ライフサイエンスコーパス: dietary iron

1 by long-term consumption of large amounts of dietary iron.

2 trol; P = 0.016), plasma lipoprotein(a), and dietary iron.

3 leading to up-regulation of transporters for dietary iron.

4 ulation of DMT1, and increased absorption of dietary iron.

5 it, likely because of a lack of bioavailable dietary iron.

6 t did not increase intensity with increasing dietary iron.

7 ortin-1, consistent with increased uptake of dietary iron.

8 gluconeogenic enzymes seen with variation of dietary iron.

9 repair and pathogen recognition changed with dietary iron.

10 ection), hepcidin powerfully controls use of dietary iron.

11 enterocytes, which mediate the absorption of dietary iron.

12 nisms must be available for the reduction of dietary iron.

13 um iron (0.8; 95% CI, 0.7 to 1.0), and total dietary iron (0.8; 95% CI, 0.7 to 1.1).

14 Infected animals from the intermediate-dietary iron (40- and 100-ppm) groups exhibited greater

15 was to investigate combined effects of high dietary iron (650 mg/kg diet) and radiation exposure (0.

16 f blood to be phlebotomized when restricting dietary iron absorbed was estimated in the 3 longitudina

17 at HFE modulates erythropoiesis by affecting dietary iron absorption and erythroid iron intake.

18 isease associated with loss of regulation of dietary iron absorption and excessive iron deposition in

19 imaging scans of individuals with excessive dietary iron absorption and hemochromatosis risk.

20 entation, Beninese women had lower long-term dietary iron absorption and higher iron losses in the pr

21 r of iron metabolism characterized by excess dietary iron absorption and iron deposition in several t

22 At the whole-body level, dietary iron absorption and iron export from the tissues

23 e in the negative-feedback mechanism between dietary iron absorption and iron status.

24 ulator of iron metabolism, hepcidin inhibits dietary iron absorption and macrophage iron recycling.

25 hormone produced by the liver that inhibits dietary iron absorption and macrophage iron release.

26 Hepcidin reduces dietary iron absorption and may contribute to declines i

27 contribute to anemia, but their influence on dietary iron absorption and recycling is unknown.

28 To meet these iron requirements, both dietary iron absorption and the mobilization of iron fro

29 women.An interactive program for calculating dietary iron absorption at any concentration of serum fe

30 dom, were used to develop a model to predict dietary iron absorption at different serum ferritin conc

31 esponse to physical activity and declines in dietary iron absorption compared with energy balance.

32 Strenuous physical activity decreases dietary iron absorption compared with rest.

33 erum ferritin, to substantial differences in dietary iron absorption for 8 wk.

34 injection of excess apotransferrin enhances dietary iron absorption in mice and triggers accumulatio

35 Dietary iron absorption in the small intestine is requir

36 ectively, these findings indicate that while dietary iron absorption is reduced in children with vira

37 PCBP1 deletion and the resulting unregulated dietary iron absorption led to poor growth, severe anemi

38 it is uncertain whether luminal enhancers of dietary iron absorption such as ascorbic acid can be eff

39 In iron-sufficient children, median (95% CI) dietary iron absorption was 32 (28, 34) ug/(d x kg), com

40 concentrations of 15, 30, and 60 mg/L, mean dietary iron absorption would be 22.3%, 16.3%, and 11.6%

41 ent iron overload is the result of excessive dietary iron absorption, most commonly caused in populat

42 is is under the normal regulatory control of dietary iron absorption, namely via ferroportin-dependen

43 By this mechanism, hepcidin inhibits dietary iron absorption, the efflux of recycled iron fro

44 ism by which HFE mutations lead to increased dietary iron absorption.

45 issue iron deposition secondary to excessive dietary iron absorption.

46 is not required in the intestinal lumen for dietary iron absorption.

47 pcidin, including the intestine, the site of dietary iron absorption.

48 he intestinal epithelium but not involved in dietary iron absorption.

49 on, preventing iron recycling and decreasing dietary iron absorption.

50 that increases serum hepcidin and decreases dietary iron absorption.

51 from single meals cannot be used to estimate dietary iron absorption.

52 ocks Hamp transcription, permitting enhanced dietary iron absorption.

53 the ability to modulate iron metabolism and dietary iron absorption.

54 Dietary iron affects circadian glucose metabolism throug

55 Discovery of this new form of dietary iron and elucidation of its pathway of intestina

56 demonstrated an inverse relationship between dietary iron and endothelial ferroportin expression.

57 we used Hfe-KO mice in conditions of altered dietary iron and erythropoiesis.

58 We assessed the association of intakes of dietary iron and heme iron with risk of postmenopausal b

59 ential for iron homeostasis and regulated by dietary iron and inflammation, is a target gene of the t

60 ors probably modulate the bioavailability of dietary iron and influence the accumulation of iron stor

61 Similarly, HEI component associations with dietary iron and iron status were often inconsistent and

62 lly increased to limit further absorption of dietary iron and its release from stores.

63 and that counter-regulatory factors such as dietary iron and luminal lipocalin 2 should be taken int

64 sorder characterized by excess absorption of dietary iron and progressive iron deposition in several

65 sorder characterized by excess absorption of dietary iron and progressive iron deposition in several

66 These data demonstrate that dietary iron and radiation, alone and combined, contribu

67 provided evidence of an interaction between dietary iron and SLC40A1.

68 that mTORC1 activity in RBCs is regulated by dietary iron and that genetic activation or inhibition o

69 udy provide a mechanistic connection between dietary iron and the appetite-regulating hormone leptin.

70 Hepcidin controls the absorption of dietary iron and the distribution of iron among cell typ

71 c iron balance by limiting the absorption of dietary iron and the release of iron from macrophage sto

72 Intakes of dietary iron and, in particular, heme iron may increase

73 se to iron, allowing increased absorption of dietary iron, and eventually iron overload.

74 s between Healthy Eating Index (HEI) scores, dietary iron, and iron status indicators (body iron, fer

75 utations in HFE result in over absorption of dietary iron, and patterns of tissue iron deposition in

76 ongest evidence to date of the importance of dietary iron as a determinant of iron status in vulnerab

77 Iron-replete men partially adapted to dietary iron bioavailability and iron absorption from a

78 n whether iron absorption in women adapts to dietary iron bioavailability and whether adaptation refl

79 Values for dietary iron bioavailability are required for setting di

80 Values for dietary iron bioavailability can be derived for any targ

81 Adaptation of iron absorption in response to dietary iron bioavailability is less likely in premenopa

82 ts suggest that these diets would have lower dietary iron bioavailability than nonvegetarian diets, b

83 o adapt in response to a 12-wk difference in dietary iron bioavailability, whether absorption was tes

84 developed a new interactive tool to predict dietary iron bioavailability.Iron intake and serum ferri

85 total scores were positively associated with dietary iron, but not iron status.

86 , a disease in which excessive absorption of dietary iron can lead to liver cirrhosis, diabetes, arth

87 phenotype results from reduced absorption of dietary iron caused by high levels of hepcidin and is du

88 Moreover, excess dietary iron caused significant elevation of serum iron

89 Consistent with the changes in leptin, dietary iron content was also directly related to food i

90 hemojuvelin in skeletal muscle regardless of dietary iron content.

91 of dietary iron overload (2% carbonyl iron), dietary iron deficiency (gastric parietal cell ablation)

92 shown that Mn accumulation is exacerbated by dietary iron deficiency (ID) and disturbances in norepin

93 Here, we interrogate the impact of dietary iron deficiency (ID) on the uptake of FTH1- and

94 Dietary iron deficiency can rapidly deplete brain iron c

95 nd Risk Factors Study (GBD) 2021 to estimate dietary iron deficiency prevalence and disability-adjust

96 Despite global improvements, dietary iron deficiency remains a major health concern w

97 for DMT1 up-regulation was a murine model of dietary iron deficiency that demonstrated greatly increa

98 to whether a causal relation exists between dietary iron deficiency with (ID+A) or without (ID-A) an

99 DCT1 is upregulated by dietary iron deficiency, and may represent a key mediato

100 is study, we quantified the global burden of dietary iron deficiency, focusing on where inadequate di

101 mice, which can be partially ameliorated by dietary iron depletion.

102 The aim of this study was to determine how dietary iron derived in this fashion is absorbed in the

103 etion in the Heph protein are able to absorb dietary iron despite reduced expression and mislocalizat

104 Mice receiving the lowest level of dietary iron exhibited borderline iron deficiency, with

105 ing porphyrin heme provides a rich source of dietary iron for mammals.

106 onheme iron absorption requires reduction of dietary iron for uptake by the divalent metal ion transp

107 ing hormone that regulates the absorption of dietary iron from the duodenum.

108 III)-selective chelators capable of removing dietary iron from the gastrointestinal tract and prevent

109 lso significantly higher in the intermediate-dietary-iron groups.

110 nding of how HFE regulates the absorption of dietary iron has been slow, but much can be learnt from

111 The kinetics of dietary iron import into various organs of mice were eva

112 levels of enterocyte iron, poor retention of dietary iron in enterocyte ferritin, and excess efflux o

113 uld provide a sustainable and rich source of dietary iron in the diet.

114 a non-absorbed, oral therapeutic that binds dietary iron in the gut, preventing absorption and promo

115 Dietary iron intake and iron absorption did not change d

116 ood groups recommended in the DGAs relate to dietary iron intake and iron status in subsets of the Un

117 Adherence to the DGAs supports dietary iron intake but not iron status.

118 While dietary iron intake by Yupiks was similar to that of a r

119 ron deficiency, focusing on where inadequate dietary iron intake leads to clinical manifestations suc

120 High dietary iron intake triggered the accumulation of serum

121 Dietary iron intake was assessed by frequency questionna

122 ate hepcidin production and, thus, increased dietary iron intake, and iron-loading anemias whereby bo

123 , bariatric surgical procedures), inadequate dietary iron intake, and pregnancy.

124 , body composition, physical activity level, dietary iron intake, delta-efficiency, or ventilatory th

125 eficiency occurs after insufficient maternal dietary iron intake, maternal hypertension, and maternal

126 Mean dietary iron intake, mean serum vitamin C concentrations

127 mic microcytic anemia and better adequacy of dietary iron intake, thereby suggesting the beneficial i

128 the severity of NOD disease correlates with dietary iron intake.

129 onsistently within the reference ranges) and dietary iron intakes did not differ significantly betwee

130 ta examining the risk of GDM associated with dietary iron, iron supplementation, and iron status as m

131 e of these disorders, the mechanism by which dietary iron is absorbed into the body is poorly underst

132 ion of hepcidin expression in hepatocytes by dietary iron is associated with an elevation of Bmp6 mRN

133 mochromatosis (HH), intestinal absorption of dietary iron is increased, leading to excessive iron acc

134 Absorption of dietary iron is largely regulated by the liver hormone h

135 ction and consequent excessive absorption of dietary iron, leading to iron overload.

136 ectively), and this effect did not depend on dietary iron levels.

137 and only Bmp6 and Bmp2 mRNA were induced by dietary iron loading in wild-type mice.

138 Dietary iron loading increased hepcidin and Id1 expressi

139 pression of TfR2 was not down-regulated with dietary iron loading or in the HFE -/- model of HH.

140 Dietary iron loading resulted in a substantially increas

141 Notably, dietary iron loading still induced liver SMAD5 phosphory

142 and Tfr2 up-regulate hepcidin in response to dietary iron loading without increases in liver Bmp6 mes

143 ffer in basal iron status and sensitivity to dietary iron loading.

144 to induce hepcidin in response to long-term dietary iron loading.

145 creases in P-Smad1,5,8 levels in response to dietary iron loading.

146 opriately regulate Hamp expression following dietary iron manipulations or holo-transferrin injection

147 Unabsorbed dietary iron may increase free radical production in the

148 Despite abundant dietary iron, mice with hepcidin-producing tumors develo

149 Dietary iron modulates levels of peroxisome proliferator

150 ory T cell responses using a murine model of dietary iron modulation in the context of influenza infe

151 E C282Y-heterozygous subjects did not absorb dietary iron more efficiently, even when foods were high

152 g the body of excess iron, the absorption of dietary iron must be precisely regulated.

153 We assessed the effects of dietary iron on circadian gluconeogenesis.

154 infections, we examined the effect of excess dietary iron on disease severity in HCV-infected chimpan

155 We examined the effect of dietary iron on regulation of hepcidin expression via th

156 s usually attributed to the malabsorption of dietary iron or the loss of iron from the intestinal muc

157 pression in normal mice and murine models of dietary iron overload (2% carbonyl iron), dietary iron d

158 Dietary iron overload caused a modest (30%) rise in plas

159 Dietary iron overload did not mitigate hepcidin inductio

160 isited the 'iron hypothesis' by showing that dietary iron overload or elevated non-transferrin bound

161 he genetic basis is still uncertain (African dietary iron overload), and several less frequent or rar

162 These findings indicate that levels of dietary iron play an important role in regulation of app

163 Insufficient dietary iron, reduced iron absorption due to increases i

164 arly hallmark of aging and demonstrated that dietary iron reduction improves iron turnover efficacy.

165 Most dietary iron remains unabsorbed and hence may be availab

166 Dietary iron repletion completely reversed ID anemia and

167 entation did not prevent steatosis; instead, dietary iron restriction and antioxidant therapy with vi

168 These data suggest that severe dietary iron restriction impairs hookworm development in

169 ed in order to test the hypothesis that host dietary iron restriction mediates susceptibility to hook

170 of the chemistry and biology of each type of dietary iron source (ferritin, heme, Fe2+ ion, etc.), an

171 footprint and could serve as an alternative dietary iron source.

172 being advocated to use high and bioavailable dietary iron sources to prevent iron deficiency.

173 A member of the nonheme iron group of dietary iron sources, ferritin is a complex with Fe3+ ir

174 urpose of these studies was to determine how dietary iron supplementation affected the severity of al

175 gh PCBP1-deleted livers were iron deficient, dietary iron supplementation did not prevent steatosis;

176 Dietary iron supplementation is associated with increase

177 im of this study was to assess the effect of dietary iron supplementation on insulin resistance and t

178 sent study, we used a rat model of long term dietary iron supplementation to identify stellate cell g

179 To elucidate connections between dietary iron, the microbiome, and SCD pathogenesis, we t

180 ndent upon carefully regulated absorption of dietary iron, thus these genes are of fundamental import

181 These changes may increase dietary iron uptake and allow release of stored iron to

182 Inefficient dietary iron uptake promotes many diseases, but mechanis

183 ropriately low levels of hepcidin, increased dietary iron uptake, and systemic iron accumulation, has

184 or older children without adverse effects on dietary iron utilization.

185 ired hepatic response was observed even when dietary iron was limited.

186 nal DMT1, the main transporter for uptake of dietary iron, were higher in the TfR2-mutant mice as com

187 e differentiating enterocytes to absorb more dietary iron when they mature into villus enterocytes.

188 lability diet absorbed up to 4.5 mg (30-35%) dietary iron with minimal influence of the diet consumed

189 Dilution of enriched body iron by dietary iron with natural isotopic composition was used