosis via a specific lactoferrin receptor (LfR). Recently, lactoferrin has become popular as a food additive and may enhance iron status in several age groups. Ferritin is present in meat, but also in plants. The ferritin content of plants can be enhanced by conventional breeding or genetic engineering, and thereby increase iron intake of populations consuming plant-based diets. Ferritin is a bioavailable source of iron, as shown in recent human studies. Ferritin can be taken up by intestinal cells via endocytosis, suggesting a receptor-mediated mechanism.

scholarly journals The Effectiveness of Different Doses of Iron Supplementation and the Prenatal Determinants of Maternal Iron Status in Pregnant Spanish Women: ECLIPSES Study

Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2418 ◽  
Author(s):  
Lucía Iglesias Vázquez ◽  
Victoria Arija ◽  
Núria Aranda ◽  
Estefanía Aparicio ◽  
Núria Serrat ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Early Pregnancy ◽  
Iron Supplementation ◽  
Iron Status ◽  
Deficiency Anemia ◽  
Hfe Gene ◽  
Excess Iron ◽  
Spanish Women ◽  
Maternal Iron ◽  
Different Doses

Iron deficiency (ID), anemia, iron deficiency anemia (IDA) and excess iron (hemoconcentration) harm maternal–fetal health. We evaluated the effectiveness of different doses of iron supplementation adjusted for the initial levels of hemoglobin (Hb) on maternal iron status and described some associated prenatal determinants. The ECLIPSES study included 791 women, randomized into two groups: Stratum 1 (Hb = 110–130g/L, received 40 or 80mg iron daily) and Stratum 2 (Hb > 130g/L, received 20 or 40mg iron daily). Clinical, biochemical, and genetic information was collected during pregnancy, as were lifestyle and sociodemographic characteristics. In Stratum 1, using 80 mg/d instead of 40 mg/d protected against ID on week 36. Only women with ID on week 12 benefited from the protection against anemia and IDA by increasing Hb levels. In Stratum 2, using 20 mg/d instead of 40 mg/d reduced the risk of hemoconcentration in women with initial serum ferritin (SF) ≥ 15 μg/L, while 40 mg/d improved SF levels on week 36 in women with ID in early pregnancy. Mutations in the HFE gene increased the risk of hemoconcentration. Iron supplementation should be adjusted to early pregnancy levels of Hb and iron stores. Mutations of the HFE gene should be evaluated in women with high Hb levels in early pregnancy.

The Serine Protease Tmprss6 Regulates Hepcidin Expression, but Its Loss Does Not Cause Systemic Iron Deficiency In the Fetal and Neonatal Periods

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4258-4258
Author(s):  
Ramsey M. Wehbe ◽  
Rebecca L. Whittlesey ◽  
Nancy C. Andrews ◽  
Karin E. Finberg
Keyword(s):  
Iron Deficiency ◽  
Iron Homeostasis ◽  
Iron Concentration ◽  
Fold Increase ◽  
Heme Iron ◽  
Hepcidin Expression ◽  
Non Heme Iron ◽  
Iron Parameters ◽  
Maternal Iron ◽  
Hepcidin Mrna

Abstract Abstract 4258 Mutations in TMPRSS6 (matriptase-2), a transmembrane serine protease expressed by the liver, result in the clinical phenotype of iron refractory iron deficiency anemia (IRIDA). Additionally, common polymorphisms in TMPRSS6 have been associated with variation in laboratory parameters of iron homeostasis in healthy populations. TMPRSS6 increases iron absorption by reducing expression of the hepatic hormone, hepcidin, via down-regulation of a BMP/SMAD signaling cascade. Hepcidin promotes the internalization and degradation of the duodenal iron transporter, ferroportin, thereby inhibiting iron absorption. Previous studies have demonstrated that adult mice with Tmprss6 deficiency exhibit elevated hepatic hepcidin mRNA levels that are associated with decreased hepatic iron stores. In one study, genetic loss of Tmprss6 was shown to result in significant elevation of hepatic hepcidin expression in mice at birth; however, whether this hepcidin elevation was associated with abnormalities in iron homeostasis was not reported. We therefore asked if the elevated hepcidin levels present in newborn Tmprss6-/- pups correlate with abnormal parameters of iron homeostasis in the fetal or neonatal periods. To answer this question, we intercrossed Tmprss6+/− mice to generate Tmprss6+/+, Tmprss6+/−, and Tmprss6-/- progeny for phenotypic characterization at either gestational day 17.5 (E17.5) or postnatal day 0 (P0). Consistent with prior observations, Tmprss6-/- pups at P0 showed a 4.6-fold increase in hepatic hepcidin mRNA compared to Tmprss6+/+ littermates (p=.006). However, despite this elevation in hepcidin expression, Tmprss6-/- pups were not pale, and they showed no significant differences in body mass or hepatic non-heme iron concentration compared to Tmprss6+/+ and Tmprss6+/− littermates. At E17.5, Tmprss6-/- fetuses showed a 50-fold increase in hepatic hepcidin mRNA compared to Tmprss6+/+ littermates (p=.005). However, Tmprss6-/- fetuses also were not pale, and they showed no significant difference in body mass compared to Tmprss6+/+ and Tmprss6+/− littermates. Surprisingly, hepatic non-heme iron concentration at E17.5 was significantly higher in Tmprss6-/- fetuses than in Tmprss6+/+ fetuses (p=.003). To determine if the increased hepcidin expression of Tmprss6-/- fetuses might affect iron homeostasis in their pregnant mothers, we measured iron parameters in Tmprss6+/− females gestating E17.5 litters that were enriched for either Tmprss6+/+ or Tmprss6-/- fetuses. No significant effects of fetal genotype on maternal iron parameters were observed. In summary, our results demonstrate that Tmprss6 regulates hepcidin expression in the fetal and neonatal periods in mice. However, Tmprss6 deficiency does not appear to be associated with systemic iron deficiency at these stages of development, and fetal Tmprss6 expression does not have a significant effect on maternal iron homeostasis in late gestation. These results may have implications for understanding the maintenance of iron homeostasis in early development, and may provide insight into the evolution of IRIDA as well as other disorders of iron homeostasis. Disclosures: No relevant conflicts of interest to declare.

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