ライフサイエンスコーパス: iron absorption

1 hepcidin (HAMP), the hormone that regulates iron absorption.

2 l tranporter-1, as well as enhanced duodenal iron absorption.

3 n normal hematologic values due to increased iron absorption.

4 e expression of key genes that contribute to iron absorption.

5 gle meals cannot be used to estimate dietary iron absorption.

6 d doses increases serum hepcidin and reduces iron absorption.

7 n solubility and bioavailability and improve iron absorption.

8 uodenal enterocytes, is required for optimal iron absorption.

9 ich increased the surface area available for iron absorption.

10 a regulatory mechanism for limiting further iron absorption.

11 would further exacerbate anemia and increase iron absorption.

12 cted 36% of the interindividual variation in iron absorption.

13 epcidin explain interindividual variation in iron absorption.

14 p transcription, permitting enhanced dietary iron absorption.

15 ly to be due to a TNF-alpha-induced block in iron absorption.

16 ys a pivotal role as a negative regulator of iron absorption.

17 heme intakes, zinc intakes may increase heme-iron absorption.

18 tely predict the influence of polyphenols on iron absorption.

19 w Hamp1 levels are responsible for increased iron absorption.

20 that higher zinc intakes would decrease heme-iron absorption.

21 of an iron-sensing mechanism that regulates iron absorption.

22 dietary inhibitor of both heme- and nonheme-iron absorption.

23 role in determining the level of intestinal iron absorption.

24 a multicopper oxidase essential for enteric iron absorption.

25 no significant effect of dietary calcium on iron absorption.

26 eterogeneous disease caused by inappropriate iron absorption.

27 ice resulted in nearly a 4-fold reduction in iron absorption.

28 e mutant mice retain the ability to regulate iron absorption.

29 n a shared pathway with HFE in regulation of iron absorption.

30 ciency of the duodenal mucosa, and increased iron absorption.

31 but does not influence the up-regulation of iron absorption.

32 d-type animals for their ability to regulate iron absorption.

33 thereby possibly reflecting greater colonic iron absorption.

34 s gastric acid production, which can inhibit iron absorption.

35 itory effect, resulting in increased nonheme iron absorption.

36 hypercoagulability, and increased intestinal iron absorption.

37 s gastric acid production, which can inhibit iron absorption.

38 act on nutrition whereby they interfere with iron absorption.

39 ation and serum hepcidin and thereby improve iron absorption.

40 1.41, -0.28)] were significant predictors of iron absorption.

41 tinal epithelium but not involved in dietary iron absorption.

42 enting iron recycling and decreasing dietary iron absorption.

43 tivated in the intestine and is essential in iron absorption.

44 affected inflammation biomarkers nor altered iron absorption.

45 creases serum hepcidin and decreases dietary iron absorption.

46 However, calcium administration may inhibit iron absorption.

47 rge variations were observed in mean nonheme-iron absorption (0.7-22.9%) between studies, which depen

48 dividuals (all from US studies): log[nonheme-iron absorption, %] = -0.73 log[ferritin, mug/L] + 0.11

49 Longitudinal, paired iron-absorption ((5)(8)Fe) studies were conducted in 59

50 ctivity is essential for intestinal non-heme iron absorption after birth.

51 provides a tool for investigating the excess iron absorption and abnormal iron distribution in iron-o

52 e essential role of HIF-2alpha in regulating iron absorption and also demonstrate that hypoxia sensin

53 We measured iron absorption and body composition with the use of dua

54 understanding of the mechanisms that control iron absorption and body iron stores.

55 ghts a role of HIF-2 in the dysregulation of iron absorption and chronic iron accumulation, as observ

56 activity of ferroportin, hepcidin modulates iron absorption and delivery from the body's stores.

57 ial for all cells but is toxic in excess, so iron absorption and distribution are tightly regulated.

58 et the body's iron requirements and regulate iron absorption and distribution.

59 the necessity of the gastric proton pump for iron absorption and effective erythropoiesis.

60 odulates erythropoiesis by affecting dietary iron absorption and erythroid iron intake.

61 a transmembrane protein crucial for duodenal iron absorption and erythroid iron transport.

62 We examined iron absorption and growth in exclusively breastfed infa

63 Hepcidin-25 is a peptide hormone involved in iron absorption and homeostasis and found at increased s

64 thesized in the liver, is a key regulator of iron absorption and homeostasis in mammals.

65 es examined a variety of genes that regulate iron absorption and homeostasis.

66 Inflammation reduces duodenal iron absorption and increases macrophage iron retention,

67 n metabolism characterized by excess dietary iron absorption and iron deposition in several tissues.

68 At the whole-body level, dietary iron absorption and iron export from the tissues into th

69 osed to be a central regulator of intestinal iron absorption and iron recycling by macrophages.

70 ystemic iron levels by inhibiting intestinal iron absorption and iron recycling.

71 r, has been shown to inhibit both intestinal iron absorption and iron release from macrophages.

72 negative-feedback mechanism between dietary iron absorption and iron status.

73 gastric bypass (RYGBP) on heme- and nonheme-iron absorption and iron status.

74 n (Hp) plays an important role in intestinal iron absorption and is predicted to be a ferroxidase bas

75 major transporter responsible for intestinal iron absorption and its expression is regulated by body

76 iency of hepcidin, the hormone that controls iron absorption and its tissue distribution, is the caus

77 rmone hepcidin is the principal regulator of iron absorption and its tissue distribution.

78 f iron metabolism, hepcidin inhibits dietary iron absorption and macrophage iron recycling.

79 a peptide hormone that decreases intestinal iron absorption and macrophage iron release, is a potent

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

81 d TNF-alpha is thought to inhibit intestinal iron absorption and macrophage iron release.

82 -like peptide hormone that inhibits duodenal iron absorption and macrophage iron release.

83 sed red blood cell survival, and a defect in iron absorption and macrophage iron retention, which int

84 tory diseases, up-regulated hepcidin impairs iron absorption and macrophage release, causing anemia.

85 of vitamin C that result from its effects on iron absorption and metabolism has not been confirmed in

86 alternate days and in single doses optimises iron absorption and might be a preferable dosing regimen

87 regulatory hormone hepcidin allows increased iron absorption and mobilization from stores.

88 iron-regulatory hormone hepcidin to increase iron absorption and mobilization of iron from stores.

89 cell types leads to the increased intestinal iron absorption and plasma iron levels characteristic of

90 ne 6 (TMPRSS6) gene, an enzyme that promotes iron absorption and recycling by inhibiting hepcidin ant

91 te to anemia, but their influence on dietary iron absorption and recycling is unknown.

92 roportin in the gut and spleen, the sites of iron absorption and recycling respectively.

93 levels of hepcidin, a negative regulator of iron absorption and recycling, underlie the pathophysiol

94 diated by Hamp up-regulation, which inhibits iron absorption and recycling.

95 ating iron balance by controlling intestinal iron absorption and recycling.

96 is, is deficient in HH, leading to unchecked iron absorption and subsequent iron overload.

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

99 cessive condition characterized by increased iron absorption and tissue deposition.

100 iron-loading anemias whereby both increased iron absorption and transfusion therapy contribute to th

101 n supplementation on their expression and on iron absorption and utilization during infancy.

102 Defects in iron absorption and utilization lead to iron deficiency

103 nding of the genetic circuitry that controls iron absorption and utilization.

104 Iron absorption and zinc absorption from the food produc

105 romatosis (involved in venous ulceration and iron absorption), and various types of collagen (contrib

106 microcytic anemia due to impaired intestinal iron absorption, and defective iron utilization in red c

107 one marrow iron stores, increased intestinal iron absorption, and hemoglobin response to SF) among no

108 o measure inflammation biomarkers, hepcidin, iron absorption, and utilization pre- and posttreatment

109 t adaptation, substantially influenced total iron absorption (approximately 6-fold).

110 alues, 36% of interindividual differences in iron absorption are explained by differences in circulat

111 ed hepatic peptide that regulates intestinal iron absorption as well as maternal-fetal iron transport

112 e iron bioavailability (total and fractional iron absorption), assessed by measuring the isotopic lab

113 An apparent reduction in heme-iron absorption associated with the lavage procedure sug

114 t-milk copper (P < 0.01) predicted increased iron absorption at 5M.

115 interactive program for calculating dietary iron absorption at any concentration of serum ferritin i

116 e used to develop a model to predict dietary iron absorption at different serum ferritin concentratio

117 In these women, iron absorption averaged 14.71 +/- 10.7% from the supple

118 There was no significant difference in iron absorption between ferritin and ferrous sulfate: lo

119 The difference in whole-body iron absorption between heat-treated (24.6 +/- 20.8%; n

120 isotope studies have shown no difference in iron absorption between infants with high or low hemoglo

121 The difference in whole-body iron absorption between the groups given lactoferrin (20

122 y was to evaluate the influence of inulin on iron absorption, bifidobacteria, total bacteria, short-c

123 nflammation, increases hepcidin, and reduces iron absorption but not utilization.

124 en shown to be a potent inhibitor of nonheme iron absorption, but it remains unclear whether the timi

125 to MNP and MNP+RUTF significantly increased iron absorption by 1.85-fold (95% CI: 1.49-, 2.29-fold;

126 0.001).GOS consumption by infants increased iron absorption by 62% from an MNP containing FeFum+NaFe

127 Increasing intestinal iron absorption by activation of HIF-2alpha or parentera

128 orchestrate hepatic hepcidin production and iron absorption by the intestine.

129 hat regulates iron homeostasis by inhibiting iron absorption by the small intestine and release of ir

130 ) and that from FeSO4 (34.3 +/- 23.6%) or in iron absorption calculated from red blood cell incorpora

131 blood transfusions and excessive intestinal iron absorption can be a complication of chronic anemias

132 enotype stems from impaired gastrointestinal iron absorption caused by a point mutation of the gastri

133 to repeated blood transfusions and increased iron absorption, chronic hemolysis is the major cause of

134 ) transporter internalization, impairing the iron absorption; clinically manifested as anemia of infl

135 Iron absorption correlated with fecal pH in the placebo

136 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

137 Nonheme-iron absorption decreased from 11.1% to 4.7% (P < 0.0001

138 Dietary iron intake and iron absorption did not change during the study.

139 igate at a molecular level the regulation of iron absorption during infancy in a rat pup model.

140 wn about the molecular mechanisms regulating iron absorption during infancy.

141 fine structure range beyond the onset of the iron absorption edge.

142 Dietary factors affecting iron absorption, eg, ascorbic acid, phytate, and calcium

143 ulated to play important roles in intestinal iron absorption, erythroid iron utilization, hepatic iro

144 Median percentage increases in iron absorption for -AA to +AA meals were 56% in the NW

145 2 x 2 factorial experiments compared women's iron absorption from 2 maize varieties (ACR and TZB; n =

146 In this study, we compared iron absorption from a meal with ascorbic acid (+AA) and

147 ermine whether prebiotic consumption affects iron absorption from a micronutrient powder (MNP) contai

148 h an iron-fortified maize meal and 2) assess iron absorption from a micronutrient powder (MNP) given

149 increase in serum hepcidin and a decrease in iron absorption from adiposity-related inflammation.

150 tion was observed between serum ferritin and iron absorption from both ferritin and FeSO4, which sugg

151 Infant iron absorption from breast milk averaged 7.1% and 13.9%

152 Heme- and nonheme-iron absorption from either high- or low-bioavailability

153 The median percentages of fractional iron absorption from FeFum+NaFeEDTA and from FeSO4 in th

154 ore or with the meal significantly increased iron absorption from FePP by 2.55-fold (95% CI: 1.48-, 4

155 ls, the addition of lipids more than doubles iron absorption from FePP.

156 mineral (animal-type) and to compare it with iron absorption from ferrous sulfate.

157 orhydria reduced the normal increase in heme-iron absorption from hemoglobin in response to iron defi

158 stimated from predictive algorithms, nonheme iron absorption from meals, and models of iron intake, s

159 Our study aim was to compare iron absorption from oral iron supplements given on cons

160 The objective was to examine iron absorption from purified soybean ferritin.

161 was no significant difference in whole-body iron absorption from soybean ferritin (29.9 +/- 19.8%) a

162 g might increase serum hepcidin and decrease iron absorption from subsequent doses.

163 t prohepcidin, was inversely associated with iron absorption from supplemental and food-based nonheme

164 iron regulatory hormone capable of blocking iron absorption from the duodenum and iron release from

165 riately raised hepcidin levels, which impair iron absorption from the gut, may be a factor.

166 ron exporter ferroportin, hepcidin decreases iron absorption from the intestine and iron release from

167 In contrast with iron absorption from the low-bioavailability diet, that

168 (P < 0.05), it accurately predicted relative iron absorption from the maize meals.

169 ective was to conduct a systematic review of iron absorption from whole diets.

170 cal effectors mediating the up-regulation of iron absorption genes are unknown.

171 a in the intestine abolished the increase in iron absorption genes as assessed by quantitative real-t

172 By day 20, DMT1 and FPN1 expression and iron absorption had decreased significantly with iron su

173 receptors for lactoferrin, a role for it in iron absorption has been suggested.

174 se dependence, and its effects on subsequent iron absorption have not been characterized in humans.

175 t developmental changes in the regulation of iron absorption; however, little is known about the mole

176 less well understood than the regulation of iron absorption in adults, which is inverse to iron stat

177 time interval of tea consumption on nonheme iron absorption in an iron-containing meal in a cohort o

178 and oligofructose have been shown to improve iron absorption in animals through colonic uptake, but t

179 The mechanism of increased iron absorption in beta-thalassemia is unclear.

180 Fractional iron absorption in children was significantly affected b

181 the effect of iron and zinc intakes on heme-iron absorption in children.

182 The same compound promotes gut iron absorption in DMT1-deficient rats and ferroportin-d

183 export protein ferroportin (FPN1) to adjust iron absorption in enterocytes, iron recycling through r

184 ion between serum or urinary prohepcidin and iron absorption in healthy premenopausal women.

185 y prohepcidin concentrations were related to iron absorption in healthy women.

186 (CA/TSC) mixture before extrusion increases iron absorption in humans from FePP-fortified extruded r

187 isotopes has provided valuable insights into iron absorption in humans, but the data have been limite

188 dies have examined the effect of hepcidin on iron absorption in humans.

189 cidin agonists might help treat the abnormal iron absorption in individuals with beta-thalassemia and

190 Whether consumption of prebiotics increases iron absorption in infants is unclear.We set out to dete

191 th a reduction in the normal upregulation of iron absorption in iron-deficient obese subjects, and th

192 Adaptation of iron absorption in response to dietary iron bioavailabil

193 own-regulate intestinal iron transporters or iron absorption in response to iron supplementation, whe

194 be reproduced by increasing the setpoint of iron absorption in the duodenum to a level where the sys

195 n homeostasis is maintained by regulation of iron absorption in the duodenum, iron recycling from ery

196 uction of Fe(III) to Fe(II) is essential for iron absorption in the gastrointestinal tract.

197 nderstanding why probiotic bacteria increase iron absorption in the gastrointestinal tract.

198 of full-length mRNA would predict deficient iron absorption in the intestine and deficient iron util

199 Mean fractional iron absorption in the inulin (15.2%; 95% CI: 8.0%, 28.9

200 hepcidin and serum prohepcidin with nonheme-iron absorption in the presence and absence of food with

201 Dietary iron absorption in the small intestine is required for s

202 din is the predominant negative regulator of iron absorption in the small intestine, iron transport a

203 Heme-iron absorption in these subjects has not been reported.

204 ective of the study was to ascertain whether iron absorption in women adapts to dietary iron bioavail

205 ivity, we were unable to show an increase in iron absorption in women with low iron status.

206 Geometric mean iron absorptions in the afebrile malaria and hookworm gr

207 Geometric mean (95% CI) iron absorptions in the NW and OW/OB were 19.0% (15.2%,

208 ascorbic acid (or other luminal enhancers of iron absorption) in obese individuals to improve iron st

209 t subjects (n = 17), geometric mean (95% CI) iron absorption increased by 28% [from 9.7% (6.5%, 14.6%

210 istribution of iron by inhibiting intestinal iron absorption, iron recycling by macrophages, and iron

211 iron homeostasis by coordinately regulating iron absorption, iron recycling, and mobilization of sto

212 Iron absorption is controlled chiefly by hepcidin, the i

213 The magnitude of the decrease in heme-iron absorption is greater than that of nonheme iron.

214 iron during erythropoiesis, small intestinal iron absorption is increased through an undefined mechan

215 The function of hepcidin in regulating iron absorption is modeled through an inverse relationsh

216 Excessive iron absorption is one of the main features of beta-thal

217 and the enhancing effect of ascorbic acid on iron absorption is one-half of that in normal-weight wom

218 The effect of bariatric surgery on iron absorption is only partially known.

219 Iron absorption is proposed to be regulated by circulati

220 In neonates, efficient intestinal iron absorption is required to scavenge as much iron as

221 In overweight and obese women, iron absorption is two-thirds that in normal-weight wome

222 liver-derived protein that restricts enteric iron absorption, is the key regulator of body iron conte

223 These cells then overexpress genes for iron absorption, leading to inappropriate cellular iron

224 As a consequence, iron absorption must be strictly regulated to ensure ade

225 der the normal regulatory control of dietary iron absorption, namely via ferroportin-dependent efflux

226 e objectives were to 1) assess the effect on iron absorption of a lipid emulsion given 20 min before

227 st the possibility of an enhancing effect on iron absorption of lipid-rich RUTFs, but more research i

228 iron-induced increase in hepcidin influences iron absorption of successive daily iron doses and twice

229 se serum hepcidin, and it does not influence iron absorption or utilization.

230 molar ratios of AA:iron) roughly tripled the iron absorption (P < 0.0001) from all test meals.

231 and serum hepcidin (P = 0.004) and improved iron absorption (P = 0.003).

232 significant group-by-compound interaction on iron absorption (P = 0.011).

233 emenopausal women, the efficiency of nonheme-iron absorption (P = 0.06, two-tailed test), but not of

234 gastric residence time, which could increase iron absorption, particularly from poorly soluble iron c

235 Iron absorption, plasma iron concentrations, and tissue

236 e hypothesized that HIF-2 could mediate high iron absorption rates in HH.

237 he duodenum, spleen, and liver, the sites of iron absorption, recycling, and storage respectively.

238 ith iron-unresponsive anemia due to impaired iron absorption/redistribution from tuberculosis-associa

239 iron without significantly affecting nonheme-iron absorption, regardless of meal bioavailability.

240 Mammalian nonheme iron absorption requires reduction of dietary iron for u

241 SO4, which suggested that sensors regulating iron absorption respond similarly to iron provided as fe

242 Caco-2 predictions confirmed human iron absorption results for maize meals but not for bean

243 e genotyping of 103 participants in previous iron-absorption studies, 5 C282Y-heterozygous subjects w

244 Stored samples from a human iron absorption study were used to test the hypothesis t

245 certain whether luminal enhancers of dietary iron absorption such as ascorbic acid can be effective i

246 (P = 0.06, two-tailed test), but not of heme-iron absorption, tended to adapt in response to a 12-wk

247 ed particles (50 nm in diameter) had a lower iron absorption than unexposed or chronically exposed bi

248 atosis is an inherited disorder of increased iron absorption that can result in cirrhosis, diabetes,

249 mechanistic understanding for the increased iron absorption that is present in this disorder.

250 HH) is characterized by increased intestinal iron absorption that may result in iron overload.

251 In the present study, we report a defect in iron absorption that results in iron-deficiency anemia,

252 mRNA levels of most of the genes involved in iron absorption that were tested; however, it did corres

253 By this mechanism, hepcidin inhibits dietary iron absorption, the efflux of recycled iron from spleni

254 ort of heme across membranes is critical for iron absorption, the formation of hemoglobin and other h

255 ad due to both transfused iron and increased iron absorption, the latter mediated by suppression of t

256 e intrinsic ability to regulate the rates of iron absorption, the spotlight in the past decade has be

257 hough hepcidin is proposed as a regulator of iron absorption, this has not been assessed in humans.

258 on of hepcidin expression serves to modulate iron absorption to meet body iron demand.

259 a level where the system cannot downregulate iron absorption to meet the iron excretion rate.

260 showed that dysregulation of the intestinal iron absorption transporter divalent metal transporter-1

261 abel, randomised controlled trials assessing iron absorption using ((54)Fe)-labelled, ((57)Fe)-labell

262 nd hematologic indexes and heme- and nonheme-iron absorption-using a standardized meal containing 3 m

263 e-day group (p=0.0013), and cumulative total iron absorption was 131.0 mg (71.4, 240.5) versus 175.3

264 Heme-iron absorption was 23.9% before and 6.2% 12 mo after su

265 Mean (+/-SD) iron absorption was 36 +/- 19% (range: 4-81%), and serum

266 by the erythrocyte iron incorporation method.Iron absorption was 5.7% +/- 8.5% (TM-1), 3.6% +/- 4.2%

267 Iron absorption was assessed by isotope incorporation in

268 Iron absorption was calculated from erythrocyte incorpor

269 e control subjects were recruited, and their iron absorption was compared by using a hamburger test m

270 cidin was increased (P < .01) and fractional iron absorption was decreased by 35% to 45% (P < .01).

271 A regression equation to calculate iron absorption was derived by pooling data for iron sta

272 Iron absorption was determined by analyzing blood sample

273 e, blood samples were collected for 8 h, and iron absorption was estimated by erythrocyte incorporati

274 Fractional iron absorption was estimated by the erythrocyte iron in

275 Mean fractional iron absorption was found to be significantly higher (2.

276 In this study, erythropoietic induction of iron absorption was further investigated.

277 Between groups, iron absorption was greater from the FeFum+NaFeEDTA (P =

278 0.0375), but, contrary to expectations, heme-iron absorption was higher at higher zinc intakes.

279 Absolute heme-iron absorption was higher in the group with higher zinc

280 Iron absorption was measured after 3 wk of inulin and pl

281 Iron absorption was measured as the erythrocyte incorpor

282 ion, and dietary intakes were also assessed; iron absorption was measured in a subgroup of women.

283 Iron absorption was measured in a whole-body counter aft

284 Iron absorption was measured in a whole-body counter aft

285 At 3 wk, iron absorption was negatively correlated with fecal pH

286 Log iron absorption was negatively correlated with serum fer

287 ation on DMT1 and FPN1 gene expression or on iron absorption was observed.

288 Iron absorption was predicted from serum ferritin concen

289 Fractional iron absorption was significantly higher from CA/TSC-ext

290 Serum ferritin and iron absorption were inversely correlated in subjects wh

291 metric mean (-SD, +SD) cumulative fractional iron absorptions were 16.3% (9.3, 28.8) in the consecuti

292 g, exclusively breastfed infants upregulated iron absorption when iron stores were depleted at both 2

293 lassemia, results in sustained elevations in iron absorption, which cause iron overload with associat

294 signals induced dysregulation of intestinal iron absorption, which contributed to liver iron overloa

295 evidence of the developmental regulation of iron absorption, which emphasizes the need for caution w

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

298 We hypothesized that fractional heme-iron absorption would decrease as heme-iron intake incre

299 zinc (1 or 9 mg); successful measurements of iron absorption, zinc absorption, or both were made in 4

300 Mean iron absorption, zinc absorption, protein quality and be