low-Fe Diet Research Articles

Dietary Iron Intake in Excess of Requirements Impairs Intestinal Copper Absorption in Sprague‐Dawley Rat Dams, Causing Copper Deficiency in Neonatal Pups

Consumption of a high-iron diet by previously iron-deficient rat dams causes copper insufficiency; however, pathophysiological outcomes in their offspring are unknown. We hypothesized that high-iron consumption by dams would also lead to copper depletion in suckling pups. Accordingly, 8-9-week-old, pregnant Sprague-Dawley rats were randomized and initially fed a low-Fe diet for ≍7 days (to induce iron deficiency), and then switched to one of five AIN-93G-based diets, with variable iron levels (normal [80 ppm] to high [up to 1600 ppm]) and marginal copper content (2 ppm; normal is 6-7 ppm). Dams were fed these diets throughout the remainder of pregnancy and during lactation, until the termination of the experiments (when suckling pups were 13-15 days of age). Subsequently, hematological parameters and serum and tissue iron concentrations were measured, and copper biomarker analyses were performed. Intestinal 64Cu absorption and tissue distribution in dams, and 64Cu delivery to the suckling pups, were also assessed. Results showed that serum para-phenylenediamine (pPD) oxidase activity (reflecting serum ceruloplasmin [Cp]) was suppressed (p<0.05) in dams consuming 5-fold excess iron and in pups suckling dams that consumed iron at 10-fold excess. Hepatic nonheme iron concentrations increased in dams and pups (p<0.05) as dietary iron levels increased (possibly due to inhibition of Cp activity, which is required for iron release from hepatocytes). When dams consumed iron at 20-fold above requirements, pup growth was impaired (p<0.05), possibly due to copper depletion, as also indicated by decreases in erythrocyte SOD activity (which accurately reflects copper status) (p<0.05). Moreover, in iron-supplemented dams, intestinal copper (64Cu) absorption and 64Cu activity in blood, liver, and spleen were all decreased (p<0.05). A similar trend was also noted in pups suckling dams consuming exces iron, with 64Cu accumulation in blood, liver, and spleen (p<0.05) being lower than in controls. We conclude that maternal intake of excessive iron (~10-fold above the dietary recommendation) impairs absorption of dietary copper and concomitantly depletes copper in neonatal pups. Low milk copper content was the most likely explanation for this outcome, although this remains to be experimentally proven.

Pemberian Ekstrak Kacang Hijau (Phaseolus Radiatus) terhadap Peningkatan Hemoglobin dan Ferritin pada Wistar Putih Anemia

Kacang hijau, selain mengandung protei, karbohidrat dan lemak juga mengandung zat besi dan vitamin C yang terbukti dapat memperbaiki anemia pada wanita hamil. Kadar zat besi yang tinggi berpotensi meningkatkan produksi ROS reaksi fenton. Penelitian ini untuk membuktikan bahwa pemberian ekstrak kacang hijau dapat meningkatkan kadar Hb dan kadar Ferritin pada tikus wistar putih.Penelitian ini menggunakan rancangan Post Test Only Control Group Design.Sebanyak 25 ekor tikus wistar dibagi menjadi 5 kelompok yaitu kelompok normal (Nor-G), kelompok control negative(Neg-G)dan kelompok perlakuan yang mendapatkan ekstrak kacang hijau 0,18g (GP-0,18), 0,36g (GP-0,36) dan 0,72g(GP-0,72). Diet rendah Fe dan ekstrak kacang hijau diberikan semala 14 hari. Kadar Hb diukur dengan metode Sahli dan Kadar Ferritin menggunakan Kit Immulite Ferritin. Kadar Hd dan ferritin pada kelompok yang mendapatkan ekstrak kacang hijau 0,18g (75,56), 0,36g (90,98) dan 0,72g (95,87) lebih tinggi bermakna, p&lt;0,05. Hasil penelitian ini menunjukkan bahwa pemberian ekstrak kacang hijau terbukti meningkatkan kadar Hb dan Kadar Ferritin.

Iron deficiency induces female infertile in order to failure of follicular development in mice.

Iron is important for many cellular functions, including ATP synthesis and cell proliferation. Insufficient of iron in the diet causes iron deficiency anemia (IDA), which often occurs in people living in the world. Since 50% of women with IDA show amenorrhea, the relationship of between iron deficiency and reproductive function was assessed using mice fed a low Fe diet (LFD). The estrous cycle in the LFD mice was blocked at diestrus, which impair follicle development, and fertility. Further, even LFD mice were injected with exogenous pregnant mare serum gonadotropin (PMSG), follicular development was ceased at the secondary follicle stage, and preovulatory follicles were not observed. Amount of ATP decreased in the ovary of the LFD mice, and expression of follicle development markers (Fshr, Cyp19a1, Ccnd2) and estradiol-17β (E2) was low level compared to levels mice fed a normal diet. Feeding a normal diet with sufficient iron to the LFD mice for an additional 3 weeks completely reversed absence the effects of iron insufficient on the estrous cycle and infertility. Thus, iron restriction depresses ovary functions, especially follicular development from secondary follicle to antral follicles and infertility. These effects are fully reversible by supplementation of a normal diet containing iron.

Iron status, weight changes and body composition during anemia recovery in an experimental model: the effect of fermented goat or cow milk

Objective: to provide detailed information on iron status, body changes, food intake, hepatosomatic index, and body composition during recovery from severe iron deficiency anemia with fermented cow or goat milk. Material and methods: sixty male Wistar albino rats were divided into two experimental groups (control and anemic) and fed ad libitum an AIN-93G diet for 40 days, receiving a normal Fe diet (45 mg/kg of diet) or a low-Fe diet (5 mg/kg of diet), respectively. After induction of anemia, both the control and anemic groups were additionally fed for 30 days either a fermented cow milk-based or fermented goat milk-based diet with normal Fe content. Hematological and iron-related biochemical parameters, weight changes, food intake, hepatosomatic index, and body composition were assessed. Results: The hepatosomatic index was higher in the anemic group versus the control group. In both groups fed a fermented goat milk-based diet the hepatosomatic index was higher due to lower body weight and a higher liver weight. Food intake, weight gain, and total body fat were lower, whereas lean mass and free and total water were higher in the anemic group as compared to the control group. In both animal groups fed a fermented goat milk-based diet body weight and body fat were lower and the percentages of lean mass and free water and total water were higher. Conclusion: Iron deficiency decreased weight gain, lean mass, and body fat, indicating lower energy stores. Fermented goat milk-based diet recovers more efficiently iron status, decreased adiposity, and increased energy expenditure.

Fermented Goat Milk Consumption Enhances Brain Molecular Functions during Iron Deficiency Anemia Recovery.

Iron deficiency anemia (IDA) is one of the most prevalent nutritional deficiencies worldwide. Iron plays critical roles in nervous system development and cognition. Despite the known detrimental consequences of IDA on cognition, available studies do not provide molecular mechanisms elucidating the role of iron in brain functions during iron deficiency and recovery with dairy components. In this study, 100 male Wistar rats were placed on a pre-experimental period of 40 days and randomly divided in two groups: a control group receiving a normal-Fe diet, (45 mg/kg), and an Fe-deficient group receiving a low-Fe diet (5 mg/kg). At day 40, 10 rats per group were sacrificed to anemia control, and 80 rats were divided into eight experimental groups fed with fermented goat or cow milk-based diets, with normal Fe content or Fe overload (450 mg/kg) for 30 days. IDA decreased most of the parameters related to brain molecular functions, namely dopamine, irisin, MAO-A, oxytocin, β-endorphin, and α-MSH, while it increased synaptophysin. These alterations result in an impairment of brain molecular functions. In general, during anemia recovery, fermented goat milk diet consumption increased dopamine, oxytocin, serotonin, synaptophysin, and α-MSH, and decreased MAO-A and MAO-B, suggesting a potential neuroprotective effect in brain functions, which could enhance brain molecular functions.

Iron Deficiency and Neuroendocrine Regulators of Basal Metabolism, Body Composition and Energy Expenditure in Rats.

Although dietary iron is a determinant of iron status in animals, body fat mass has been reported to have an inverse association with iron status in human studies. The goal of this study was to determine the relationship between Fe homeostasis, body composition, energy expenditure and neuroendocrine regulators for severe Fe-deficiency anaemia. Forty male Wistar albino rats recently weaned were divided at random into two groups: the control group was fed the basal diet, AIN-93G diet (normal-Fe) and the anaemic group received a low-Fe diet for 40 days. Neuroendocrine parameters that regulate basal metabolism and appetite (thyroid hormones, ghrelin, glucose-dependent insulinotropic polypeptide (GIP), glucagon, insulin, adrenocorticotropic hormone and corticosterone), body composition, respiratory volumes, energy expenditure, haematological and biochemical were assessed. Total body fat was lower, whereas lean mass, free and total water were higher in the anemic group. O2 consumption, CO2 production, energy expenditure (EE) and respiratory quotient (RQ) were lower in the Fe-deficient animals. Triiodothyronine and thyroxine hormones decreased, while thyroid-stimulating hormone increased in the anemic group. Circulating levels of ghrelin were lower in the anemic group, while GIP, glucagon, insulin, corticosterone and adrenocorticotropic hormone levels were higher. Fe-deficiency impairs weight gain in the rats, with marked reductions in lean mass and body fat, indicating lower energy stores.

Protective effects of fermented goat milk on genomic stability, oxidative stress and inflammatory signalling in testis during anaemia recovery

Oxidative stress is a harmful factor for male reproductive function, and a major cause of infertility. On the other hand, fermented goat milk has positive effects on anemia recovery and mineral metabolism. This study evaluated the effect of feeding rats with fermented milks during anaemia recovery on molecular mechanisms linked to oxidative stress and inflammatory signalling in rats reproductive system. Forty male Wistar rats were placed on a pre-experimental period of 40 days (control group, receiving normal-Fe diet and Fe-deficient group, receiving low-Fe diet). Lately, rats were fed with fermented goat or cow milk-based diets during 30 days. After feeding the fermented milks, Total antioxidant status (TAS) and non-esterified fatty acids (NEFA) increased and 8-hydroxy-2’-deoxyguanosine (8-OHdG), 15-F2t-isoprostanes and thiobarbituric acid reactive substances (TBARS) decreased in testis. DNA oxidative damage in testis germ cells was lower with fermented goat milk. Fermented goat milk reduced IL-6 and TNF-α in control animals, increasing INF-γ in control and anaemic rats. NRF2 and PGC-1α protein levels increased in testis after fermented goat milk consumption in control and anaemic rats. Fermented goat milk also increased TAS and decreased oxidative damage, protecting the main testis cell bioconstituents (lipids, proteins, DNA, prostaglandins) from oxidative damage and reduced inflammatory activity, preventing injuries to testis germinal epithelium. Fermented goat milk enhanced lipolysis, fatty acids degradation and immune response, attenuating inflammatory signalling, representing a positive growth advantage for testicular cells.

Administration of Mung Bean Extract (Phaseolus radiatus) in Increasing Hb and Ferritin Level and Decreasing Malondyaldehide (MDA) Level in Anaemic Rats

BACKGROUND: Mung bean, not only contains protein, carbohydrates, and fats, but also contains iron and vitamin C which are proven to overcome anemia in pregnant woman. High iron levels are potential to increase ROS production through fenton reaction.OBJECTIVE: to prove the administration of mungbean can increase Hb and ferritin levels and decreasing malondihaldehyde (MDA) in anaemic rats.METHODS: This research uses Post Test Only Control Group Design. A total of 25 anaemic rats were divided into 5 groups: normal group (Nor-G);negative control group (Neg-G), were given low Fe diet; and treatment group with low Fe and mung bean extract at dose of 0,18g/200g/days (GP-0,18), 0,36g/200g/days (GP-0.36), dan 0,72g/200g/days (GP-0.72). Low Fe diet and mung bean extract were administered for 14 days. Hb levels were measured using Sahli method, ferritine level using Immulite Ferritine Kit, and MDA were measured using TBA.RESULTS: Compare to Nor-G and Neg-G, levels of ferritin and Hb on groups with mung bean extract 0,18g (75.56), 0,36g (90.98) and 0,72g (95.87) were significantly higher (p &lt; 0.05). While MDA levels on groups with mung bean 0,18g (4.646), 0,36g (3.396) and 0,72g (1.92) were significantly lower than on Nor-G and Neg-G groups (p &lt; 0.05).CONCLUSION: The administration of mung bean extract can increase Hb and ferritin, also lower MDA level on anaemic rats.

Fermented goat milk consumption during anaemia recovery: ergogenic effect and improvement of skeletal muscle homeostasis.

Anaemia is associated with fatigue and diminished muscular oxygenation, which may affect skeletal muscle (SM). No studies are available about the SM modifications during anaemia recovery; therefore, the aim of this study is to study SM homeostasis during anaemia recovery with fermented milks. Forty male Wistar rats were placed on a pre-experimental period of 40days, divided in two groups (control group receiving normal-Fe diet and Fe-deficient group receiving low-Fe diet). Lately, rats were fed with fermented goat or cow milk-based diets, with normal-Fe content during 30days. After feeding the fermented milks, leptin, adiponectin, non-esterified fatty acids (NEFA) and protein expression (UCP1, PepT1 and irisin) within the SM were assessed. Adiponectin decreased in both groups of animals fed fermented goat milk, while leptin and NEFA increased. UCP1 protein expression increased in control and anaemic animals fed fermented goat milk. UCP1 also increased in both group of anaemic animals fed either fermented cow or goat milk in comparison with their controls. Irisin increased in both group of animals fed fermented goat milk. Finally, PepT1 also showed an increased expression in control and anaemic rats fed fermented goat milk and the anaemia also induced an over-expression of this transporter in animals fed either fermented cow or goat milk. Fermented goat milk consumption during anaemia recovery diminishes adiposity depots and enhances lipolysis, increasing UCP1, PepT1 and irisin protein expression, featuring an ergogenic effect in the SM which is an important endocrine regulator of body metabolism.

The effect of a low iron diet and early life methylmercury exposure in Daphnia pulex

Iron (Fe) deficiency increases risk for adverse health outcomes in humans; however little is known about the potential interaction with methylmercury (MeHg) exposure. Studies testing multiple stressor hypotheses are expensive and time consuming in mammalian model systems; therefore, determining relevance of alternative models is important. Daphnia pulex were fed standard or low-Fe diets of freshwater algae, Ankistrodesmus falcatus. MeHgCl (1600 ng/L) or vehicle was added to culture media for 24 h during early life, and the combinatorial effects of a low-Fe diet and MeHg exposure on lifespan, maturation time, and reproduction were evaluated. Lipid storage effects were measured using image analysis of Oil Red O staining and triacylglyceride quantification. Our results show a dose-dependent reduction in lifespan in D. pulex fed low Fe diets. Lipid analysis suggests an interactive effect of diet and MeHg exposure, with MeHg exposure increasing lipid storage in D. pulex fed a low-Fe diet. These findings suggest the effects of dietary iron intake and early life MeHg exposure in D. pulex may be mediated by changes in energetics that result in differential lipid storage. Therefore, lipid storage in D. pulex may be a useful screen for detecting long-term effects of multiple stressors early in life.

Identifying the threshold of iron deficiency in the central nervous system of the rat by the auditory brainstem response.

The deleterious effects of anemia on auditory nerve (AN) development have been well investigated; however, we have previously reported that significant functional consequences in the auditory brainstem response (ABR) can also occur as a consequence of marginal iron deficiency (ID). As the ABR has widespread clinical use, we evaluated the ability of this electrophysiological method to characterize the threshold of tissue ID in rats by examining the relationship between markers of tissue ID and severity of ABR latency defects. To generate various levels of ID, female Long-Evans rats were exposed to diets containing sufficient, borderline, or deficient iron (Fe) concentrations throughout gestation and offspring lifetime. We measured hematological indices of whole body iron stores in dams and offspring to assess the degree of ID. Progression of AN ID in the offspring was measured as ferritin protein levels at different times during postnatal development to complement ABR functional measurements. The severity of ABR deficits correlated with the level of Fe restriction in each diet. The sufficient Fe diet did not induce AN ID and consequently did not show an impaired ABR latency response. The borderline Fe diet, which depleted AN Fe stores but did not cause systemic anemia resulted in significantly increased ABR latency isolated to Peak I.The low Fe diet, which induced anemia and growth retardation, significantly increased ABR latencies of Peaks I to IV. Our findings indicate that changes in the ABR could be related to various degrees of ID experienced throughout development.

Folic acid supplemented goat milk has beneficial effects on hepatic physiology, haematological status and antioxidant defence during chronic Fe repletion.

The aim of the current study was to asses the effect of goat or cow milk-based diets, either normal or Fe-overloaded and folic acid supplement on some aspects of hepatic physiology, enzymatic antioxidant defence and lipid peroxidation in liver, brain and erythrocyte of control and anaemic rats after chronic Fe repletion. 160 male Wistar rats were placed on 40d in two groups, a control group receiving normal-Fe diet and the Fe-deficient group receiving low Fe diet. Lately, the rats were fed with goat and cow milk-based diets during 30d, with normal-Fe content or Fe-overload and either with normal folic or folic acid supplemented. Fe-overload increased plasma alanine transaminase and aspartate transaminase levels when cow milk was supplied. Dietary folate supplementation reduced plasma transaminases levels in animals fed goat milk with chronic Fe overload. A remarkable increase in the superoxide dismutase activity was observed in the animals fed cow milk. Dietary folate supplement lead to a decrease on the activity of this enzyme in all the tissues studied with both milk-based diets. A concomitant increment in catalase was also observed. The increase in lipid peroxidation products levels in rats fed cow milk with Fe-overload, suggest an imbalance in the functioning of the enzymatic antioxidant defence. In conclusion, dietary folate-supplemented goat milk reduces both plasma transaminases levels, suggesting a hepatoprotective effect and has beneficial effects in situation of Fe-overload, improving the antioxidant enzymes activities and reducing lipid peroxidation.

Goat milk consumption modulates liver divalent metal transporter 1 (DMT1) expression and serum hepcidin during Fe repletion in Fe-deficiency anemia

Iron deficiency is the most prevalent micronutrient deficiency worldwide. In spite of the crucial role of hepatocyte divalent metal transporter 1 (DMT1) and hepcidin in Fe metabolism, to date, no studies have directly tested the role of these proteins in liver Fe metabolism during Fe repletion after induced Fe-deficiency anemia. Therefore, the aim of the current study was to assess the effect of goat or cow milk-based diets on Fe metabolism in one of the main body storage organs, the liver, during the course of Fe repletion with goat or cow milk-based diets in anemic rats. Animals were placed on a preexperimental period of 40 d, a control group receiving a normal-Fe diet and the Fe-deficient group receiving a low-Fe diet (5mg of Fe/kg of diet). Rats were fed for 30 d with goat or cow milk-based diets with normal Fe content (45mg of Fe/kg of diet). The hematological parameters, serum hepcidin, hepatosomatic index, liver Fe content, and liver DMT1 expression were determined. During the recovery of the anemia with milk-based diets, the restoration of liver Fe content and hematological parameters, especially with goat milk, increased the red blood cell count, favoring the oxygen supply and weight gain. Moreover, goat milk consumption potentiates liver DMT1 expression, enhancing Fe metabolism and storage. In addition, the increase in serum hepcidin in anemic rats observed in the current study also explains and supports the higher liver Fe content after supplying goat milk, because it blocks the liberation of Fe from hepatocytes, increasing its storage in liver.

The Effect of Date (Phoenix dactylifera) Juice on Haemoglobin Level An Experimental Study in Iron Supplemented Rats

There has been more research on the iron supplementation. Date juice has been shown to be rich in iron. It has been reported to increase the hemoglobin level in rats. Few studies has been conducted on the effect of date juice on the hemoglobin level in male white Wistar rats fed low iron diet.This research was conducted to evaluate the effect of (Phoenix dactylifera) juice on haemoglobin level in iron supplemented rats. In this experimental study using post test control group design, 24 male white Wistar rats were divided into 4 groups. G-I served as the control group (standard diet and aquadest). G II was given the low Fe diet and aquadest for 21 d. G-III,IV were given the low fe diet and aquadest plus date juice at the concentration of 50%, 100% respectively. The treatment was given for 14 days. Spectrophotometer was used to assess the haemoglobin level of rats. One way anova followed by Post Hoc LSD was applied for the data analysis. Mean of hemoglobin (g/dl) level for the four groups were 12,03, 7.72, 9.25, 10.35 respectively. Test resulted in p&lt;0.05. Post Hoc LSD test resulted in a significant different between K-I and G-II, G-III, G-IV ;G-II and G-III, G-IV ;G-III and G-IV. In conclusion, date juice increases the haemoglobin level in male white rats fed on the low fe diet.

Plasma and liver lipids of iron‐deficient rats with excessive dietary manganese

Recently, manganese (Mn) toxicity in a child with iron (Fe) deficiency was reported. Since there is a possibility that effect of Fe deficiency is augmented by excessive Mn, plasma and liver lipids in rats were analyzed. Thirty‐two 3‐week‐old male Wistar rats were randomly assigned in a 2×2 factorial design (eight rats each): FeA/MnA group fed AIN‐93G diet, FeA/MnE group fed a high Mn diet (1000 ppm), FeD/MnA group fed a low‐Fe diet (no supplemental Fe), and FeD/MnE group fed a low Fe/high Mn diet. Rats were fed ad libitum for six weeks and then fasted overnight. Plasma and liver lipids were measured enzymatically. Data were analyzed by two‐way ANOVA and P values less than 0.05 was considered significant. The low Fe diet increased plasma triglycerides, phospholipids and free fatty acids. The low Fe diet decreased plasma glucose and HDL cholesterol, and concomitant high Mn augmented their reduction. The low Fe diet increased liver triglycerides. Both the low Fe and high Mn diets increased liver phospholipids. The low Fe diet increased liver cholesterol, and concomitant high Mn attenuated its rise. These results suggest that concomitant high dietary Mn modulates changes in plasma and liver lipids induced by Fe deficiency. Partly supported by Japan Society for the Promotion of Science Grants‐in‐Aid for Scientific Research (C) (22500772).

Iron Metabolism in a Rodent Model of Menkes Disease (Brindled Mice)

The Menkes copper‐transporting ATPase (Atp7a) is induced in the rodent duodenum during iron deficiency. To understand its role in intestinal iron metabolism, we thus initiated an investigation in Atp7a mutant mice (Brindled). As mutant mice die perinatally of severe copper deficiency, IP copper injections were administered at 7 and 9 days‐of‐age. Mice developed normally thereafter and were similar in size and activity level to wt littermates. Subsequently, mice were deprived of dietary iron for 3 wks and iron and copper homeostasis was studied. Several important observations arose from these analyses, including: 1) mutant mice on control diet were copper deficient and anemic with no changes in iron status; 2) mutant mice on iron‐deficient diet were iron and copper deficient and more significantly anemic; 3) the transcriptional response to iron deficiency in enterocytes was seen only in mutant mice on low Fe diet, suggesting that the HIF2α‐mediated induction of iron and copper homeostasis‐related genes is triggered by iron levels and not hypoxia per se; and 4) Brindled mice had increased hepatic copper levels during iron deprivation, leading to a concomitant increase in serum ferroxidase activity, while no such changes were noted in control or low Fe wt mice. This study has thus revealed novel aspects of the iron‐copper connection and is the first to investigate iron homeostasis in a model of genetic copper deficiency.Grant Funding Source: NIH

Effect of Iron-nanoparticles and Iron-microparticles on Erythropoiesis and Iron-storage in Iron-deficiency Anemic Mice

Iron is an essential trace element for normal body’s functions. The restriction of iron availability directly limits erythropoiesis. The objective of this experiment was to compare the bioavailability of iron nanoparticles (Fe-NPs) with iron-microparticles (Fe-MPs) in anemic mice. There were four experimental groups including normal control group, iron-deficiency anemia (IDA) group, Fe-NPs group, and Fe-MPs group. Animals in normal group fed on an adequate iron-containing diet (45 ppm Fe). Meanwhile, the animals in the other three groups fed on a low Fe diet (4.5 ppm Fe) for 7 weeks. Double deionized water was supplied as drinking water ad libitum. After feeding for 3 weeks with the low Fe diet, the animals in Fe-NPs and Fe-MPs groups were orally treated with Fe-NPs or Fe-MPs at the daily dose of 40 mg/kg for 4 weeks. IDA group showed a markedly decreased red blood cell (RBC) count, hematocrit (Hct), and hemoglobin (Hb) values compared with normal group throughout experimental periods. Treatments of Fe-NPs or Fe-MPs for 4 weeks restored the decreased RBC count and hematological values similar to normal values. Fe-NPs group showed the faster restoration in the values than Fe-MPs as time passes. The iron contents of the upper small intestine in Fe-NPs and Fe-MPs groups were higher than normal group at weeks 2 and 4. Hepatic iron contents and lipid peroxidation were significantly increased by Fe-NPs and Fe-MPs treatments compared with IDA group as time increase. The iron contents in liver and ferritin deposits in spleen were identified in Fe-NPs and Fe-MPs groups similarly to normal group. These results indicate that oral administration of both Fe-NPs and Fe-MPs can recover anemia and Fe-NPs is more absorbable and available in the body than Fe-MPs.

Influence of cow or goat milk consumption on antioxidant defence and lipid peroxidation during chronic iron repletion

Despite Fe deficiency and overload having been widely studied, no studies are available about the influence of milk consumption on antioxidant defence and lipid peroxidation during the course of these highly prevalent cases. The objective of the present study was to assess the influence of cow or goat milk-based diets, either with normal or Fe-overload, on antioxidant defence and lipid peroxidation in the liver, brain and erythrocytes of control and anaemic rats after chronic Fe repletion. Weanling male rats were randomly divided into two groups: a control group receiving a normal-Fe diet (45 mg/kg) and an anaemic group receiving a low-Fe diet (5 mg/kg) for 40 d. Control and anaemic rats were fed goat or cow milk-based diets, either with normal Fe or Fe-overload (450 mg/kg), for 30 or 50 d. Fe-deficiency anaemia did not have any effect on antioxidant enzymes or lipid peroxidation in the organs studied. During chronic Fe repletion, superoxide dismutase (SOD) activity was higher in the group of animals fed the cow milk diet compared with the group consuming goat milk. The slight modification of catalase and glutathione peroxidise activities in animals fed the cow milk-based diet reveals that these enzymes are unable to neutralise and scavenge the high generation of free radicals produced. The animals fed the cow milk diet showed higher rates of lipid peroxidation compared with those receiving the goat milk diet, which directly correlated with the increase in SOD activity. It was concluded that goat milk has positive effects on antioxidant defence, even in a situation of Fe overload, limiting lipid peroxidation.

Iron absorption in hepcidin1 knockout mice

Hepcidin, the Fe-regulatory peptide, has been shown to inhibit Fe absorption and reticuloendothelial Fe recycling. The present study was conducted to explore the mechanism of in vivo Fe regulation through genetic disruption of hepcidin1 and acute effects of hepcidin treatment in hepcidin1 knockout (Hepc1-/-) and heterozygous mice. Hepcidin1 disruption resulted in significantly increased intestinal Fe uptake. Hepcidin injection inhibited Fe absorption in both genotypes, but the effects were more evident in the knockout mice. Hepcidin administration was also associated with decreased membrane localisation of ferroportin in the duodenum, liver and, most significantly, in the spleen of Hepc1-/- mice. Hypoferraemia was induced in heterozygous mice by hepcidin treatment, but not in Hepc1-/- mice, 4 h after injection. Interestingly, Fe absorption and serum Fe levels in Hepc1-/- and heterozygous mice fed a low-Fe diet were not affected by hepcidin injection. The present study demonstrates that hepcidin deficiency causes increased Fe absorption. The effects of hepcidin were abolished by dietary Fe deficiency, indicating that the response to hepcidin may be influenced by dietary Fe level or Fe status.

Iron bioavailability from ferric pyrophosphate in rats fed with fructan-containing yacon (Smallanthus sonchifolius) flour

The effects of inulin-type fructans (ITF)-containing yacon flour (YF) on Fe bioavailability from ferric pyrophosphate (FP) were evaluated in Fe-deficient rats using the Hb repletion efficiency (HRE) assay. Weanling male Wistar rats were fed a low-Fe diet (12mg/kg) for 15days followed by 2 weeks of Fe repletion with diets providing 35mg Fe/kg as either ferrous sulphate (FS) or FP, supplemented with 7.5% ITF as either YF or Raftilose (RAF), a purified ITF. ITF increased caecal fermentation, whereas YF was more butyrogenic than RAF. ITF improved HRE in FP-fed rats, and those fed YF had a higher relative biological value compared with those fed FP and RAF. Liver Fe was increased by ITF, but only YF led to values similar to those in the FS group. It is observed that ITF increased caecal fermentation and Fe bioavailability. These effects were more pronounced when YF was the ITF source.