Plasma Iron Concentration Research Articles

APPLICATION OF NANOCLUSTER IRON–MOLYBDENE POLYOXOMETALATES FOR CORRECTION OF EXPERIMENTAL POSTHEMORRHAGIC ANEMIA

The widespread occurrence of anemia and the presence of side-effects of existing iron-containing drugs require the search for new drugs. In an experiment on male rats of the Wistar strain, posthemorrhagic anemia is simulated by collecting blood from the tail vein in an amount of 1.5% of body weight. Intramuscular administration of iron–molybdenum polyoxometallates in an amount of 1.5 mg/kg to rats with anemia results in a faster restoration of the content of red blood cells and hemoglobin, the hematocrit value in the blood, the concentration of iron in the blood plasma, and the content of erythrocyte precursors in the bone marrow, which recover one to seven days earlier than the parameters measured in a control group of untreated animals.

Rapid growth is a dominant predictor of hepcidin suppression and declining ferritin in Gambian infants.

Iron deficiency and iron deficiency anemia are highly prevalent in low-income countries, especially among young children. Hepcidin is the major regulator of systemic iron homeostasis. It controls dietary iron absorption, dictates whether absorbed iron is made available in circulation for erythropoiesis and other iron-demanding processes, and predicts response to oral iron supplementation. Understanding how hepcidin is itself regulated is therefore important, especially in young children. We investigated how changes in iron-related parameters, inflammation and infection status, seasonality, and growth influenced plasma hepcidin and ferritin concentrations during infancy using longitudinal data from two birth cohorts of infants in rural Gambia (n=114 and n=193). This setting is characterized by extreme seasonality, prevalent childhood anemia, undernutrition, and frequent infection. Plasma was collected from infants at birth and at regular intervals, up to 12 months of age. Hepcidin, ferritin and plasma iron concentrations declined markedly during infancy, with reciprocal increases in soluble transferrin receptor and transferrin concentrations, indicating declining iron stores and increasing tissue iron demand. In cross-sectional analyses at 5 and 12 months of age, we identified expected relationships of hepcidin with iron and inflammatory markers, but also observed significant negative associations between hepcidin and antecedent weight gain. Correspondingly, longitudinal fixed effects modeling demonstrated weight gain to be the most notable dynamic predictor of decreasing hepcidin and ferritin through infancy across both cohorts. Infants who grow rapidly in this setting are at particular risk of depletion of iron stores, but since hepcidin concentrations decrease with weight gain, they may also be the most responsive to oral iron interventions.

Iron Oxide Nanoparticle Formulations for Supplementation.

Intravenous (IV) iron is widely used to provide supplementation when oral iron is ineffective or not tolerated. All commercially available intravenous iron formulations are comprised of iron oxyhydroxide cores coated with carbohydrates of varying structure and branch characteristics. The diameter of the iron-carbohydrate complexes ranges from 5-100 nm and meets criteria for nanoparticles. Clinical use of IV iron formulations entered clinical practice beginning of the late 1950s, which preceded the nanomedicine exploration frontier. Thus, these agents were approved without full exploration of labile iron release profiles or comprehensive biodistribution studies. The hypothesis for the pathogenesis of acute oxidative stress induced by intravenous iron formulations is the release of iron from the iron-carbohydrate structure, resulting in transient concentrations of labile plasma iron and induction of the Fenton chemistry and the Haber-Weiss reaction promoting formation of highly reactive free radicals such as the hydroxyl radical. Among available IV iron formulations, products with smaller carbohydrate shells are more labile and more likely to release labile iron directly into the plasma (i.e., before metabolism by the reticuloendothelial system). The proposed biologic targets of labile-iron-induced oxidative stress include nearly all systemic cellular components including endothelial cells, myocardium, liver as well as low density lipoprotein and other plasma proteins. Most studies have relied on plasma pharmacokinetic analyses that require many model assumptions to estimate contribution of the iron-carbohydrate complex to elevations in serum iron indices and hemoglobin. Additionally, the commercially available formulations have not been well studied with regard to optimal dosing regimens, long-term safety and comparative efficacy. The IV iron formulations fall into a class defined by the Food and Drug Administration as "Complex Drugs" and thus present considerable challenges for bioequivalence evaluation.

Levels of Zinc, Magnesium and Iron in Children with Attention Deficit Hyperactivity Disorder

Background: Attention deficit hyperactivity disorder is a common multifactorial and complex neuro developmental disorder often persisting through adolescence and adulthood. Indications of nutritional treatments with omega-3 fatty acids, and minerals like zinc, magnesium, iron, etc. are gaining importance. We therefore sought to estimate ,and compare the mineral content of zinc, magnesium, and iron in the plasma of ADHD diagnosed children with normal non-ADHD children, and establish a correlation if any with the disorder symptoms. Methods and findings: Psychiatric evaluation was performed using the Diagnostic and Statistical Manual IV and plasma elemental analysis using atomic absorption spectrophotometry. Low levels of zinc, magnesium and iron were observed in ADHD children when compared to their healthy controls. Conclusion: Children with ADHD exhibit lower concentrations of plasma zinc, magnesium, and iron as compared to normal controls which could be correlated with the disorder symptoms in ADHD.

Evaluation of Serum Iron and Transferrin in Idiopathic Nephrotic Syndrome Patients Attending Al-Hussein Pediatric Nephrology Clinic

Background: Nephrotic syndrome is characterized by excessive urinary excretion of albumin and other intermediated-size plasma proteins such as transferrin.. Excessive urinary losses of transferrin can produce low serum transferrin level that may lead to low plasma iron concentration and consequently the development of iron resistant microcytic hypochromic anemia. The aim of the work to evaluate changes in serum iron and transferrin and the relationship between the serum and urinary transferrin in the active and remission state of nephrotic syndrome Patients and methods: The present work included fifty children with idiopathic nephrotic syndrome (INS), divided into 2 groups: group A (25 cases in activity) and group B (25 cases in remission). These two groups were age and sex matched with a mean age of (7.74 ± 2.45). All patients in this work were clinically evaluated together with routine laboratory investigations. Serum albumin and urinary alb. /creatinine were assessed. Levels of serum iron, serum ferritin, serum transferrin and urinary transferrin were measured. Results: This work shows that the level of hemoglobin, MCV, HCT were statistically significantly lower in the cases in active state than cases in remission. The mean serum iron, serum ferritin and serum transferrin were significantly lower in the cases in active state than in the cases in remission .The mean urinary transferrin was statistically significantly higher in the cases in active state than in the cases with remission. Conclusion: Urinary transferrin can be considered a reliable parameter for early prediction of iron deficiency anemia in children with active nephrotic syndrome.

Regulators of hepcidin expression.

Iron, an essential nutrient, is required for many biological processes but is also toxic in excess. The lack of a mechanism to excrete excess iron makes it crucial for the body to regulate the amount of iron absorbed from the diet. This regulation is mediated by the hepatic hormone hepcidin. Hepcidin also controls iron release from macrophages that recycle iron and from hepatocytes that store iron. Hepcidin binds to the only known iron export protein, ferroportin, inducing its internalization and degradation and thus limiting the amount of iron released into the plasma. Important regulators of hepcidin, and therefore of systemic iron homeostasis, include plasma iron concentrations, body iron stores, infection and inflammation, hypoxia and erythropoiesis, and, to a lesser extent, testosterone. Dysregulation of hepcidin production contributes to the pathogenesis of many iron disorders: hepcidin deficiency causes iron overload in hereditary hemochromatosis and non-transfused β-thalassemia, whereas overproduction of hepcidin is associated with iron-restricted anemias seen in patients with chronic inflammatory diseases and inherited iron-refractory iron-deficiency anemia. The present review summarizes our current understanding of the molecular mechanisms and signaling pathways contributing to hepcidin regulation by these factors and highlights the issues that still need clarification.

Nutritional Infertility and Ameliorative Measures in Dairy Animals of Middle Gujarat

Fertility improvement camps were organized in different villages of middle Gujarat covering 1481 breedable cattle and buffaloes with the history of impaired fertility. The reproductive status of animals was ascertained through gynaeco-clinical examination per rectum. Blood sampling (n=305) was done from representative groups of animals to know the nutritional status. All non-infectious infertile animals were dewormed using either Inj. Ivermectin 100 mg s/c or bolus Fenbendazole + Ivermectin 3.0 g orally. Anestrus animals (n=265) were then nutritionally supplemented either with chelated area specific mineral mixture (ASMM, 50-60 g/d/h) or multi-minerals boli - one on alternate day, with and without bypass fat (75-80 g/d/h) for one month along with an advice to improve feeding level, estrus detection and timely breeding. Revisits were made after 2.5-3.0 months to check the reproductive status. The mean blood glucose concentrations were significantly lower (p less than 0.05), while total cholesterol and zinc levels were higher (p less than 0.05) in anestrus than in subestrus and/or repeat breeding cows and buffaloes. Moreover, the plasma total cholesterol levels in buffaloes were just one half to those of cows. Further, the plasma total protein, calcium, phosphorus, magnesium, iron, copper and cobalt concentrations were found to be nonsignificantly higher in repeat breeders than in anestrus or subestrus cows and buffaloes. Calcium was deficient in some 20% animals and calcium: phosphorus ratio varied from 1:1 to 1.8:1 in animals under different areas of study indicating its role in causing infertility in dairy animals. Supplementation of ASMM, multi-mineral boli alone or in combination with bypass fat in pubertal /postpartum anestrus animals resulted in 34-56% estrus induction response and 33-50% conception rate, both being better with mineral plus bypass fat supplementation than minerals alone.

A Simple and Portable Reader to Analyze Concentration of Iron in Blood Plasma via Colorimetric Analysis

This paper presents a simple and portable body iron reader to analyze the concentration of iron via colorimetric analysis. Through this approach, early diagnosis can be made for diseases such as iron deficiency anemia (IDA) and thalassemia. The uses of spectrophotometer to analyze a concentration of analyte in a sample can be reconsidered. Spectrophotometer nowadays is bulky and very expensive. The proposed portable reader can gives the user a result of concentration of analyte in a sample solution almost the same as the commercially available spectrophotometer. Through a comparison, the portable body iron reader managed to obtain a 0.9986 coefficient of determination value which has only 0.13% of error. Moreover, this device can works with a battery without the needs of power source.

Use of radiative properties to determine temperature and vapours concentration in MAG welding arc (Ar–CO2–Fe plasmas)

This paper introduces a method allowing a fast determination of space- and time-resolved plasma temperature and iron concentration in MAG arcs during the high-current phase. This method consists of measuring the plasma spectral radiation of a 82%Ar–18%CO2 plasma with iron vapours using a high-speed camera filtered by narrow band filters in the spectral intervals of 570–590 nm and 606–627 nm respectively; calculating theoretically the dependence of the absolute emissivity ε570–590 nm and relative emissivity ε570–590 nm/ε607–627 nm versus the plasma temperature and the iron concentration, and comparing the two results in order to deduce the plasma temperature (T) and iron concentration (YFe) fields of the experimental measurements. The evolution of their profile in time and space are coupled to arc recorded images. This method has also been validated for three layers of plasma at the positions of 0.5 mm, 1.5 mm and 2.5 mm above the workpiece by using a high-resolution spectrometer and adopting other existing diagnostics such as Stark broadening. The plasma temperature and iron concentration show good agreement throughout the different methods, which demonstrates the effectiveness of this new method.

Hepcidin Protects against Lethal Escherichia coli Sepsis in Mice Inoculated with Isolates from Septic Patients.

Iron is an essential micronutrient for most microbes and their hosts. Mammalian hosts respond to infection by inducing the iron-regulatory hormone hepcidin, which causes iron sequestration and a rapid decrease in the plasma and extracellular iron concentration (hypoferremia). Previous studies showed that hepcidin regulation of iron is essential for protection from infection-associated mortality with the siderophilic pathogens Yersinia enterocolitica and Vibrio vulnificus However, the evolutionary conservation of the hypoferremic response to infection suggests that not only rare siderophilic bacteria but also common pathogens may be targeted by this mechanism. We tested 10 clinical isolates of Escherichia coli from children with sepsis and found that both genetic iron overload (by hepcidin-1 knockout [HKO]) and iatrogenic iron overload (by intravenous iron) potentiated infection with 8 out of the 10 studied isolates: after peritoneal injection of E. coli, iron-loaded mice developed sepsis with 60% to 100% mortality within 24 h, while control wild-type mice suffered 0% mortality. Using one strain for more detailed study, we show that iron overload allows rapid bacterial multiplication and dissemination. We further found that the presence of non-transferrin-bound iron (NTBI) in the circulation is more important than total plasma or tissue iron in rendering mice susceptible to infection and mortality. Postinfection treatment of HKO mice with just two doses of the hepcidin agonist PR73 abolished NTBI and completely prevented sepsis-associated mortality. We demonstrate that the siderophilic phenotype extends to clinically common pathogens. The use of hepcidin agonists promises to be an effective early intervention in patients with infections and dysregulated iron metabolism.

Iron bioavailability of four iron sources used to fortify infant cereals, using anemic weaning pigs as a model.

Iron (Fe) deficiency anemia in young children is a global health concern which can be reduced by Fe fortification of foods. Cereal is often one of the first foods given to infants, providing adequate quantities of Fe during weaning. In this work, we have compared iron bioavailability and iron status of four iron sources used to fortify infant cereals, employing piglets as an animal model. The study was conducted on 36 piglets, 30 of them with induced anemia. From day 28 of life, the weaned piglets were fed with four experimental diets (n = 6) each fortified with 120mg Fe/kg by ferrous sulfate heptahydrate (FSH), electrolytic iron (EI), ferrous fumarate (FF), or micronized dispersible ferric pyrophosphate (MDFP) for another 21days. In addition, one group of six anemic piglets fed with the basal diet with no iron added (Control-) and a Control+ group of non-anemic piglets (n = 6) were also studied. Blood indicators of iron status were measured after depletion and during the repletion period. The Fe content in organs, hemoglobin regeneration efficiency, and relative bioavailability (RBV) was also determined. The Fe salts adequately treated anemia in the piglets, allowing the animals to recover from the anemic state, although EI was less efficient with regard to replenishing Fe stores giving lower concentrations of plasma ferritin and iron in the spleen, liver, lung, and kidney. In addition, the RBV of EI was 88.27% with respect to the reference iron salt (FSH). Ferrous fumarate and MDFP were equally as bioavailable as the reference salt, and were used significantly better than EI in piglets. These results contribute to extend the evidence-based results for recommending the most suitable fortificant for infant cereals.

Haemochromatosis.

Haemochromatosis is defined as systemic iron overload of genetic origin, caused by a reduction in the concentration of the iron regulatory hormone hepcidin, or a reduction in hepcidin-ferroportin binding. Hepcidin regulates the activity of ferroportin, which is the only identified cellular iron exporter. The most common form of haemochromatosis is due to homozygous mutations (specifically, the C282Y mutation) in HFE, which encodes hereditary haemochromatosis protein. Non-HFE forms of haemochromatosis due to mutations in HAMP, HJV or TFR2 are much rarer. Mutations in SLC40A1 (also known as FPN1; encoding ferroportin) that prevent hepcidin-ferroportin binding also cause haemochromatosis. Cellular iron excess in HFE and non-HFE forms of haemochromatosis is caused by increased concentrations of plasma iron, which can lead to the accumulation of iron in parenchymal cells, particularly hepatocytes, pancreatic cells and cardiomyocytes. Diagnosis is noninvasive and includes clinical examination, assessment of plasma iron parameters, imaging and genetic testing. The mainstay therapy is phlebotomy, although iron chelation can be used in some patients. Hepcidin supplementation might be an innovative future approach.

Genetic hemochromatosis: Pathophysiology, diagnostic and therapeutic management

The term hemochromatosis (HC) corresponds to several diseases characterized by systemic iron overload of genetic origin and affecting both the quality of life and life expectancy. Major improvement in the knowledge of iron metabolism permits to divide these diseases into two main pathophysiological categories. For most HC forms (types 1, 2, 3 and 4B HC) iron overload is related to cellular hepcidin deprivation which causes an increase of plasma iron concentration and the appearance of plasma non-transferrin bound iron. In contrast, iron excess in type 4A ferroportin disease is related to decreased cellular iron export. Whatever the HC type, the diagnosis rests on a non-invasive strategy, combining clinical, biological and imaging data. The mainstay of the treatment remains venesection therapy with the perspective of hepcidin supplementation for hepcidin deprivation-related HC. Prevention of HC is critical at the family level and, for type 1 HC, remains a major goal, although still debated, at the population level.

Iron supplementation in mouse expands cellular innate defences in spleen and defers lethal malaria infection

The co-endemicity of malnutrition, erythrocytopathies, transmissible diseases and iron-deficiency contribute to the prevalence of chronic anaemia in many populations of the developing world. Although iron dietary supplementation is applied or recommended in at risk populations, its use is controversial due to undesirable outcomes, particularly regarding the response to infections, including highly prevalent malaria. We hypothesized that a boosted oxidative stress due to iron supplementation have a similar impact on malaria to that of hereditary anaemias, enhancing innate response and conditioning tissues to prevent damage during infection. Thus, we have analysed antioxidant and innate responses against lethal Plasmodium yoelii during the first five days of infection in an iron-supplemented mouse. This murine model showed high iron concentration in plasma with upregulated expression of hemoxygenase-1. The sustained homeostasis after this extrinsic iron conditioning, delayed parasitemia growth that, once installed, developed without anaemia. This protection was not conferred by the intrinsic iron overload of hereditary hemochromatosis. Upon iron-supplementation, a large increase of the macrophages/dendritic cells ratio and the antigen presenting cells was observed in the mouse spleen, independently of malaria infection. Complementary, malaria promoted the splenic B and T CD4 cells activation. Our results show that the iron supplementation in mice prepares host tissues for oxidative-stress and induces unspecific cellular immune responses, which could be seen as an advantage to promote early defences against malaria infection.

Can iron work for pigs as a booster?

AbstractIron deficiency is a common health problem in mammals, especially in growing piglets hence iron administration to suckling piglets is a routine practice in swine production.A total number of 160 weaners were allotted to two experimental groups according to body weight (I – cachectic underweight piglets; II – piglets with appropriate weaning body weight). Additionally, each group was divided into two subgroups, with iron administered to piglets in subgroups IA and IIA on the first day of the experiment. In order to monitor the weight gains in pigs, they were weighed twice. To estimate the haematological status, blood samples were taken on the weaning day from selected piglets (10 in each subgroup). Haematological analyses were conducted using Hb, Ht, RBC, MCV, MCH, MCHC as early anaemia indicators. Additionally plasma iron (PI) and total iron-binding capacity (TIBC) were assessed as parameters of the actual and potential circulating extracellular iron.The aim of the study was to investigate the effect of additional postweaning Fe supplementation on production results. A lower concentration of PI was noted in weaker piglets (Group IA and IB). Throughout the experiment higher daily gains were noted in Group II; differences between Group IIA and IA as well as IB were statistically confirmed at p≤ 0,01.It might be expected that an additional Fe dose applied in weaning piglets can be used as a growth promoter. On the other hand, in case of cachectic animals toxicity of supplemental iron must be taken into consideration.

The uremic toxin indoxyl sulfate interferes with iron metabolism by regulating hepcidin in chronic kidney disease.

Hepcidin secreted by hepatocytes is a key regulator of iron metabolism throughout the body. Hepcidin concentrations are increased in chronic kidney disease (CKD), contributing to abnormalities in iron metabolism. Levels of indoxyl sulfate (IS), a uremic toxin, are also elevated in CKD. However, the effect of IS accumulation on iron metabolism remains unclear. We used HepG2 cells to determine the mechanism by which IS regulates hepcidin concentrations. We also used a mouse model of adenine-induced CKD. The CKD mice were divided into two groups: one was treated using AST-120 and the other received no treatment. We examined control mice, CKD mice, CKD mice treated using AST-120 and mice treated with IS via drinking water. In the in vitro experiments using HepG2 cells, IS increased hepcidin expression in a dose-dependent manner. Silencing of the aryl hydrocarbon receptor (AhR) inhibited IS-induced hepcidin expression. Furthermore, IS induced oxidative stress and antioxidant drugs diminished IS-induced hepcidin expression. Adenine-induced CKD mice demonstrated an increase in hepcidin concentrations; this increase was reduced by AST-120, an oral adsorbent of the uremic toxin. CKD mice showed renal anemia, decreased plasma iron concentration, increased plasma ferritin and increased iron content in the spleen. Ferroportin was decreased in the duodenum and increased in the spleen. These changes were ameliorated by AST-120 treatment. Mice treated by direct IS administration showed hepatic hepcidin upregulation. IS affects iron metabolism in CKD by participating in hepcidin regulation via pathways that depend on AhR and oxidative stress.

Effect of physical activity and age on plasma copper, zinc, iron, and magnesium concentration in physically active healthy males

The concentration of nutritionally important minerals in circulation is under tight homeostatic control, however, physical activity and aging influence their body stores and nutritional requirement. The aim of this study was to evaluate the effect of both physical activity and age on plasma concentrations of copper, zinc, iron, and magnesium. Stratified cluster sampling was used for selection of study participants (N=360) belonging to three physical activity groups: sedentary, moderately active, and highly active on the basis of their physical activity levels as 1.53, 1.8, and 2.3, respectively. They were also divided into six different age groups (18-20, 21-25, 26-30, 31-35, 36-40, and 41-45y). We assessed nutritional status by determining their body composition using bioelectrical impedance method and measuring intake levels. Fasting blood samples were taken to separate plasma for analysis of copper, zinc, magnesium, and iron. There was a major difference (P<0.001) in the mean value of plasma copper, zinc, magnesium, and iron for the three activity groups. The plasma copper and iron concentrations were higher in the moderately active group (copper: 1.59±0.05mg/L, iron: 0.79±0.22mg/L) whereas zinc concentration was higher in the sedentary group (2.37±0.29mg/L). Both the highly and moderately active groups had higher plasma magnesium levels compared with the sedentary group. Plasma copper, zinc, magnesium, and iron levels also were influenced by age in a different pattern with respect to physical activity. Physical activity-related energy expenditure and age play a remarkable role in deciphering the plasma mineral levels in the healthy individuals.

MRNA Levels of Placental Iron and Zinc Transporter Genes Are Upregulated in Gambian Women with Low Iron and Zinc Status

Background: The role of the placenta in regulating micronutrient transport in response to maternal status is poorly understood.Objective: We investigated the effect of prenatal nutritional supplementation on the regulation of placental iron and zinc transport.Methods: In a randomized trial in rural Gambia [ENID (Early Nutrition and Immune Development)], pregnant women were allocated to 1 of 4 nutritional intervention arms: 1) iron and folic acid (FeFol) tablets (FeFol group); 2) multiple micronutrient (MMN) tablets (MMN group); 3) protein energy (PE) as a lipid-based nutrient supplement (LNS; PE group); and 4) PE and MMN (PE+MMN group) as LNS. All arms included iron (60 mg/d) and folic acid (400 μg/d). The MMN and PE+MMN arms included 30 mg supplemental Zn/d. In a subgroup of ∼300 mother-infant pairs, we measured maternal iron status, mRNA levels of genes encoding for placental iron and zinc transport proteins, and cord blood iron levels.Results: Maternal plasma iron concentration in late pregnancy was 45% and 78% lower in the PE and PE+MMN groups compared to the FeFol and MMN groups, respectively (P < 0.001). The mRNA levels of the placental iron uptake protein transferrin receptor 1 were 30–49% higher in the PE and PE+MMN arms than in the FeFol arm (P < 0.031), and also higher in the PE+MMN arm (29%; P = 0.042) than in the MMN arm. Ferritin in infant cord blood was 18–22% lower in the LNS groups (P < 0.024). Zinc supplementation in the MMN arm was associated with higher maternal plasma zinc concentrations (10% increase; P < 0.001) than in other intervention arms. mRNA levels for intracellular zinc-uptake proteins, in this case zrt, irt-like protein (ZIP) 4 and ZIP8, were 96–205% lower in the PE+MMN arm than in the intervention arms without added zinc (P < 0.025). Furthermore, mRNA expression of ZIP1 was 85% lower in the PE+MMN group than in the PE group (P = 0.003).Conclusion: In conditions of low maternal iron and in the absence of supplemental zinc, the placenta upregulates the gene expression of iron and zinc uptake proteins, presumably in order to meet fetal demands in the face of low maternal supply. The ENID trial was registered at www.controlled-trials.com as ISRCTN49285450.

Regulation of the Iron Homeostatic Hormone Hepcidin.

Iron is required for many biological processes but is also toxic in excess; thus, body iron balance is maintained through sophisticated regulatory mechanisms. The lack of a regulated iron excretory mechanism means that body iron balance is controlled at the level of absorption from the diet. Iron absorption is regulated by the hepatic peptide hormone hepcidin. Hepcidin also controls iron release from cells that recycle or store iron, thus regulating plasma iron concentrations. Hepcidin exerts its effects through its receptor, the cellular iron exporter ferroportin. Important regulators of hepcidin, and therefore of systemic iron homeostasis, include plasma iron concentrations, body iron stores, infection and inflammation, and erythropoiesis. Disturbances in the regulation of hepcidin contribute to the pathogenesis of many iron disorders: hepcidin deficiency causes iron overload in hereditary hemochromatosis and nontransfused β-thalassemia, whereas overproduction of hepcidin is associated with iron-restricted anemias seen in patients with chronic kidney disease, chronic inflammatory diseases, some cancers, and inherited iron-refractory iron deficiency anemia. This review summarizes our current understanding of the molecular mechanisms and signaling pathways involved in the control of hepcidin synthesis in the liver, a principal determinant of plasma hepcidin concentrations.

Comparative Effects of Inulin with Different Polymerization Degrees on Growth Performance, Blood Trace Minerals, and Erythrocyte Indices in Growing-Finishing Pigs

There are numerous reports of the effect of inulin on the bioavailability of mineral compounds. However, there are no conclusive reports concerning its beneficial impact (or lack thereof) in the case of such essential trace elements as iron, copper, or zinc. The aim of the study was to compare the effects of inulin addition with different degrees of polymerization (DPs) on growth performance in fatteners as well as on blood plasma concentrations of iron, copper, and zinc and selected hematological indices. The experiment was conducted throughout the fattening period (up to a body weight of approximately 115 kg) on 112 weaners with an initial weight of 25.0 ± 0.5 kg divided into 7 groups. The first group served as a control, while the other groups received increasing doses (1, 2, and 3 %) of standard inulin (SI; DPav ≥ 10) or long-chain inulin (LCI, DPav ≥ 23) in complete mixtures. Compared with the control, the supplementation of the mixtures with inulin increased the average daily gains, the final body weight, and the plasma content of trace elements (P < 0.05). An increased plasma zinc concentration was noted after application of inulin with a lower polymerization degree (P < 0.05). In turn, at a higher inulin polymerization degree, a higher final body weight and increased copper (P < 0.05), iron (P < 0.1), hemoglobin, mean corpuscular hemoglobin concentration (MCHC), and packed cell volume (PCV) levels were detected in animal blood (P < 0.05). The inulin addition was found to have modified the analyzed indices, and the optimal supplementation level was estimated at 20 g·kg−1 diet. Inulin with the higher DP exerted a more pronounced effect on the analyzed properties.