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1 tinal epithelium but not involved in dietary iron absorption.
2 enting iron recycling and decreasing dietary iron absorption.
3 tivated in the intestine and is essential in iron absorption.
4 affected inflammation biomarkers nor altered iron absorption.
5 creases serum hepcidin and decreases dietary iron absorption.
6 However, calcium administration may inhibit iron absorption.
7 hepcidin (HAMP), the hormone that regulates iron absorption.
8 l tranporter-1, as well as enhanced duodenal iron absorption.
9 n normal hematologic values due to increased iron absorption.
10 e expression of key genes that contribute to iron absorption.
11 gle meals cannot be used to estimate dietary iron absorption.
12 3 months following disruption of intestinal iron absorption.
13 n solubility and bioavailability and improve iron absorption.
14 uodenal enterocytes, is required for optimal iron absorption.
15 a battery of genes essential for intestinal iron absorption.
16 ich increased the surface area available for iron absorption.
17 a regulatory mechanism for limiting further iron absorption.
18 ermore, hypoxia can also affect and increase iron absorption.
19 would further exacerbate anemia and increase iron absorption.
20 cted 36% of the interindividual variation in iron absorption.
21 epithelial cells leads to loss of intestinal iron absorption.
22 epcidin explain interindividual variation in iron absorption.
23 p transcription, permitting enhanced dietary iron absorption.
24 ly to be due to a TNF-alpha-induced block in iron absorption.
25 ys a pivotal role as a negative regulator of iron absorption.
26 lity to modulate iron metabolism and dietary iron absorption.
27 heme intakes, zinc intakes may increase heme-iron absorption.
28 tely predict the influence of polyphenols on iron absorption.
29 w Hamp1 levels are responsible for increased iron absorption.
30 that higher zinc intakes would decrease heme-iron absorption.
31 of an iron-sensing mechanism that regulates iron absorption.
32 dietary inhibitor of both heme- and nonheme-iron absorption.
33 role in determining the level of intestinal iron absorption.
34 a multicopper oxidase essential for enteric iron absorption.
35 no significant effect of dietary calcium on iron absorption.
36 hypercoagulability, and increased intestinal iron absorption.
37 d doses increases serum hepcidin and reduces iron absorption.
38 thereby possibly reflecting greater colonic iron absorption.
39 s gastric acid production, which can inhibit iron absorption.
40 itory effect, resulting in increased nonheme iron absorption.
41 s gastric acid production, which can inhibit iron absorption.
42 ingested tracer underestimated true maternal iron absorption.
43 act on nutrition whereby they interfere with iron absorption.
44 ation and serum hepcidin and thereby improve iron absorption.
45 1.41, -0.28)] were significant predictors of iron absorption.
46 rge variations were observed in mean nonheme-iron absorption (0.7-22.9%) between studies, which depen
47 dividuals (all from US studies): log[nonheme-iron absorption, %] = -0.73 log[ferritin, mug/L] + 0.11
50 Our objective was to re-evaluate maternal iron absorption after factoring in these losses and iden
51 e essential role of HIF-2alpha in regulating iron absorption and also demonstrate that hypoxia sensin
54 iron homeostasis, hepcidin, block intestinal iron absorption and cause iron retention in reticuloendo
55 ghts a role of HIF-2 in the dysregulation of iron absorption and chronic iron accumulation, as observ
57 ial for all cells but is toxic in excess, so iron absorption and distribution are tightly regulated.
62 Hepcidin-25 is a peptide hormone involved in iron absorption and homeostasis and found at increased s
71 n (Hp) plays an important role in intestinal iron absorption and is predicted to be a ferroxidase bas
72 major transporter responsible for intestinal iron absorption and its expression is regulated by body
73 iency of hepcidin, the hormone that controls iron absorption and its tissue distribution, is the caus
76 a peptide hormone that decreases intestinal iron absorption and macrophage iron release, is a potent
80 tory diseases, up-regulated hepcidin impairs iron absorption and macrophage release, causing anemia.
82 of vitamin C that result from its effects on iron absorption and metabolism has not been confirmed in
83 alternate days and in single doses optimises iron absorption and might be a preferable dosing regimen
85 iron-regulatory hormone hepcidin to increase iron absorption and mobilization of iron from stores.
86 cell types leads to the increased intestinal iron absorption and plasma iron levels characteristic of
89 ne 6 (TMPRSS6) gene, an enzyme that promotes iron absorption and recycling by inhibiting hepcidin ant
93 levels of hepcidin, a negative regulator of iron absorption and recycling, underlie the pathophysiol
97 ing porridge meal leads to decreased nonheme iron absorption and that a 1-h time interval between a m
98 o meet these iron requirements, both dietary iron absorption and the mobilization of iron from stores
101 iron-loading anemias whereby both increased iron absorption and transfusion therapy contribute to th
106 romatosis (involved in venous ulceration and iron absorption), and various types of collagen (contrib
107 at leads to increased EPO production, better iron absorption, and amelioration of anemia in chronic k
109 microcytic anemia due to impaired intestinal iron absorption, and defective iron utilization in red c
110 one marrow iron stores, increased intestinal iron absorption, and hemoglobin response to SF) among no
111 o measure inflammation biomarkers, hepcidin, iron absorption, and utilization pre- and posttreatment
112 alues, 36% of interindividual differences in iron absorption are explained by differences in circulat
113 ed hepatic peptide that regulates intestinal iron absorption as well as maternal-fetal iron transport
114 e iron bioavailability (total and fractional iron absorption), assessed by measuring the isotopic lab
116 interactive program for calculating dietary iron absorption at any concentration of serum ferritin i
117 e used to develop a model to predict dietary iron absorption at different serum ferritin concentratio
121 isotope studies have shown no difference in iron absorption between infants with high or low hemoglo
123 y was to evaluate the influence of inulin on iron absorption, bifidobacteria, total bacteria, short-c
125 en shown to be a potent inhibitor of nonheme iron absorption, but it remains unclear whether the timi
126 to MNP and MNP+RUTF significantly increased iron absorption by 1.85-fold (95% CI: 1.49-, 2.29-fold;
127 0.001).GOS consumption by infants increased iron absorption by 62% from an MNP containing FeFum+NaFe
129 regulatory hormone hepcidin enable excessive iron absorption by ferroportin, the unique cellular iron
131 hat regulates iron homeostasis by inhibiting iron absorption by the small intestine and release of ir
132 ) and that from FeSO4 (34.3 +/- 23.6%) or in iron absorption calculated from red blood cell incorpora
133 blood transfusions and excessive intestinal iron absorption can be a complication of chronic anemias
134 enotype stems from impaired gastrointestinal iron absorption caused by a point mutation of the gastri
135 to repeated blood transfusions and increased iron absorption, chronic hemolysis is the major cause of
136 ) transporter internalization, impairing the iron absorption; clinically manifested as anemia of infl
137 e days increases PHep and modestly decreases iron absorption compared with alternate day dosing, and
139 1% [8.2, 20.7] twice daily; p=0.33) or total iron absorption (day 1-3: 44.3 mg [29.4, 66.7] once dail
142 good quantitative and dynamic description of iron absorption, distribution, storage and mobilization
147 ulated to play important roles in intestinal iron absorption, erythroid iron utilization, hepatic iro
150 2 x 2 factorial experiments compared women's iron absorption from 2 maize varieties (ACR and TZB; n =
152 ermine whether prebiotic consumption affects iron absorption from a micronutrient powder (MNP) contai
153 h an iron-fortified maize meal and 2) assess iron absorption from a micronutrient powder (MNP) given
154 increase in serum hepcidin and a decrease in iron absorption from adiposity-related inflammation.
155 tion was observed between serum ferritin and iron absorption from both ferritin and FeSO4, which sugg
158 ore or with the meal significantly increased iron absorption from FePP by 2.55-fold (95% CI: 1.48-, 4
161 orhydria reduced the normal increase in heme-iron absorption from hemoglobin in response to iron defi
162 stimated from predictive algorithms, nonheme iron absorption from meals, and models of iron intake, s
165 was no significant difference in whole-body iron absorption from soybean ferritin (29.9 +/- 19.8%) a
167 t prohepcidin, was inversely associated with iron absorption from supplemental and food-based nonheme
168 iron regulatory hormone capable of blocking iron absorption from the duodenum and iron release from
170 ron exporter ferroportin, hepcidin decreases iron absorption from the intestine and iron release from
176 a in the intestine abolished the increase in iron absorption genes as assessed by quantitative real-t
179 se dependence, and its effects on subsequent iron absorption have not been characterized in humans.
180 t developmental changes in the regulation of iron absorption; however, little is known about the mole
181 ed on the modulation of pathways that reduce iron absorption (ie, using hepcidin activators like Tmpr
182 less well understood than the regulation of iron absorption in adults, which is inverse to iron stat
183 time interval of tea consumption on nonheme iron absorption in an iron-containing meal in a cohort o
184 and oligofructose have been shown to improve iron absorption in animals through colonic uptake, but t
190 export protein ferroportin (FPN1) to adjust iron absorption in enterocytes, iron recycling through r
193 (CA/TSC) mixture before extrusion increases iron absorption in humans from FePP-fortified extruded r
194 isotopes has provided valuable insights into iron absorption in humans, but the data have been limite
196 cidin agonists might help treat the abnormal iron absorption in individuals with beta-thalassemia and
197 Whether consumption of prebiotics increases iron absorption in infants is unclear.We set out to dete
198 th a reduction in the normal upregulation of iron absorption in iron-deficient obese subjects, and th
199 be reproduced by increasing the setpoint of iron absorption in the duodenum to a level where the sys
200 n homeostasis is maintained by regulation of iron absorption in the duodenum, iron recycling from ery
203 of full-length mRNA would predict deficient iron absorption in the intestine and deficient iron util
205 hepcidin and serum prohepcidin with nonheme-iron absorption in the presence and absence of food with
208 ective of the study was to ascertain whether iron absorption in women adapts to dietary iron bioavail
212 ascorbic acid (or other luminal enhancers of iron absorption) in obese individuals to improve iron st
213 t subjects (n = 17), geometric mean (95% CI) iron absorption increased by 28% [from 9.7% (6.5%, 14.6%
214 istribution of iron by inhibiting intestinal iron absorption, iron recycling by macrophages, and iron
215 iron homeostasis by coordinately regulating iron absorption, iron recycling, and mobilization of sto
218 iron during erythropoiesis, small intestinal iron absorption is increased through an undefined mechan
221 and the enhancing effect of ascorbic acid on iron absorption is one-half of that in normal-weight wom
226 liver-derived protein that restricts enteric iron absorption, is the key regulator of body iron conte
228 der the normal regulatory control of dietary iron absorption, namely via ferroportin-dependent efflux
229 e objectives were to 1) assess the effect on iron absorption of a lipid emulsion given 20 min before
230 st the possibility of an enhancing effect on iron absorption of lipid-rich RUTFs, but more research i
231 iron-induced increase in hepcidin influences iron absorption of successive daily iron doses and twice
236 gastric residence time, which could increase iron absorption, particularly from poorly soluble iron c
239 he duodenum, spleen, and liver, the sites of iron absorption, recycling, and storage respectively.
240 ith iron-unresponsive anemia due to impaired iron absorption/redistribution from tuberculosis-associa
241 iron without significantly affecting nonheme-iron absorption, regardless of meal bioavailability.
243 SO4, which suggested that sensors regulating iron absorption respond similarly to iron provided as fe
245 e genotyping of 103 participants in previous iron-absorption studies, 5 C282Y-heterozygous subjects w
247 certain whether luminal enhancers of dietary iron absorption such as ascorbic acid can be effective i
248 ed particles (50 nm in diameter) had a lower iron absorption than unexposed or chronically exposed bi
249 atosis is an inherited disorder of increased iron absorption that can result in cirrhosis, diabetes,
251 mals requires sustained postnatal intestinal iron absorption that maintains intracellular iron concen
253 In the present study, we report a defect in iron absorption that results in iron-deficiency anemia,
254 mRNA levels of most of the genes involved in iron absorption that were tested; however, it did corres
255 By this mechanism, hepcidin inhibits dietary iron absorption, the efflux of recycled iron from spleni
256 ort of heme across membranes is critical for iron absorption, the formation of hemoglobin and other h
257 ad due to both transfused iron and increased iron absorption, the latter mediated by suppression of t
258 e intrinsic ability to regulate the rates of iron absorption, the spotlight in the past decade has be
259 hough hepcidin is proposed as a regulator of iron absorption, this has not been assessed in humans.
262 showed that dysregulation of the intestinal iron absorption transporter divalent metal transporter-1
263 abel, randomised controlled trials assessing iron absorption using ((54)Fe)-labelled, ((57)Fe)-labell
264 nd hematologic indexes and heme- and nonheme-iron absorption-using a standardized meal containing 3 m
265 e-day group (p=0.0013), and cumulative total iron absorption was 131.0 mg (71.4, 240.5) versus 175.3
268 by the erythrocyte iron incorporation method.Iron absorption was 5.7% +/- 8.5% (TM-1), 3.6% +/- 4.2%
271 e control subjects were recruited, and their iron absorption was compared by using a hamburger test m
272 cidin was increased (P < .01) and fractional iron absorption was decreased by 35% to 45% (P < .01).
275 e, blood samples were collected for 8 h, and iron absorption was estimated by erythrocyte incorporati
284 ion, and dietary intakes were also assessed; iron absorption was measured in a subgroup of women.
292 metric mean (-SD, +SD) cumulative fractional iron absorptions were 16.3% (9.3, 28.8) in the consecuti
293 g, exclusively breastfed infants upregulated iron absorption when iron stores were depleted at both 2
294 lassemia, results in sustained elevations in iron absorption, which cause iron overload with associat
295 signals induced dysregulation of intestinal iron absorption, which contributed to liver iron overloa
296 not from FeSO4 There was a trend to increase iron absorption with the MNP+RUTF meal, which did not re
297 rations of 15, 30, and 60 mg/L, mean dietary iron absorption would be 22.3%, 16.3%, and 11.6%, respec
299 zinc (1 or 9 mg); successful measurements of iron absorption, zinc absorption, or both were made in 4