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1 leading to up-regulation of transporters for dietary iron.
2 ulation of DMT1, and increased absorption of dietary iron.
3 ortin-1, consistent with increased uptake of dietary iron.
4 gluconeogenic enzymes seen with variation of dietary iron.
5 repair and pathogen recognition changed with dietary iron.
6 ection), hepcidin powerfully controls use of dietary iron.
7 enterocytes, which mediate the absorption of dietary iron.
8 nisms must be available for the reduction of dietary iron.
9 by long-term consumption of large amounts of dietary iron.
10 trol; P = 0.016), plasma lipoprotein(a), and dietary iron.
11 um iron (0.8; 95% CI, 0.7 to 1.0), and total dietary iron (0.8; 95% CI, 0.7 to 1.1).
12       Infected animals from the intermediate-dietary iron (40- and 100-ppm) groups exhibited greater
13  was to investigate combined effects of high dietary iron (650 mg/kg diet) and radiation exposure (0.
14 f blood to be phlebotomized when restricting dietary iron absorbed was estimated in the 3 longitudina
15 at HFE modulates erythropoiesis by affecting dietary iron absorption and erythroid iron intake.
16 isease associated with loss of regulation of dietary iron absorption and excessive iron deposition in
17 r of iron metabolism characterized by excess dietary iron absorption and iron deposition in several t
18                     At the whole-body level, dietary iron absorption and iron export from the tissues
19 e in the negative-feedback mechanism between dietary iron absorption and iron status.
20 ulator of iron metabolism, hepcidin inhibits dietary iron absorption and macrophage iron recycling.
21  hormone produced by the liver that inhibits dietary iron absorption and macrophage iron release.
22 contribute to anemia, but their influence on dietary iron absorption and recycling is unknown.
23        To meet these iron requirements, both dietary iron absorption and the mobilization of iron fro
24 women.An interactive program for calculating dietary iron absorption at any concentration of serum fe
25 dom, were used to develop a model to predict dietary iron absorption at different serum ferritin conc
26 erum ferritin, to substantial differences in dietary iron absorption for 8 wk.
27                                              Dietary iron absorption in the small intestine is requir
28 it is uncertain whether luminal enhancers of dietary iron absorption such as ascorbic acid can be eff
29  concentrations of 15, 30, and 60 mg/L, mean dietary iron absorption would be 22.3%, 16.3%, and 11.6%
30 is is under the normal regulatory control of dietary iron absorption, namely via ferroportin-dependen
31         By this mechanism, hepcidin inhibits dietary iron absorption, the efflux of recycled iron fro
32 issue iron deposition secondary to excessive dietary iron absorption.
33  is not required in the intestinal lumen for dietary iron absorption.
34 he intestinal epithelium but not involved in dietary iron absorption.
35 on, preventing iron recycling and decreasing dietary iron absorption.
36  that increases serum hepcidin and decreases dietary iron absorption.
37 from single meals cannot be used to estimate dietary iron absorption.
38 ocks Hamp transcription, permitting enhanced dietary iron absorption.
39 ism by which HFE mutations lead to increased dietary iron absorption.
40                                              Dietary iron affects circadian glucose metabolism throug
41 we used Hfe-KO mice in conditions of altered dietary iron and erythropoiesis.
42    We assessed the association of intakes of dietary iron and heme iron with risk of postmenopausal b
43 ors probably modulate the bioavailability of dietary iron and influence the accumulation of iron stor
44 lly increased to limit further absorption of dietary iron and its release from stores.
45  and that counter-regulatory factors such as dietary iron and luminal lipocalin 2 should be taken int
46 sorder characterized by excess absorption of dietary iron and progressive iron deposition in several
47 sorder characterized by excess absorption of dietary iron and progressive iron deposition in several
48                  These data demonstrate that dietary iron and radiation, alone and combined, contribu
49  provided evidence of an interaction between dietary iron and SLC40A1.
50 that mTORC1 activity in RBCs is regulated by dietary iron and that genetic activation or inhibition o
51 udy provide a mechanistic connection between dietary iron and the appetite-regulating hormone leptin.
52          Hepcidin controls the absorption of dietary iron and the distribution of iron among cell typ
53 c iron balance by limiting the absorption of dietary iron and the release of iron from macrophage sto
54                                   Intakes of dietary iron and, in particular, heme iron may increase
55 se to iron, allowing increased absorption of dietary iron, and eventually iron overload.
56 utations in HFE result in over absorption of dietary iron, and patterns of tissue iron deposition in
57 ongest evidence to date of the importance of dietary iron as a determinant of iron status in vulnerab
58        Iron-replete men partially adapted to dietary iron bioavailability and iron absorption from a
59 n whether iron absorption in women adapts to dietary iron bioavailability and whether adaptation refl
60                                   Values for dietary iron bioavailability are required for setting di
61                                   Values for dietary iron bioavailability can be derived for any targ
62 Adaptation of iron absorption in response to dietary iron bioavailability is less likely in premenopa
63 ts suggest that these diets would have lower dietary iron bioavailability than nonvegetarian diets, b
64 o adapt in response to a 12-wk difference in dietary iron bioavailability, whether absorption was tes
65  developed a new interactive tool to predict dietary iron bioavailability.Iron intake and serum ferri
66 , a disease in which excessive absorption of dietary iron can lead to liver cirrhosis, diabetes, arth
67 phenotype results from reduced absorption of dietary iron caused by high levels of hepcidin and is du
68                             Moreover, excess dietary iron caused significant elevation of serum iron
69       Consistent with the changes in leptin, dietary iron content was also directly related to food i
70 hemojuvelin in skeletal muscle regardless of dietary iron content.
71 of dietary iron overload (2% carbonyl iron), dietary iron deficiency (gastric parietal cell ablation)
72 shown that Mn accumulation is exacerbated by dietary iron deficiency (ID) and disturbances in norepin
73                                              Dietary iron deficiency can rapidly deplete brain iron c
74 for DMT1 up-regulation was a murine model of dietary iron deficiency that demonstrated greatly increa
75  to whether a causal relation exists between dietary iron deficiency with (ID+A) or without (ID-A) an
76                       DCT1 is upregulated by dietary iron deficiency, and may represent a key mediato
77  mice, which can be partially ameliorated by dietary iron depletion.
78   The aim of this study was to determine how dietary iron derived in this fashion is absorbed in the
79 etion in the Heph protein are able to absorb dietary iron despite reduced expression and mislocalizat
80           Mice receiving the lowest level of dietary iron exhibited borderline iron deficiency, with
81 ing porphyrin heme provides a rich source of dietary iron for mammals.
82 onheme iron absorption requires reduction of dietary iron for uptake by the divalent metal ion transp
83 ing hormone that regulates the absorption of dietary iron from the duodenum.
84 III)-selective chelators capable of removing dietary iron from the gastrointestinal tract and prevent
85 lso significantly higher in the intermediate-dietary-iron groups.
86 nding of how HFE regulates the absorption of dietary iron has been slow, but much can be learnt from
87                              The kinetics of dietary iron import into various organs of mice were eva
88                                              Dietary iron intake and iron absorption did not change d
89                                        While dietary iron intake by Yupiks was similar to that of a r
90                                              Dietary iron intake was assessed by frequency questionna
91 ate hepcidin production and, thus, increased dietary iron intake, and iron-loading anemias whereby bo
92 , body composition, physical activity level, dietary iron intake, delta-efficiency, or ventilatory th
93 eficiency occurs after insufficient maternal dietary iron intake, maternal hypertension, and maternal
94                                         Mean dietary iron intake, mean serum vitamin C concentrations
95 onsistently within the reference ranges) and dietary iron intakes did not differ significantly betwee
96 ta examining the risk of GDM associated with dietary iron, iron supplementation, and iron status as m
97 e of these disorders, the mechanism by which dietary iron is absorbed into the body is poorly underst
98 ion of hepcidin expression in hepatocytes by dietary iron is associated with an elevation of Bmp6 mRN
99 mochromatosis (HH), intestinal absorption of dietary iron is increased, leading to excessive iron acc
100 ction and consequent excessive absorption of dietary iron, leading to iron overload.
101 ectively), and this effect did not depend on dietary iron levels.
102                                              Dietary iron loading increased hepcidin and Id1 expressi
103 pression of TfR2 was not down-regulated with dietary iron loading or in the HFE -/- model of HH.
104                                              Dietary iron loading resulted in a substantially increas
105 and Tfr2 up-regulate hepcidin in response to dietary iron loading without increases in liver Bmp6 mes
106 ffer in basal iron status and sensitivity to dietary iron loading.
107 creases in P-Smad1,5,8 levels in response to dietary iron loading.
108                                   Unabsorbed dietary iron may increase free radical production in the
109                             Despite abundant dietary iron, mice with hepcidin-producing tumors develo
110                                              Dietary iron modulates levels of peroxisome proliferator
111 E C282Y-heterozygous subjects did not absorb dietary iron more efficiently, even when foods were high
112                   We assessed the effects of dietary iron on circadian gluconeogenesis.
113 infections, we examined the effect of excess dietary iron on disease severity in HCV-infected chimpan
114                    We examined the effect of dietary iron on regulation of hepcidin expression via th
115 s usually attributed to the malabsorption of dietary iron or the loss of iron from the intestinal muc
116 pression in normal mice and murine models of dietary iron overload (2% carbonyl iron), dietary iron d
117                                              Dietary iron overload caused a modest (30%) rise in plas
118 he genetic basis is still uncertain (African dietary iron overload), and several less frequent or rar
119       These findings indicate that levels of dietary iron play an important role in regulation of app
120                                         Most dietary iron remains unabsorbed and hence may be availab
121                                              Dietary iron repletion completely reversed ID anemia and
122               These data suggest that severe dietary iron restriction impairs hookworm development in
123 ed in order to test the hypothesis that host dietary iron restriction mediates susceptibility to hook
124 of the chemistry and biology of each type of dietary iron source (ferritin, heme, Fe2+ ion, etc.), an
125        A member of the nonheme iron group of dietary iron sources, ferritin is a complex with Fe3+ ir
126 urpose of these studies was to determine how dietary iron supplementation affected the severity of al
127                                              Dietary iron supplementation is associated with increase
128 im of this study was to assess the effect of dietary iron supplementation on insulin resistance and t
129 sent study, we used a rat model of long term dietary iron supplementation to identify stellate cell g
130 ndent upon carefully regulated absorption of dietary iron, thus these genes are of fundamental import
131                   These changes may increase dietary iron uptake and allow release of stored iron to
132 ropriately low levels of hepcidin, increased dietary iron uptake, and systemic iron accumulation, has
133 or older children without adverse effects on dietary iron utilization.
134 nal DMT1, the main transporter for uptake of dietary iron, were higher in the TfR2-mutant mice as com
135 e differentiating enterocytes to absorb more dietary iron when they mature into villus enterocytes.
136 lability diet absorbed up to 4.5 mg (30-35%) dietary iron with minimal influence of the diet consumed

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