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1

TURNBULL, ADAM, FRANS CLETON, CLEMENT A. FINCH, LEE THOMPSON, and JOAN MARTIN. "IRON ABSORPTION. IV. THE ABSORPTION OF HEMOGLOBIN IRON." Nutrition Reviews 47, no. 2 (April 27, 2009): 51–53. http://dx.doi.org/10.1111/j.1753-4887.1989.tb02786.x.

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2

Fuqua, Brie K., Christopher D. Vulpe, and Gregory J. Anderson. "Intestinal iron absorption." Journal of Trace Elements in Medicine and Biology 26, no. 2-3 (June 2012): 115–19. http://dx.doi.org/10.1016/j.jtemb.2012.03.015.

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3

Beard, John L., Laura E. Murray-Kolb, Jere D. Haas, and Frank Lawrence. "Iron Absorption Prediction Equations Lack Agreement and Underestimate Iron Absorption." Journal of Nutrition 137, no. 7 (July 1, 2007): 1741–46. http://dx.doi.org/10.1093/jn/137.7.1741.

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4

Garry, Philip J. "Iron stores related to iron absorption." American Journal of Clinical Nutrition 66, no. 6 (December 1, 1997): 1483–84. http://dx.doi.org/10.1093/ajcn/66.6.1483a.

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5

Roughead, Zamzam K., and Janet R. Hunt. "Adaptation in iron absorption: iron supplementation reduces nonheme-iron but not heme-iron absorption from food." American Journal of Clinical Nutrition 72, no. 4 (October 1, 2000): 982–89. http://dx.doi.org/10.1093/ajcn/72.4.982.

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6

Fleming, Robert E., and Robert S. Britton. "Iron Imports. VI. HFE and regulation of intestinal iron absorption." American Journal of Physiology-Gastrointestinal and Liver Physiology 290, no. 4 (April 2006): G590—G594. http://dx.doi.org/10.1152/ajpgi.00486.2005.

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The majority of clinical cases of iron overload is caused by mutations in the HFE gene. However, the role that HFE plays in the physiology of intestinal iron absorption remains enigmatic. Two major models have been proposed: 1) HFE exerts its effects on iron homeostasis indirectly, by modulating the expression of hepcidin; and 2) HFE exerts its effects directly, by changing the iron status (and therefore the iron absorptive activity) of intestinal enterocytes. The first model places the primary role of HFE in the liver (hepatocytes and/or Kupffer cells). The second model places the primary role in the duodenum (crypt cells or villus enterocytes). These models are not mutually exclusive, and it is possible that HFE influences the iron status in each of these cell populations, leading to cell type-specific downstream effects on intestinal iron absorption and body iron distribution.
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7

Li, Xiaofei, Lingyan Zhang, Liyang Zhang, Lin Lu, and Xugang Luo. "Effect of iron source on iron absorption by in situ ligated intestinal loops of broilers." Animal Production Science 57, no. 2 (2017): 308. http://dx.doi.org/10.1071/an15531.

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Two experiments were conducted to investigate the effect of iron (Fe) source on Fe absorption by in situ ligated intestinal loops of broilers. In Experiment 1, in situ ligated intestinal loops from Fe-deficient chicks (29 days old) were perfused with solutions containing 0.45 mmol Fe/L from FeSO4 (FeSO4·7H2O), Fe-Gly chelate, Fe-Met chelate, one of three Fe-amino acid or protein complexes with weak, moderate or extremely strong complex strength (Fe-Met W, Fe-Pro M, or Fe-Pro ES), or the mixtures of FeSO4 with either Gly or Met (Fe + Gly or Fe + Met), respectively, up to 30 min. In Experiment 2, in situ ligated duodenal loops from Fe-deficient chicks (29 days old) were perfused with solutions containing 0–3.58 mmol Fe/L from FeSO4, Fe-Met W, Fe-Pro M, or Fe-Pro ES up to 30 min. The absorptions of Fe from both inorganic and organic Fe sources in the ligated duodenum were ~1.35–2.8 times higher (P < 0.05) than that in the ligated jejunum or ileum. The absorption of Fe as Fe-Pro M or Fe-Pro ES was higher (P < 0.05) than that of Fe as inorganic Fe or Fe-Met W at Fe concentration of 3.58 mmol/L. The absorption kinetics of Fe from organic and inorganic Fe sources in the ligated duodenal loops followed a saturable process as determined by regression analysis of concentration-dependent absorption rates. The maximum absorption rate and Michaelis–Menten constant values in the ligated duodenal loops were higher (P < 0.05) for Fe-Pro M and Fe-Pro ES than for FeSO4 and Fe-Met W. The results from this study indicate that the duodenum was the main site of Fe absorption in the intestines of broilers; organic Fe sources with stronger complex strength values showed higher Fe absorptions at a higher concentration of added Fe; and the simple mixture of FeSO4 with amino acids did not increase Fe absorption.
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8

Sotos, John G. "Beeturia and iron absorption." Lancet 354, no. 9183 (September 1999): 1032. http://dx.doi.org/10.1016/s0140-6736(05)76638-1.

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9

Conrad, Marcel E., Jay N. Umbreit, and Elizabeth G. Moore. "Iron Absorption and Transport." American Journal of the Medical Sciences 318, no. 4 (October 1999): 213–29. http://dx.doi.org/10.1016/s0002-9629(15)40626-3.

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10

ANDERSON, GREGORY J. "Control of iron absorption." Journal of Gastroenterology and Hepatology 11, no. 11 (November 1996): 1030–32. http://dx.doi.org/10.1111/j.1440-1746.1996.tb00029.x.

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11

Hauge, Bodil Nexmand. "The Iron Absorption Test." Acta Medica Scandinavica 168, no. 2 (April 24, 2009): 109–16. http://dx.doi.org/10.1111/j.0954-6820.1960.tb06651.x.

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12

SØRENSEN, EINAR WOLFF. "Studies on Iron Absorption." Acta Medica Scandinavica 175, no. 6 (April 24, 2009): 763–70. http://dx.doi.org/10.1111/j.0954-6820.1964.tb00633.x.

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13

Sørensen, Einar Wolff. "Studies on Iron Absorption." Acta Medica Scandinavica 178, no. 4 (April 24, 2009): 385–92. http://dx.doi.org/10.1111/j.0954-6820.1965.tb04283.x.

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14

Anderson, Gregory J., David M. Frazer, and Gordon D. McLaren. "Iron absorption and metabolism." Current Opinion in Gastroenterology 25, no. 2 (March 2009): 129–35. http://dx.doi.org/10.1097/mog.0b013e32831ef1f7.

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15

Conrad, Marcel E., and Jay N. Umbreit. "Pathways of Iron Absorption." Blood Cells, Molecules, and Diseases 29, no. 3 (November 2002): 336–55. http://dx.doi.org/10.1006/bcmd.2002.0564.

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16

Hallberg, Leif, and Lena Hulthén. "Perspectives on Iron Absorption." Blood Cells, Molecules, and Diseases 29, no. 3 (November 2002): 562–73. http://dx.doi.org/10.1006/bcmd.2002.0603.

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17

O??Neil-Cutting, Mary A., and William H. Crosby. "Antacids and Iron Absorption." Nurse Practitioner 11, no. 8 (August 1986): 70. http://dx.doi.org/10.1097/00006205-198608000-00015.

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18

Andrews, Nancy C. "Iron metabolism and absorption." Reviews in Clinical and Experimental Hematology 4, no. 4 (December 2000): 283–301. http://dx.doi.org/10.1046/j.1468-0734.2000.00021.x.

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19

Sörensen, Einar Wolff. "Studies on Iron Absorption." Acta Medica Scandinavica 180, no. 2 (April 24, 2009): 241–44. http://dx.doi.org/10.1111/j.0954-6820.1966.tb02831.x.

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20

Sörensen, Einar Wolff. "Studies on Iron Absorption." Acta Medica Scandinavica 181, no. 6 (April 24, 2009): 707–16. http://dx.doi.org/10.1111/j.0954-6820.1967.tb07989.x.

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21

Sörensen, Einar Wolff. "Studies on Iron Absorption." Acta Medica Scandinavica 181, no. 6 (April 24, 2009): 739–46. http://dx.doi.org/10.1111/j.0954-6820.1967.tb07995.x.

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22

CONRAD, MARCEL E., JAY N. UMBREIT, and ELIZABETH G. MOORE. "Iron Absorption and Transport." American Journal of the Medical Sciences 318, no. 4 (October 1999): 213. http://dx.doi.org/10.1097/00000441-199910000-00002.

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23

Magnusson, B., E. Bjorn-Rasmussen, L. Hallberg, and L. Rossander. "Iron Absorption in Relation to Iron Status." Scandinavian Journal of Haematology 27, no. 3 (April 24, 2009): 201–8. http://dx.doi.org/10.1111/j.1600-0609.1981.tb00473.x.

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24

BOTHWELL, T. H., R. D. BAYNES, B. J. MACFARLANE, and A. P. MACPHAIL. "Nutritional iron requirements and food iron absorption." Journal of Internal Medicine 226, no. 5 (November 1989): 357–65. http://dx.doi.org/10.1111/j.1365-2796.1989.tb01409.x.

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25

Huebers, H. A., E. Csiba, B. Josephson, and C. A. Finch. "Iron absorption in the iron-deficient rat." Blut 60, no. 6 (June 1990): 345–51. http://dx.doi.org/10.1007/bf01737850.

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26

Ajioka, Richard S., Ivana De Domenico, and James P. Kushner. "Hepcidin-Independent Regulation of Dietary Iron Absorption." Blood 112, no. 11 (November 16, 2008): 3853. http://dx.doi.org/10.1182/blood.v112.11.3853.3853.

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Abstract Iron homeostasis in mammals is maintained at the level of iron absorption by the gut. Hepcidin plays a central role in homeostasis by binding to ferroportin and regulating cellular iron export. We found that mice weaned onto diets ranging from 35–350 mg Fe/kg for a period of 4 wk did not change body iron levels as measured by organ iron content and hematological parameters. Direct measure of absorption of 59Fe administered by gavage revealed an inverse correlation between dietary iron content and absorption. Gavage experiments were done following a 4h fast when the stomach and proximal small bowel were free of dietary content. Although iron absorption changed, liver expression of hepcidin mRNA did not. We measured the absorptive response in mice weaned onto diets containing 35 mg Fe/kg for 4 wk and abruptly changed to 350 mg Fe/kg. There was no change in iron absorption at day 1 but by day 3 absorption was reduced nearly 3-fold compared to controls and remained at this level for at least 7d. During this time neither liver nor spleen iron content changed but transferrin saturation increased approximately 1.5-fold. Most importantly, serum hepcidin levels, measured by a competitive binding assay (De Domenico et al. Cell Metab.2008, 8:146–156), were unchanged. Mice were then changed from diets containing 350 mg Fe/kg to diets containing 35 mg Fe/kg. Within 24h mice increased absorption of 59Fe 3-fold. Elevated absorption continued for at least 3d, declined by 7d and at 14d was at a level found in mice maintained on a diet containing 35 mg Fe/kg. During this period there was no change in organ iron content or in transferrin saturation. Serum hepcidin did not change on day 1, but was reduced by approximately 40% on days 3 through 7. Increased iron absorption could be attributed in part to increased expression of Dmt1 but no change in ferroportin message was detected. Enterocyte ferritin levels doubled on day 1 but returned to control levels on days 3 through 7. Finally, mice with a targeted disruption of the hepcidin gene were challenged with an abrupt reduction in dietary iron content and absorption increased approximately 3-fold. These data suggest that iron absorption can respond to changes in dietary iron content independent of hepcidin and that response to changes in luminal iron content are at the level of uptake and storage in a manner intrinsic to the enterocyte.
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27

Lynch, SR, BS Skikne, and JD Cook. "Food iron absorption in idiopathic hemochromatosis." Blood 74, no. 6 (November 1, 1989): 2187–93. http://dx.doi.org/10.1182/blood.v74.6.2187.2187.

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Abstract The relationship between iron status and food iron absorption was evaluated in 75 normal volunteers, 15 patients with idiopathic hemochromatosis, and 22 heterozygotes by using double extrinsic radioiron tags to label independently the nonheme and heme iron components of a hamburger meal. In normal subjects, absorption from each of these pools was inversely correlated with storage iron, as measured by the serum ferritin concentration. In patients with hemochromatosis, absorption of both forms of iron was far greater than would be predicted from the relationship between absorption and serum ferritin observed in normal volunteers. Nevertheless, there was still a modest but statistically significant reduction in absorption of nonheme iron with increasing serum ferritin. This relationship could not be demonstrated in the case of heme iron absorption. In heterozygotes, nonheme iron absorption from a hamburger meal containing no supplementary iron did not differ significantly from that observed in normal volunteers. However, when this meal was both modified to promote bioavailability and supplemented with iron, absorption of nonheme iron was significantly elevated. These studies confirm the presence of excessive nonheme iron absorption even from unfortified meals in patients with idiopathic hemochromatosis and suggest in addition that they are particularly susceptible to iron loading from diets containing a high proportion of heme iron. Impaired regulation of nonheme iron absorption was also observed in heterozygous individuals, but a statistically significant abnormality was demonstrable only when the test meal contained a large highly bioavailable iron supplement.
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28

Lynch, SR, BS Skikne, and JD Cook. "Food iron absorption in idiopathic hemochromatosis." Blood 74, no. 6 (November 1, 1989): 2187–93. http://dx.doi.org/10.1182/blood.v74.6.2187.bloodjournal7462187.

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The relationship between iron status and food iron absorption was evaluated in 75 normal volunteers, 15 patients with idiopathic hemochromatosis, and 22 heterozygotes by using double extrinsic radioiron tags to label independently the nonheme and heme iron components of a hamburger meal. In normal subjects, absorption from each of these pools was inversely correlated with storage iron, as measured by the serum ferritin concentration. In patients with hemochromatosis, absorption of both forms of iron was far greater than would be predicted from the relationship between absorption and serum ferritin observed in normal volunteers. Nevertheless, there was still a modest but statistically significant reduction in absorption of nonheme iron with increasing serum ferritin. This relationship could not be demonstrated in the case of heme iron absorption. In heterozygotes, nonheme iron absorption from a hamburger meal containing no supplementary iron did not differ significantly from that observed in normal volunteers. However, when this meal was both modified to promote bioavailability and supplemented with iron, absorption of nonheme iron was significantly elevated. These studies confirm the presence of excessive nonheme iron absorption even from unfortified meals in patients with idiopathic hemochromatosis and suggest in addition that they are particularly susceptible to iron loading from diets containing a high proportion of heme iron. Impaired regulation of nonheme iron absorption was also observed in heterozygous individuals, but a statistically significant abnormality was demonstrable only when the test meal contained a large highly bioavailable iron supplement.
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29

LINAKIS, JAMES G., PETER G. LACOUTURE, and ALAN WOOLF. "Iron absorption from chewable vitamins with iron versus iron tablets." Pediatric Emergency Care 8, no. 6 (December 1992): 321–24. http://dx.doi.org/10.1097/00006565-199212000-00003.

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30

S Nagalakshmi, S. Nagalakshmi, and Arun Prem Kumar. "Importance of Iron in Maize (Zea mays L.) genotypes and quantification of iron content by Atomic Absorption Spectrophotometry." International Journal of Scientific Research 2, no. 5 (June 1, 2012): 13–14. http://dx.doi.org/10.15373/22778179/may2013/6.

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31

Olivares, Manuel, Eva Hertrampf, and Fernando Pizarro. "Effect of iron stores on heme iron absorption." Nutrition Research 13, no. 6 (June 1993): 633–38. http://dx.doi.org/10.1016/s0271-5317(05)80555-x.

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32

KAWAKAMI, Hiroshi, Makiko HIRATSUKA, and Shun''ichi DOSAKO. "Effects of iron-saturated lactoferrin on iron absorption." Agricultural and Biological Chemistry 52, no. 4 (1988): 903–8. http://dx.doi.org/10.1271/bbb1961.52.903.

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33

Magnusson, Bengt, Lennart Sölvell, Bertil Arvidsson, and Christer Siösteen. "Iron Absorption during Iron Supplementation in Blood Donors." Scandinavian Journal of Haematology 14, no. 5 (April 24, 2009): 337–46. http://dx.doi.org/10.1111/j.1600-0609.1975.tb02705.x.

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34

Conrad, Marcel E., and Jay N. Umbreit. "Iron absorption: Relative importance of iron transport pathways." American Journal of Hematology 67, no. 3 (2001): 215. http://dx.doi.org/10.1002/ajh.1114.

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35

Kawakami, Hiroshi, Makiko Hiratsuka, and Shun’ichi Dosako. "Effects of Iron-saturated Lactoferrin on Iron Absorption." Agricultural and Biological Chemistry 52, no. 4 (April 1988): 903–8. http://dx.doi.org/10.1080/00021369.1988.10868784.

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36

Barrett, Jon F. R., Paul G. Whittaker, John D. Fenwick, John G. Williams, and Tom Lind. "Comparison of Stable Isotopes and Radioisotopes in the Measurement of Iron Absorption in Healthy Women." Clinical Science 87, no. 1 (July 1, 1994): 91–95. http://dx.doi.org/10.1042/cs0870091.

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1. Stable isotope methods are being used to investigate the absorption of dietary iron. In order to be certain that this new methodology is accurate, we have compared results obtained using stable isotopes and inductively coupled plasma mass spectrometry with those determined using a radioisotope and whole body counting. 2. The stable isotope 54Fe (2.8 mg) was given to 10 healthy non-pregnant women. Six women received the isotope in aqueous form, and four took it with a meat meal. The 54Fe served as a carrier for 10 ng of the radioisotope 59Fe. An ampoule (200 μg) of the isotope 57Fe or 58Fe was then given intravenously, and in serum samples taken over the next 10 h the ratios of the stable iron isotopes were measured by inductively coupled plasma mass spectrometry and the oral iron absorption was calculated. This was then compared with the results obtained by using a whole body counter to measure (on day 0 and day 14) the γ-activity emitted by the radioisotope. 3. The mean iron absorption measured by both methods ranged from 8% to 45%. Measurement of the post-absorptive serum enrichment of the stable isotopes provided estimates of absorption from both aqueous and food iron which were similar to that yielded by whole body counting, the mean difference being −1.5% (95% confidence interval −5.2 to 2.1%). Absorption estimated by stable isotopes exhibited the same inverse relationship with the serum ferritin level (body iron stores) to that known to exist with whole body counting. Similar estimates of food iron absorption were obtained irrespective of the type of isotope used as an extrinsic label, implying that stable isotopes are as valid as radioisotopes in reflecting intrinsic food iron absorption. 4. This study validates the use of stable isotopes and post-absorption curves as a new and accurate technique in the measurement of iron absorption.
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37

Ekenved, Gunnar. "ABSORPTION FROM DIFFERENT TYPES OF IRON TABLETS - CORRELATION BETWEEN SERUM IRON INCREASE AND TOTAL ABSORPTION OF IRON." Scandinavian Journal of Haematology 17, S28 (April 24, 2009): 51–63. http://dx.doi.org/10.1111/j.1600-0609.1976.tb00348.x.

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38

Szymlek-Gay, Ewa A., Magnus Domellöf, Olle Hernell, Richard F. Hurrell, Torbjörn Lind, Bo Lönnerdal, Christophe Zeder, and Ines M. Egli. "Mode of oral iron administration and the amount of iron habitually consumed do not affect iron absorption, systemic iron utilisation or zinc absorption in iron-sufficient infants: a randomised trial." British Journal of Nutrition 116, no. 6 (August 22, 2016): 1046–60. http://dx.doi.org/10.1017/s0007114516003032.

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AbstractDifferent metabolic pathways of supplemental and fortification Fe, or inhibition of Zn absorption by Fe, may explain adverse effects of supplemental Fe in Fe-sufficient infants. We determined whether the mode of oral Fe administration or the amount habitually consumed affects Fe absorption and systemic Fe utilisation in infants, and assessed the effects of these interventions on Zn absorption, Fe and Zn status, and growth. Fe-sufficient 6-month-old infants (n72) were randomly assigned to receive 6·6 mg Fe/d from a high-Fe formula, 1·3 mg Fe/d from a low-Fe formula or 6·6 mg Fe/d from Fe drops and a formula with no added Fe for 45 d. Fractional Fe absorption, Fe utilisation and fractional Zn absorption were measured with oral (57Fe and67Zn) and intravenous (58Fe and70Zn) isotopes. Fe and Zn status, infection and growth were measured. At 45 d, Hb was 6·3 g/l higher in the high-Fe formula group compared with the Fe drops group, whereas serum ferritin was 34 and 35 % higher, respectively, and serum transferrin 0·1 g/l lower in the high-Fe formula and Fe drops groups compared with the low-Fe formula group (allP<0·05). No intervention effects were observed on Fe absorption, Fe utilisation, Zn absorption, other Fe status indices, plasma Zn or growth. We concluded that neither supplemental or fortification Fe nor the amount of Fe habitually consumed altered Fe absorption, Fe utilisation, Zn absorption, Zn status or growth in Fe-sufficient infants. Consumption of low-Fe formula as the only source of Fe was insufficient to maintain Fe stores.
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39

Blachier, François, Pierre Vaugelade, Véronique Robert, Bertille Kibangou, François Canonne-Hergaux, Serge Delpal, François Bureau, Hervé Blottière, and Dominique Bouglé. "Comparative capacities of the pig colon and duodenum for luminal iron absorption." Canadian Journal of Physiology and Pharmacology 85, no. 2 (February 2007): 185–92. http://dx.doi.org/10.1139/y07-007.

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Iron deficiency is the most common human nutritional disorder in the world. Iron absorptive capacity of the small intestine is known to be much limited and therefore large quantities of iron salts must be used to treat iron deficiency. As a result, significant amounts of iron may reach the large intestine. This study compared the capacities of the small and large intestine to transfer luminal iron to the venous blood in relationship with the expression in epithelial cells of proteins involved in iron absorption using a pig model. Intracaecal injection of iron sulphate corresponding with 2.5 and 5.0 mg elemental iron per kg body mass resulted in modest, transient, but significant (p < 0.05) increases in iron concentration in the portal blood plasma. By comparing portal blood plasma iron concentrations following injection in the duodenal and caecal lumen, we calculated that 5 h after injection, iron colonic absorption represented approximately 14% of duodenal absorption. Caecal and proximal colon mucosa accumulated iron to a much lower extent than the duodenal mucosa. Isolated colonocytes were found to express divalent metal transporter (DMT1) and ferritin, but to a lesser extent than the duodenal enterocytes. Ferroportin was highly expressed in colonocytes. In these cells as well as in enterocytes ferroportin was found to be glycosylated. In short term experiments and at a concentration in the range of that measured in the aqueous phases recovered from the large intestine luminal content after iron injection, iron sulphate did not alter colonocyte viability. We concluded that the colonic epithelial cells that express proteins involved in iron absorption are able to transfer luminal iron to the venous blood even if its relative participation in the overall intestinal absorption appears to be modest under our experimental conditions.
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40

Mandilaras, Konstantinos, Tharse Pathmanathan, and Fanis Missirlis. "Iron Absorption in Drosophila melanogaster." Nutrients 5, no. 5 (May 17, 2013): 1622–47. http://dx.doi.org/10.3390/nu5051622.

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41

Hunt, Janet R. "Absorption of iron from ferritin." American Journal of Clinical Nutrition 81, no. 5 (May 1, 2005): 1178–79. http://dx.doi.org/10.1093/ajcn/81.5.1178.

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42

Simpson, Robert J., Martin Lombard, Kishor B. Raja, Ray Thatcher, and Timothy J. Peters. "Iron absorption by hypotransferrinaemic mice." British Journal of Haematology 78, no. 4 (August 1991): 565–70. http://dx.doi.org/10.1111/j.1365-2141.1991.tb04490.x.

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43

Sørensen, Einar Wolff. "Studies on Iron Absorption. III." Acta Medica Scandinavica 178, no. 5 (April 24, 2009): 663–64. http://dx.doi.org/10.1111/j.0954-6820.1965.tb04316.x.

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44

Barger-Lux, M. J. "Calcium supplementation and iron absorption." American Journal of Clinical Nutrition 54, no. 3 (September 1, 1991): 607. http://dx.doi.org/10.1093/ajcn/54.3.607.

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45

Gallagher, Patrick G., and Richard A. Ehrenkranz. "Understanding Iron Absorption and Metabolism." Journal of Pediatric Gastroenterology & Nutrition 27, no. 5 (November 1998): 610–11. http://dx.doi.org/10.1097/00005176-199811000-00023.

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46

Pandey, Shyam Bahadur. "THE MECHANISM OF IRON ABSORPTION." Journal of Nepal Medical Association 15, no. 44 (January 1, 2003): I—III. http://dx.doi.org/10.31729/jnma.1002.

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47

Torrance, Colin. "Absorption and function of iron." Nursing Standard 6, no. 19 (February 4, 1992): 25–28. http://dx.doi.org/10.7748/ns.6.19.25.s37.

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48

Fomon, Samuel J., Ekhard E. Ziegler, Ronald R. Rogers, Steven E. Nelson, Barbara B. Edwards, David G. Guy, John C. Erve, and Morteza Janghorbani. "Iron Absorption from Infant Foods." Pediatric Research 26, no. 3 (September 1989): 250–54. http://dx.doi.org/10.1203/00006450-198909000-00019.

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49

Milman, Nils, and Lars Larsen. "Iron Absorption after Renal Transplantation." Acta Medica Scandinavica 200, no. 1-6 (April 24, 2009): 25–30. http://dx.doi.org/10.1111/j.0954-6820.1976.tb08191.x.

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Hallberg, Leif, Lennart Sölvell, and Bengt Zederfeldt. "Iron Absorption after Partial Gastrectomy." Acta Medica Scandinavica 179, S445 (April 24, 2009): 269–75. http://dx.doi.org/10.1111/j.0954-6820.1966.tb02370.x.

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