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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.
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
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
20 ulator of iron metabolism, hepcidin inhibits dietary iron absorption and macrophage iron recycling.
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
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
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
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
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.
53 c iron balance by limiting the absorption of dietary iron and the release of iron from macrophage sto
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
59 n whether iron absorption in women adapts to dietary iron bioavailability and whether adaptation refl
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
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
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
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
82 onheme iron absorption requires reduction of dietary iron for uptake by the divalent metal ion transp
84 III)-selective chelators capable of removing dietary iron from the gastrointestinal tract and prevent
86 nding of how HFE regulates the absorption of dietary iron has been slow, but much can be learnt from
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
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
103 pression of TfR2 was not down-regulated with dietary iron loading or in the HFE -/- model of HH.
105 and Tfr2 up-regulate hepcidin in response to dietary iron loading without increases in liver Bmp6 mes
111 E C282Y-heterozygous subjects did not absorb dietary iron more efficiently, even when foods were high
113 infections, we examined the effect of excess dietary iron on disease severity in HCV-infected chimpan
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
118 he genetic basis is still uncertain (African dietary iron overload), and several less frequent or rar
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
126 urpose of these studies was to determine how dietary iron supplementation affected the severity of al
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
132 ropriately low levels of hepcidin, increased dietary iron uptake, and systemic iron accumulation, has
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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