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1

Wang, Chia-Yu, and Jodie L. Babitt. "Liver iron sensing and body iron homeostasis." Blood 133, no. 1 (January 3, 2019): 18–29. http://dx.doi.org/10.1182/blood-2018-06-815894.

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Abstract The liver orchestrates systemic iron balance by producing and secreting hepcidin. Known as the iron hormone, hepcidin induces degradation of the iron exporter ferroportin to control iron entry into the bloodstream from dietary sources, iron recycling macrophages, and body stores. Under physiologic conditions, hepcidin production is reduced by iron deficiency and erythropoietic drive to increase the iron supply when needed to support red blood cell production and other essential functions. Conversely, hepcidin production is induced by iron loading and inflammation to prevent the toxicity of iron excess and limit its availability to pathogens. The inability to appropriately regulate hepcidin production in response to these physiologic cues underlies genetic disorders of iron overload and deficiency, including hereditary hemochromatosis and iron-refractory iron deficiency anemia. Moreover, excess hepcidin suppression in the setting of ineffective erythropoiesis contributes to iron-loading anemias such as β-thalassemia, whereas excess hepcidin induction contributes to iron-restricted erythropoiesis and anemia in chronic inflammatory diseases. These diseases have provided key insights into understanding the mechanisms by which the liver senses plasma and tissue iron levels, the iron demand of erythrocyte precursors, and the presence of potential pathogens and, importantly, how these various signals are integrated to appropriately regulate hepcidin production. This review will focus on recent insights into how the liver senses body iron levels and coordinates this with other signals to regulate hepcidin production and systemic iron homeostasis.
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2

Cook, James D. "Defining optimal body iron." Proceedings of the Nutrition Society 58, no. 2 (May 1999): 489–95. http://dx.doi.org/10.1017/s0029665199000634.

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The major liabilities of Fe lack include defects in psychomotor development in infants, impaired educational performance in schoolchildren, increased perinatal morbidity, and impaired work capacity. Few if any of the relevant investigations have demonstrated these abnormalities in the absence of anaemia. Consequently, adequate Fe nutrition can be defined as a normal haemoglobin concentration. On the other hand, optimal Fe nutrition should be regarded as sufficient body Fe to avoid any limitation in tissue Fe supply, termed Fe-deficient erythropoiesis. A variety of laboratory measurements have been used to identify this milder form of Fe deficiency, including serum ferritin, transferrin saturation, erythrocyte protoporphyrin, mean corpuscular volume, and more recently the concentration of the soluble fragment of transferrin receptor in serum. Recent studies indicate that the serum transferrin receptor is the preferred measurement, because enhanced synthesis of the transferrin receptor represent the initial cellular response to a declining Fe supply. Moreover, unlike other methods, it is not affected by chronic inflammation or infection which are often confused with Fe deficiency. In an otherwise normal healthy population the transferrin receptor: ferritin value provides a useful quantitative index of body Fe over a wide spectrum of Fe status, ranging from Fe repletion to Fe-deficiency anaemia. It is concluded that optimal Fe nutrition is best defined as a normal haemoglobin, serum ferritin and transferrin receptor concentration.
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3

Cook, James D., Carol H. Flowers, and Barry S. Skikne. "The quantitative assessment of body iron." Blood 101, no. 9 (May 1, 2003): 3359–63. http://dx.doi.org/10.1182/blood-2002-10-3071.

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Current initiatives to reduce the high prevalence of nutritional iron deficiency have highlighted the need for reliable epidemiologic methods to assess iron status. The present report describes a method for estimating body iron based on the ratio of the serum transferrin receptor to serum ferritin. Analysis showed a single normal distribution of body iron stores in US men aged 20 to 65 years (mean ± 1 SD, 9.82 ± 2.82 mg/kg). A single normal distribution was also observed in pregnant Jamaican women (mean ± 1 SD, 0.09 ± 4.48 mg/kg). Distribution analysis in US women aged 20 to 45 years indicated 2 populations; 93% of women had body iron stores averaging 5.5 ± 3.35 mg/kg (mean ± 1 SD), whereas the remaining 7% of women had a mean tissue iron deficit of 3.87 ± 3.23 mg/kg. Calculations of body iron in trials of iron supplementation in Jamaica and iron fortification in Vietnam demonstrated that the method can be used to calculate absorption of the added iron. Quantitative estimates of body iron greatly enhance the evaluation of iron status and the sensitivity of iron intervention trials in populations in which inflammation is uncommon or has been excluded by laboratory screening. The method is useful clinically for monitoring iron status in those who are highly susceptible to iron deficiency.
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4

Kohgo, Yutaka, Katsuya Ikuta, Takaaki Ohtake, Yoshihiro Torimoto, and Junji Kato. "Body iron metabolism and pathophysiology of iron overload." International Journal of Hematology 88, no. 1 (July 2008): 7–15. http://dx.doi.org/10.1007/s12185-008-0120-5.

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5

Debnam, Ted, and Kaila Srai. "Hepcidin, body iron and infection." Physiology News, Winter 2005 (January 1, 2006): 38–39. http://dx.doi.org/10.36866/pn.61.38.

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6

Cook, J. D., and B. S. Skikne. "Intestinal regulation of body iron." Blood Reviews 1, no. 4 (December 1987): 267–72. http://dx.doi.org/10.1016/0268-960x(87)90028-2.

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7

Sikström, C., L. Beckman, G. Hallmans, and K. Asplund. "Transferrin Types, Iron-Binding Capacity and Body Iron Stores." Human Heredity 43, no. 6 (1993): 337–41. http://dx.doi.org/10.1159/000154156.

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8

汪, 昕. "Brain Iron Deposition, Body Iron Overload and Cognitive Impairment." Journal of Physiology Studies 01, no. 03 (2013): 16–19. http://dx.doi.org/10.12677/jps.2013.13004.

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9

Ganz, Tomas, and Elizabeta Nemeth. "Iron imports. IV. Hepcidin and regulation of body iron metabolism." American Journal of Physiology-Gastrointestinal and Liver Physiology 290, no. 2 (February 2006): G199—G203. http://dx.doi.org/10.1152/ajpgi.00412.2005.

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Hepcidin, a small peptide synthesized in the liver, controls extracellular iron by regulating its intestinal absorption, placental transport, recycling by macrophages, and release from stores. Hepcidin inhibits the cellular efflux of iron by binding to and inducing the degradation of ferroportin, the sole iron exporter in iron-transporting cells. In turn, hepcidin synthesis is increased by iron loading and decreased by anemia and hypoxia. Hepcidin is markedly induced during inflammation, trapping iron in macrophages, decreasing plasma iron concentrations, and contributing to the anemia of inflammation. Hepcidin deficiency due to the dysregulation of its synthesis causes most known forms of hemochromatosis.
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10

Moghadam, Ali Malekshahi, Mahboobeh Mehrabani Natanzi, Mahmoud Djalali, Ahmad Saedisomeolia, Mohammad Hassan Javanbakht, Ali Akbar Saboor-Yaraghi, and Mahnaz Zareei. "Relationship between blood donors' iron status and their age, body mass index and donation frequency." Sao Paulo Medical Journal 131, no. 6 (2013): 377–83. http://dx.doi.org/10.1590/1516-3180.2013.1316554.

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CONTEXT AND OBJECTIVE: Regular blood donation may decrease body iron storage and lead to anemia. The aim here was to evaluate the iron status of Iranian male blood donors and the impact of age, body mass index (BMI) and donation frequency over one year, on iron status indices. DESIGN AND SETTING: Cross-sectional, descriptive and analytical study at Tehran Blood Transfusion Center, Tehran, Iran. METHODS: Between July and September 2011, 117 male blood donors were selected and divided into four groups according to their frequency of blood donation. Thirty male non-donors were also recruited as controls after adjusting for age, weight, height, smoking habits and monthly income. Iron status indices and some criteria such as general health and dietary measurements were determined among all subjects. RESULTS: The values of the iron-related parameters were significantly lower among donors than among non-donors. Only total iron binding capacity (TIBC) was found to be significantly higher among different donor groups than in the controls. A significant positive correlation was observed between age and serum ferritin (SF) only among the donors who had donated once within the preceding year. The iron status indices did not show any significant relationship with BMI among donors or non-donors. CONCLUSION: A donation frequency of more than twice a year had a significant influence on iron-related parameters. Therefore, without annual measurement of these parameters, further phlebotomies may lead to iron deficiency and donor rejection in the future.
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11

Balla, József, György Balla, Béla Lakatos, Viktória Jeney, and Klára Szentmihályi. "Heme-iron in the human body." Orvosi Hetilap 148, no. 36 (September 1, 2007): 1699–706. http://dx.doi.org/10.1556/oh.2007.28156.

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A vas minden élő organizmus számára nélkülözhetetlen, ugyanakkor a fölöslegben lévő aktív vas veszélyes, hiszen szabad gyökök képződését katalizálhatja. Ezért a vas abszorpciója szigorúan szabályozott folyamat, melynek eredménye a vasvesztés és a vasfelvétel egyensúlya. Azokban az országokban, ahol az étkezéssel a hemvas bevitele jelentős, a szervezet vastartalmának nagy része hemből származik. A táplálékkal bevitt hemet a vékonybél enterocyta sejtjei intakt formában receptormediált módon abszorbeálják, majd hem-oxigenáz katalizálta reakcióban degradálják, így a vas transzferrinhez kötve hagyja el az enterocytát. A hem számos protein prosztetikus csoportja, így minden sejtünk szintetizálja. Mennyiségét tekintve a legjelentősebb hemprotein a hemoglobin, mely a vörösvértestekben az oxigén transzportját végzi. A vörösvértestek hemolízise során szabaddá váló hemoglobin specifikusan vagy aspecifikusan plazmaproteinekhez kötődik, és receptormediált úton felvételre kerül, majd degradálódik. A hemoglobinmolekula szerkezeti felépítése megnehezíti, de teljes mértékben nem akadályozza meg a hemoglobin (ferro) oxidációját methemoglobinná (ferri). A reakcióban szuperoxidgyök-anion is képződik, mely további szabad gyökös reakciókaszkádokat indít el. A képződött methemoglobin a hemet nem köti olyan szorosan, mint a hemoglobin, így az oxidáció következménye szabad hem képződése. A hem a plazmaprotein hemopexinhez kötődik, és receptormediált úton a sejtek által felvételre kerül, majd a hem-oxigenázok által katalizált reakcióban degradálódik. A hem ezenkívül a plazma lipoproteinjeihez, valamint az endothelium lipidmembránjához is kapcsolódhat, aminek következtében az LDL oxidálódik, illetve az endothelium oxidatív stresszre érzékenyebbé válik. A jelen összefoglaló célja a hemmel kapcsolatos folyamatok áttekintése.
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12

Gupta, Dr C. P. "Role of Iron (Fe) in Body." IOSR Journal of Applied Chemistry 7, no. 11 (2014): 38–46. http://dx.doi.org/10.9790/5736-071123846.

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13

Auer, Johann, Robert Berent, Thomas Weber, and Bernd Eber. "Coronary atherosclerosis and body iron stores." Journal of the American College of Cardiology 41, no. 10 (May 2003): 1848–49. http://dx.doi.org/10.1016/s0735-1097(03)00325-5.

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14

Mascitelli, Luca, Francesca Pezzetta, and Mark R. Goldstein. "Altitude, body iron stores, and cancer." Medical Hypotheses 75, no. 6 (December 2010): 675–76. http://dx.doi.org/10.1016/j.mehy.2010.07.019.

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15

Dilantika, Charisma. "Iron Absorption and its Influencing Factors to Prevent Iron Deficiency." Journal of Indonesian Specialized Nutrition 1, no. 1 (September 29, 2023): 10–21. http://dx.doi.org/10.46799/jisn.v1i1.2.

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Iron is an important nutrient, required to support tissue oxygen delivery, cell growth and differentiation regulation, and energy metabolism. Body iron levels are mainly controlled by regulation of iron absorption in duodenum and proximal jejunum, allowing absorption to be accurately matched to unregulated losses. Since iron bioavailability often reduced, dietary iron absorption is controlled by cellular and systemic factors to ensure that overall body iron levels are maintained at adequate levels. A better understanding of the mechanism for iron absorption and factors influencing its absorption and bioavailability is important to avoid iron deficiency or iron overload. There are complex regulatory frameworks managing iron absorption, transportation, storage, and recycling. It is able to provide enough iron for critical body functions and react relatively quickly as iron demands increase, but mechanisms must also be in place to restrict iron absorption once the body is overwhelmed with iron. Several factors promote and impede iron absorption, such as phytate and ascorbic acid, respectively. The danger of iron deficiency for the world's population is of great significance, it is important to introduce effective strategies to tackle this issue through nutrition programs; food iron supplements; iron medication supplements; and probiotic, prebiotic, and symbiotic approaches.
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16

Cook, James D., Erick Boy, Carol Flowers, and Maria del Carmen Daroca. "The influence of high-altitude living on body iron." Blood 106, no. 4 (August 15, 2005): 1441–46. http://dx.doi.org/10.1182/blood-2004-12-4782.

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Abstract The quantitative assessment of body iron based on measurements of the serum ferritin and transferrin receptor was used to examine iron status in 800 Bolivian mothers and one of their children younger than 5 years. The survey included populations living at altitudes between 156 to 3750 m. Body iron stores in the mothers averaged 3.88 ± 4.31 mg/kg (mean ± 1 SD) and 1.72 ± 4.53 mg/kg in children. No consistent effect of altitude on body iron was detected in children but body iron stores of 2.77 ± 0.70 mg/kg (mean ± 2 standard error [SE]) in women living above 3000 m was reduced by one-third compared with women living at lower altitudes (P < .001). One half of the children younger than 2 years were iron deficient, but iron stores then increased linearly to approach values in their mothers by 4 years of age. When body iron in mothers was compared with that of their children, a striking correlation was observed over the entire spectrum of maternal iron status (r = 0.61, P < .001). This finding could provide the strongest evidence to date of the importance of dietary iron as a determinant of iron status in vulnerable segments of a population. (Blood. 2005;106:1441-1446)
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17

Aliyev, Alim Maratovich, Nikolay Mikhailovich Vladimirov, Tatiana Nikolaevna Sokolova, Yulia Amanzholovna Petrovskaya, and Vadim Viacheslavovich Leonov. "CONTEMPORARY REPRESENTATIONS ABOUT IRON HOMEOSTASIS IN THE HUMAN BODY." Scientific medical Bulletin of Ugra 29, no. 3 (2021): 4–18. http://dx.doi.org/10.25017/2306-1367-2021-29-3-4-18.

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Iron is a necessary element for all living organisms, since it is part of the functional groups of oxygentransporting proteins and enzymes that catalyze energy generation reactions and metabolic processes. New research in the fi eld of iron homeostasis has allowed to learn in more detail the molecular mechanisms of absorption, export, transport, storage, recycling of iron, the mechanisms of regulation of iron metabolism in mammals at the cellular and systemic level are disclosed in detail. This article summarizes modern scientifi c data on iron homeostasis at all stages, from absorption to recycling
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18

Tangarife, E., A. H. Romero, and J. Mejía-López. "A charge optimized many-body potential for iron/iron-fluoride systems." Physical Chemistry Chemical Physics 21, no. 36 (2019): 20118–31. http://dx.doi.org/10.1039/c9cp01927h.

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19

Fu, Shimin, Feifei Li, Jianguo Zhou, and Zhiping Liu. "The Relationship Between Body Iron Status, Iron Intake And Gestational Diabetes." Medicine 95, no. 2 (January 2016): e2383. http://dx.doi.org/10.1097/md.0000000000002383.

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20

Angelucci, Emanuele, Gary M. Brittenham, Christine E. McLaren, Marta Ripalti, Donatella Baronciani, Claudio Giardini, Maria Galimberti, Paola Polchi, and Guido Lucarelli. "Hepatic Iron Concentration and Total Body Iron Stores in Thalassemia Major." New England Journal of Medicine 343, no. 5 (August 3, 2000): 327–31. http://dx.doi.org/10.1056/nejm200008033430503.

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21

REUNANEN, A., H. TAKKUNEN, P. KNEKT, R. SEPPÄNEN, and A. AROMAA. "Body iron stores, dietary iron intake and coronary heart disease mortality." Journal of Internal Medicine 238, no. 3 (September 1995): 223–30. http://dx.doi.org/10.1111/j.1365-2796.1995.tb00926.x.

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22

Pateva, Irina, Elisabeth Kerling, Susan Carlson, Manju Reddy, Dan Chen, and Jakica Tancabelic. "Effect Of Maternal Cigarette Smoking On Newborn Iron Stores." Blood 122, no. 21 (November 15, 2013): 4671. http://dx.doi.org/10.1182/blood.v122.21.4671.4671.

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Objective Previous small-scale studies suggest that maternal smoking lowers neonatal body iron. Our objective was to study and compare the relationship between maternal and infants’ body iron in smokers and non-smokers in a large matched-pair cohort. Method This was a prospective cohort study involving 144 mothers – 72 smokers and 72 non-smokers and their respective infants. Samples were obtained from maternal blood and infants’ cord blood at delivery for serum transferrin receptor (sTfR) and ferritin levels. Serum TfR and ferritin levels were measured by RAMCO ELISA and RIA assays. The total body iron (TBI) was calculated using the sTfR/ferritin ratio. Results Maternal total body iron and smoking status Women who smoked had lower sTfR, higher ferritin and higher body iron compared to nonsmoking women. Infant’s total body iron, measurements at birth and smoking status In contrast to their respective mothers, we found a small but statistically significant negative correlation between smoking and infants’ total body iron. The number of PPD smoked was negatively correlated with infants’ ferritin and total body iron. The number of days smoked during pregnancy was also negatively correlated with infants’ ferritin and total body iron and positively correlated with infants' sTfR. Birth weight was lower in babies of smokers compared to nonsmokers (mean /- SD =3270 +/-475 vs. 3393 g +/- 475 g, p=0.03). Correlation studies revealed that birth weight in infants of smokers was negatively correlated with PPD smoked and number of days smoked. Birth length in the same infants was also negatively correlated with PPD smoked and number of days smoked. Conclusion Mothers who smoked during pregnancy had higher iron stores but their newborn infants had lower iron stores than those of non-smoking mothers. There may be a negative dose-dependent response between fetal smoke exposure and infant iron stores. Disclosures: No relevant conflicts of interest to declare.
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23

Lemanski, Clara L., Tianna J. Schott, and Young Dal Jang. "PSIV-15 Effect of Secondary Iron Injection Timing to Suckling Pigs on Pre- and Post-Weaning Growth Performance and Hematological Parameters." Journal of Animal Science 101, Supplement_2 (October 28, 2023): 309–10. http://dx.doi.org/10.1093/jas/skad341.351.

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Abstract The objective of this study was to evaluate the effects of secondary iron injection timing to suckling pigs on pre- and post-weaning growth performance and hematological variables. A total of 22 pigs (initial body weight: 1.62 ± 0.12 kg) from 4 litters were allotted into 3 treatments within litter based on body weight and sex at d 1-3 of age (d 0 of experiment) as follows: 1) Control: intramuscular injection of 150 mg iron-dextran at d 0 of experiment only, 2) Iron14: intramuscular injection of 150 mg iron-dextran at d 0 of experiment and 100 mg iron-dextran at d 10 of experiment (14 d before weaning), and 3) Iron7: intramuscular injection of 150 mg iron-dextran at d 0 of experiment and 100 mg iron-dextran at d 17 of experiment (7 d before weaning). The pigs were housed by litter in the suckling and nursery periods with a common corn-soybean meal-based diet during the nursery period. Body weight, hemoglobin concentrations and hematocrit were measured at d 0, 10, 17, 24 (weaning), 31 and 38 of experiment. The Iron14 treatment tended to have greater final weight at d 38 of experiment than the control treatment (P = 0.07; 10.97 vs. 9.38 kg) and the Iron7 treatment had intermediate value (10.15 kg). The ADG in d 24-31 postweaning tended to be greater in the Iron14 treatment than the control and Iron7 treatments (P = 0.08; 82.6, 151.8, and 53.5 g/d for the control, Iron14, and Iron7 treatments, respectively). In hemoglobin concentrations, the Iron14 treatment had greater levels than the control treatment at d 17 (P = 0.06; 12.24, 13.51, and 11.66 g/dL, respectively), 24, and 31 (P < 0.05; 10.72, 12.74, and 12.77 g/dL, respectively) of experiment whereas the Iron7 treatment had greater concentrations than the control treatment at d 24, 31, and 38 (P< 0.05; 9.46, 10.60, and 11.21 g/dL, respectively) of experiment and less than Iron14 treatment at d 17 and 24 (P < 0.05; 10.63, 12.95, 11.91 g/dL, respectively) of experiment. Hematocrit showed similar response to hemoglobin concentrations in which the Iron 14 treatment had greater hematocrit than the control treatment at d 17, 24, 31 (P < 0.05) and 38 (P = 0.10) of experiment while the Iron7 treatment had greater hematocrit levels than the control treatment at d 24, 31, and 38 (P < 0.05) of experiment. Hematocrit levels only at d 17 of experiment was greater in the Iron14 treatment than the Iron7 treatment (P < 0.05). In conclusion, the secondary iron injection to suckling piglets could improve early postweaning growth when the pigs were injected with iron at 14 d before weaning and increase hemoglobin concentrations and hematocrit regardless of timing, but the differences in hemoglobin and hematocrit values varied depending on the timing of secondary iron injection.
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24

Cable, Ritchard G., Donald Brambilla, Simone A. Glynn, Steven Kleinman, Alan E. Mast, Bryan R. Spencer, Mars Stone, and Joseph E. Kiss. "Effect of iron supplementation on iron stores and total body iron after whole blood donation." Transfusion 56, no. 8 (May 27, 2016): 2005–12. http://dx.doi.org/10.1111/trf.13659.

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25

Frazer, David M., and Gregory J. Anderson. "Iron Imports. I. Intestinal iron absorption and its regulation." American Journal of Physiology-Gastrointestinal and Liver Physiology 289, no. 4 (October 2005): G631—G635. http://dx.doi.org/10.1152/ajpgi.00220.2005.

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Our knowledge of how the body absorbs iron from the diet and how this process is controlled has increased at a rapid rate in recent years. The identification of key molecules, including the iron regulatory peptide hepcidin, and the analysis of how they are regulated and interact have led to the development of an integrated model for the control of iron absorption by body iron requirements. Research now focuses on the role of the liver as the primary regulator of iron absorption, and this review considers some of the recent highlights and controversies in this area.
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26

Baynes, R. D. "Refining the assessment of body iron status." American Journal of Clinical Nutrition 64, no. 5 (November 1, 1996): 793–94. http://dx.doi.org/10.1093/ajcn/64.5.793.

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27

Ma, Jing, and Meir J. Stampfer. "Body Iron Stores and Coronary Heart Disease." Clinical Chemistry 48, no. 4 (April 1, 2002): 601–3. http://dx.doi.org/10.1093/clinchem/48.4.601.

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28

Jandacka, Petr, Barbora Kasparova, Yvonna Jiraskova, Katerina Dedkova, Katerina Mamulova-Kutlakova, and Jana Kukutschova. "Iron-based granules in body of bumblebees." BioMetals 28, no. 1 (October 28, 2014): 89–99. http://dx.doi.org/10.1007/s10534-014-9805-9.

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29

Knekt, Paul, Antti Reunanen, Heikki Takkunen, Arpo Aromaa, Markku Heliövaara, and Timo Hakuunen. "Body iron stores and risk of cancer." International Journal of Cancer 56, no. 3 (February 1, 1994): 379–82. http://dx.doi.org/10.1002/ijc.2910560315.

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30

Leong, Weng-In, Christopher L. Bowlus, Jonas Tallkvist, and Bo Lönnerdal. "DMT1 and FPN1 expression during infancy: developmental regulation of iron absorption." American Journal of Physiology-Gastrointestinal and Liver Physiology 285, no. 6 (December 2003): G1153—G1161. http://dx.doi.org/10.1152/ajpgi.00107.2003.

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Two iron transporters, divalent metal transporter1 (DMT1) and ferroportin1 (FPN1) have been identified; however, their role during infancy is unknown. We investigated DMT1, FPN1, ferritin, and transferrin receptor expression, iron absorption and tissue iron in iron-deficient rat pups, iron-deficient rat pups given iron supplements, and controls during early ( day 10) and late infancy ( day 20). With iron deficiency, DMT1 was unchanged and FPN1 was decreased (-80%) at day 10. Body iron uptake, mucosal iron retention, and total iron absorption were unchanged. At day 20, DMT1 increased fourfold and FPN1 increased eightfold in the low-Fe group compared with controls. Body iron uptake and total iron absorption were increased, and mucosal iron retention was decreased with iron deficiency. Iron supplementation normalized expression levels of the transporters, body iron uptake, mucosal iron retention, and total iron absorption of the low-Fe group to those of controls at day 20. In summary, the molecular mechanisms regulating iron absorption during early infancy differ from late infancy when they are similar to adult animals, indicating developmental regulation of iron absorption.
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31

Matsuo-Tezuka, Yukari, Yusuke Sasaki, Toshiki Iwai, Mitsue Kurasawa, Keigo Yorozu, Yoshihito Tashiro, and Michinori Hirata. "T2∗ Relaxation Time Obtained from Magnetic Resonance Imaging of the Liver Is a Useful Parameter for Use in the Construction of a Murine Model of Iron Overload." Contrast Media & Molecular Imaging 2019 (September 22, 2019): 1–7. http://dx.doi.org/10.1155/2019/7463047.

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Aim. Iron overload is a life-threatening disorder that can increase the risks of cancer, cardiovascular disease, and liver cirrhosis. There is also a risk of iron overload in patients with chronic kidney disease. In patients with renal failure, iron storage is increased due to inadequate iron utilization associated with decreased erythropoiesis and also to the inflammatory status. To evade the risk of iron overload, an accurate and versatile indicator of body iron storage in patients with iron overload is needed. In this study, we aimed to find useful iron-related parameters that could accurately reflect body iron storage in mice in order to construct a murine model of iron overload. Methods. To select an appropriate indicator of body iron status, a variety of parameters involved in iron metabolism were evaluated. Noninvasively measured parameters were R1, R2, and R2∗ derived from magnetic resonance imaging (MRI). Invasively measured parameters included serum hepcidin levels, serum ferritin levels, and liver iron contents. Histopathological analysis was also conducted. Results/Conclusion. Among the several parameters evaluated, the MRI T2∗ relaxation time was able to detect iron storage in the liver as sensitively as serum ferritin levels. Moreover, it is expected that using an MRI parameter will allow accurate evaluation of body iron storage in mice over time.
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SAHIN, CEM, CIGDEM PALA, LEYLAGUL KAYNAR, YASEMIN ALTUNER TORUN, AYSUN CETIN, FATIH KURNAZ, SERDAR SIVGIN, and FATIH SERDAR SAHIN. "Measurement of hair iron concentration as a marker of body iron content." Biomedical Reports 3, no. 3 (January 27, 2015): 383–87. http://dx.doi.org/10.3892/br.2015.419.

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33

Costa, Attilia, Lucio N. Liberato, Pietro Palestra, and Giovanni Barosi. "Small-dose iron tolerance test and body iron content in normal subjects." European Journal of Haematology 46, no. 3 (April 24, 2009): 152–57. http://dx.doi.org/10.1111/j.1600-0609.1991.tb01269.x.

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34

Mujica-Coopman, María Fernanda, Alex Brito, Daniel López de Romaña, Fernando Pizarro, and Manuel Olivares. "Body mass index, iron absorption and iron status in childbearing age women." Journal of Trace Elements in Medicine and Biology 30 (April 2015): 215–19. http://dx.doi.org/10.1016/j.jtemb.2014.03.008.

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35

Mandelli, C., L. Cesarini, A. Pipemo, S. Fargion, A. L. Fracanzani, G. Fiorelli, P. A. Bianchi, and D. Conte. "Hepatic iron concentration and total body iron burden in genetic hemochromatosis (GH)." Journal of Hepatology 13 (January 1991): S49. http://dx.doi.org/10.1016/0168-8278(91)91183-h.

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36

Ahmed, Javed, Noor Ahmad, Bhavin Jankharia, Pradeep Krishnan, and Rashid H. Merchant. "Effect of Deferasirox Chelation on Liver Iron and Total Body Iron Concentration." Indian Journal of Pediatrics 80, no. 8 (May 29, 2013): 655–58. http://dx.doi.org/10.1007/s12098-013-1030-y.

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37

Louw, Vernon, and James Isbister. "Nonanemic Iron Deficiency: The Elusive Metrics of Iron in the Human Body." Anesthesia & Analgesia 139, no. 1 (June 17, 2024): 44–46. http://dx.doi.org/10.1213/ane.0000000000006936.

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38

McCown, Jennifer L., and Andrew J. Specht. "Iron Homeostasis and Disorders in Dogs and Cats: A Review." Journal of the American Animal Hospital Association 47, no. 3 (May 1, 2011): 151–60. http://dx.doi.org/10.5326/jaaha-ms-5553.

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Iron is an essential element for nearly all living organisms and disruption of iron homeostasis can lead to a number of clinical manifestations. Iron is used in the formation of both hemoglobin and myoglobin, as well as numerous enzyme systems of the body. Disorders of iron in the body include iron deficiency anemia, anemia of inflammatory disease, and iron overload. This article reviews normal iron metabolism, disease syndromes of iron imbalance, diagnostic testing, and treatment of either iron deficiency or excess. Recent advances in diagnosing iron deficiency using reticulocyte indices are reviewed.
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39

Kühn, Lukas C. "Iron regulatory proteins and their role in controlling iron metabolism." Metallomics 7, no. 2 (2015): 232–43. http://dx.doi.org/10.1039/c4mt00164h.

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40

Shaw, Jeremy A., Alastair Boyd, Michael House, Gary Cowin, and Boris Baer. "Multi-modal imaging and analysis in the search for iron-based magnetoreceptors in the honeybee Apis mellifera." Royal Society Open Science 5, no. 9 (September 2018): 181163. http://dx.doi.org/10.1098/rsos.181163.

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The honeybee Apis mellifera is one of many animal species for which empirical evidence of a magnetic sense has been provided. The underlying mechanisms postulated for magnetoreception in bees are varied, but most point towards the abdomen as the most likely anatomical region for its location, partly owing to the large accumulation of iron in trophocyte cells that comprise the honeybee fat body. Using a multi-modal imaging and analysis approach, we have investigated iron in the honeybee, with a particular focus on the abdomen and the utility of such techniques as applied to magnetoreception. Abdominal iron is shown to accumulate rapidly, reaching near maximum levels only 5 days after emerging from the comb and is associated with the accumulation of iron within the fat body. While fat body iron could be visualized, no regions of interest, other than perhaps the fat body itself, were identified as potential sites for magnetoreceptive cells. If an iron-based magnetoreceptor exists within the honeybee abdomen the large accumulation of iron in the fat body is likely to impede its discovery.
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41

Gopchuk, O. M. "Iron deficiency anemia." HEALTH OF WOMAN, no. 9(145) (November 30, 2019): 32–37. http://dx.doi.org/10.15574/hw.2019.145.32.

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Iron deficiency anemia is the most common group of blood diseases in the population (80–95% of all anemias), characterized by a decrease in the number of circulating red blood cells and / or hemoglobin per unit volume of blood below normal for a given age and sex. The article deals with the role of iron in the human body, the conditions associated with its deficiency, causes, clinical symptoms, diagnosis of this pathology. Recommendations are given for the treatment of iron deficiency anemia by modern iron preparations, the advantages of using in the complex correction of heme iron deficiency, ie in hemoglobin composition, iron, which is most easily absorbed by the body, have high efficiency and no side effects. Key words: iron deficiency anemia, hemoglobin, ferritin, anemic syndrome, sideropenic syndrome, pregnancy, treatment, heme iron, non-heme iron Richter FerroBio.
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42

Birghila, Semaghiul, Georgiana Baronescu, and Anca Dumbrava. "Seasonal variation and speciation of dissolved iron in an artificial surface water body." Ovidius University Annals of Chemistry 28, no. 2 (December 20, 2017): 43–48. http://dx.doi.org/10.1515/auoc-2017-0007.

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AbstractThe aquatic chemistry of iron is an important issue since iron is a micronutrient for the growth of phytoplankton. Its concentration in surface waters involves many environmental aspects, from the quality of a particular water to the control of atmospheric carbon dioxide. Dissolved iron can exist in water as ferrous and ferric iron, and the equilibrium between these two forms, as well as the precipitation and solubilization of iron, depends on many natural and anthropic factors. We studied the variation for an year of Fe(II) and total iron concentration into Poarta Alba - Midia Navodari Canal, an artificial surface water which connects Danube River with Black Sea. The results indicate a high iron concentration in surface water and a seasonal variation of iron concentration and speciation, which can be correlated with the oxidable matter content.
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43

Kiss, Joseph E., Rebecca J. Birch, Whitney R. Steele, David J. Wright, and Ritchard G. Cable. "Quantification of body iron and iron absorption in the REDS-IIDonor Iron Status Evaluation (RISE) study." Transfusion 57, no. 7 (May 19, 2017): 1656–64. http://dx.doi.org/10.1111/trf.14133.

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44

Swain, James H., LuAnn K. Johnson, and Janet R. Hunt. "Electrolytic Iron or Ferrous Sulfate Increase Body Iron in Women with Moderate to Low Iron Stores." Journal of Nutrition 137, no. 3 (March 1, 2007): 620–27. http://dx.doi.org/10.1093/jn/137.3.620.

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45

Sharp, Paul A. "Intestinal Iron Absorption: Regulation by Dietary & Systemic Factors." International Journal for Vitamin and Nutrition Research 80, no. 45 (October 1, 2010): 231–42. http://dx.doi.org/10.1024/0300-9831/a000029.

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Iron is an essential trace metal in human metabolism. However, imbalances in iron homeostasis are prevalent worldwide and have detrimental effects on human health. Humans do not have the ability to remove excess iron and therefore iron homeostasis is maintained by regulating the amount of iron entering the body from the diet. Iron is present in the human diet in number of different forms, including heme (from meat) and a variety of non-heme iron compounds. While heme is absorbed intact, the bioavailability of non-heme iron varies greatly depending on dietary composition. A number of dietary components are capable of interacting with iron to regulate its solubility and oxidation state. Interestingly, there is an emerging body of evidence suggesting that some nutrients also have direct effects on the expression and function of enterocyte iron transporters. In addition to dietary factors, body iron status is a major determinant of iron absorption. The roles of these important dietary and systemic factors in regulating iron absorption will be discussed in this review.
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46

Robalino Gonzaga, Ernesto, Irene Riestra Guiance, Richard Henriquez, Gerri Mortimore, and Jan Freeman. "The Role of the Liver in Iron Homeostasis and What Goes Wrong?" Journal of Renal and Hepatic Disorders 5, no. 2 (September 18, 2021): 26–33. http://dx.doi.org/10.15586/jrenhep.v5i2.110.

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Iron is an essential mineral that is vital for growth development, normal cellular function, synthesis of hormones and connective tissue, and most importantly, serves as a component of hemoglobin to carry oxygen to body tissues. The body finely regulates the amount of circulating and stored iron within the body to maintain concentration levels within range for optimal physiologic function. Without iron, the ability for cells to participate in electron transport and energy metabolism decreases. Furthermore, hemoglobin synthesis is altered, which leads to anemia and decreased oxygen delivery to tissue. Problems arise when there is too little or too much iron. This review explores the role of the liver in iron physiology, iron overload and discusses the most common causes of primary and secondary hepatic iron overload.
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47

Matsuo-Tezuka, Yukari, Mariko Noguchi-Sasaki, Mitsue Kurasawa, Keigo Yorozu, and Yasushi Shimonaka. "Tissue-Specific Regulation of Iron Release in Response to Body Iron Status Under Erythropoietic Stimulation." Blood 126, no. 23 (December 3, 2015): 2148. http://dx.doi.org/10.1182/blood.v126.23.2148.2148.

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Abstract Introduction: In a previous study, we demonstrated that dietary iron uptake and mobilization of stored iron are both up-regulated through suppression of serum hepcidin levels during erythropoietic stimulation by administration of Epoetin beta pegol (C.E.R.A.), a long-acting erythropoiesis-stimulating agent. It was also demonstrated that up-regulation of ferroportin (FPN) in reticuloendothelial macrophages and up-regulation of divalent metal transporter 1 (DMT1) and FPN in enterocytes are followed by hepcidin suppression; however, the quantitative contribution of dietary iron for erythropoiesis were undetermined. In this study, we investigated how utilization of dietary iron for erythropoiesis is regulated under erythropoietic stimulation by C.E.R.A. in mice with different body iron status. To quantitatively estimate utilization of dietary iron for hemoglobin synthesis, we used a dietary iron tracing method using the stable iron isotope 57Fe. Methods: To assess dietary iron-derived hemoglobin synthesis, a diet containing 200 ppm of 57Fe instead of natural iron (57Fe-diet) was used. A diet containing 200 ppm of natural iron (native Fe diet) was used as a control. C57BL/6NCrl mice were fed the native Fe diet and were intravenously administered 0.5 or 1.0 mg/mouse of iron dextran (iron-loaded condition) or dextran (control). Five days after iron loading, the diet was switched to the 57Fe-diet immediately after intravenous injection of 10 µg/kg of C.E.R.A. or vehicle. On Day 5 and 8 after C.E.R.A. treatment, mice were euthanized by exsanguination under anesthesia with isoflurane, and hemoglobin levels were measured. Expression levels of DMT1 and FPN in control and iron-loaded mice (1.0 mg/mouse) on Day 5 were estimated by immunohistochemistry. Serum hepcidin levels on Day 5 were also measured by liquid column chromatography-tandem mass spectrometry (LC-MS/MS). To quantify dietary iron-derived hemoglobin synthesis, the content of hemoglobin containing 57Fe (57Fe-hemoglobin) was measured on Day 8 by inductively coupled plasma mass spectrometry (ICP-MS). Results: Hemoglobin levels on Day 8 were significantly higher in the C.E.R.A.-treated groups than in the vehicle-treated groups for each iron conditions. In the C.E.R.A.-treated groups, although iron loading did not affect hemoglobin levels, 57Fe-hemoglobin levels were significantly decreased with iron loading. The serum hepcidin levels were significantly suppressed in each of the C.E.R.A.-treated groups. However, iron loading increased serum hepcidin levels on Day 5 in both the vehicle- and C.E.R.A.-treated groups. The expression levels of hepatic and splenic iron exporter FPN were not significantly changed by iron loading in the C.E.R.A.-treated group. In contrast, the expression levels of intestinal iron transporters DMT1 and FPN were significantly reduced by iron loading in the C.E.R.A.-treated group. Conclusion: Iron loading reduced utilization of dietary iron for hemoglobin synthesis under erythropoietic stimulation by C.E.R.A. treatment. However, iron loading did not affect total hemoglobin levels, indicating that the contribution of dietary iron and stored iron for erythropoiesis is properly controlled in response to body iron status. This was attributed to the tissue-specific regulatory mechanisms of iron transporters in iron absorptive tissue (intestine) and iron storage tissue (liver and spleen) in response to iron loading even FPN on both tissues is known to be commonly down-regulated by hepcidin-binding. Sensitive inactivation of iron importers and exporters in the duodenum under conditions of iron loading may effectively contribute to iron not being excessively incorporated under erythropoietic stimulation. Disclosures Noguchi-Sasaki: Chugai Pharmaceutical Co., Ltd.: Employment. Kurasawa:Chugai Pharmaceutical Co., Ltd.: Employment. Yorozu:Chugai Pharmaceutical Co., Ltd.: Employment. Shimonaka:Chugai Pharmaceutical Co., Ltd.: Employment.
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48

Saito, Hiroshi. "Storage Iron Turnover from a New Perspective." Acta Haematologica 141, no. 4 (2019): 201–8. http://dx.doi.org/10.1159/000496324.

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Background/Aims: Storage iron turnover has remained poorly understood since 1953. In addition, errors in measurements of the storage iron turnover rate (SIT) by ferrokinetics have been detected and the causes of those errors need to be elucidated. Methods: A new, computer-assisted method, “serum ferritin kinetics,” was introduced for the quantitation of ferritin iron and hemosiderin iron. Ferrokinetics and non-ferrokinetic methods were used to determine the body iron turnover rate. Results and Conclusion: Using serum ferritin kinetics, patients with normal iron stores and iron overload were found to have 2 iron pathways between ferritin and hemosiderin: recovery of ferritin taking iron from hemosiderin in iron mobilization and iron transformation from ferritin to hemosiderin in iron deposition. In addition, underestimation of the SIT by ferrokinetics was confirmed by comparing SIT by ferrokinetics with the standard SIT as the sum of SIT of 3 major iron-storing cells. This underestimation was caused by extra radio-iron fixation to red cells. Ferrokinetics does not give the actual body iron turnover due to the behavioral difference between radio-iron and pre-existing body iron. Recent findings on ferritin and hemosiderin iron turnover will be a potential tool for the diagnosis and therapy of hematological disorders.
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49

Ponikowska, Małgorzata, and Jacek C. Szepietowski. "Is iron deficiency involved in the pathogenesis of chronic inflammatory skin disorders?" Postępy Higieny i Medycyny Doświadczalnej 73 (August 13, 2019): 359–63. http://dx.doi.org/10.5604/01.3001.0013.3450.

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Iron is an essential microelement in the human body due to its role in hematopoiesis, involvement in energetic processes, synthesis and decomposition of lipids, proteins and nuclear acids. Iron deficiency (ID) is common in healthy populations and also frequently coincides with natural course of chronic diseases. The former is typically present when the overall iron body storages are exhausted (absolute ID), most often due to insufficient iron supply, malabsorption or increased blood loss and coincides with anemia. The latter is a result of defected iron metabolism and reflects a condition, when despite adequate iron stores in the body, iron itself is trapped in the reticuloendothelial system, becoming unavailable for the metabolic processes. It typically occurs in the presence proinflammtory activation in chronic conditions such as chronic kidney disease, inflammatory bowel disorders, malignancies and heart failure. To date there are very few publications concerning the potential role of ID in chronic dermatological disorders. We have recently found that patients with psoriasis demonstrate pattern of ID which can be characterized by negative tissue iron balance with depleted iron stores in the body. Interestingly, presence of ID was not related to the severity of psoriasis, but rather determined by patients low body mass index. We are currently investigating the hypothesis that derangements in iron metabolism resulting in ID can be also present in hidradenitis suppurativa – the other chronic dermatologic disease associated with inflammatory and autoimmune activation.
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50

Saha, Ananya, Pradip Mukhopadhyay, Indrajit Nath, Arun Kumar, and Utpal Kumar Biswas. "A quantitative assessment of body iron status and its relationship with glycemic control in patients of type 2 diabetes mellitus in a tertiary care hospital of Kolkata." Asian Journal of Medical Sciences 12, no. 5 (May 1, 2021): 69–74. http://dx.doi.org/10.3126/ajms.v12i5.33344.

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Background: Diabetes is one of the most common disease which is observed in every household of Indian population. The longevity of the diabetic patients is dependent upon the frequency of complication and comorbidity that they encounter. Serum iron and ferritin, both being the aggravators to the oxidative stress accelerating the development of complications, gives us the reason to venture into the territory exploring the possibility of monitoring the body iron stores and taking prevent measures to control such complication. The current study was designed with an aim to knot the relationship between body iron stores and glycemic control in patients of type-II diabetes mellitus. Aims and Objectives: To measure the levels of serum ferritin, serum Iron, transferrin saturation and HbA1C and finding out the relationship between body iron stores and glycemic control in patients of Type-II Diabetes Mellitus. Materials and Methods: A total of 50 diagnosed cases of type II DM and 50 healthy controls between the age group of 35-65 years were taken following inclusion and exclusion criteria. Body iron stores were assessed by measuring serum ferritin, Serum iron and Transferrin saturation and Glycemic control was assessed by measuring levels of HbA1C. Results: A significant increase in serum ferritin, serum iron and Transferrin saturation (P<0.001) was noted in diabetic patients as compared to controls. There was a positive correlation between serum iron and transferring saturation in the diabetic patients. Conclusion: The co-morbidities and complications in the Diabetic population can be prevented by monitoring Body iron stores as they can significantly contribute to the oxidative stress leading to the complication and decreased life expectancy. Early detection in the abnormality in the body iron store can help us in employing proper measures for a better management of Type-II diabetic patients and thereby improving their survival.
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