High iron intake depresses hepatic copper content in goats

1995 ◽  
Vol 17 (1) ◽  
pp. 14-17 ◽  
Author(s):  
J.Th. Schonewille ◽  
S. Yu ◽  
A.C. Beynen
2021 ◽  
pp. 1-21
Author(s):  
Celeste Tsz Hei Cheung ◽  
Anna M Rangan ◽  
Iris Mei Ying Tse ◽  
Wai Hung Sit ◽  
Jimmy Chun Yu Louie

Abstract Objectives To examine the potential effect on iron intake of 7-8 month-old infants if pre-packaged baby foods (PBFs) were used as the sole source of complementary foods. Design: Based on the 7-day recommended feeding plan for 7-8-month-old infants in Hong Kong (moderate iron-fortified rice cereal with home-cooked meals), 24 modelling scenarios were created which comprised of two milk use modes (breastmilk vs. infant formula); three modes of rice cereal use (no rice cereal; non-iron-fortified rice cereal; iron-fortified rice cereal); and four baby foods usage modes (home-cooked meals; low-iron PBFs only; high-iron PBFs only; mixed PBFs). The PBFs were randomly selected in each of the models and substituted the original meals/snacks. The average daily iron intakes of the modelled meal plans were compared against the Chinese estimated average requirement (EAR) and recommended nutrient intake (RNI) for iron. Setting: Modelling study. Participants: N/A. Results: In general, the infant-formula-based complementary feeding pattern (CFP) had higher average daily iron intake when compared with breastmilk-based CFP. The iron intake of all scenarios under the breastmilk-based CFP were below the RNI and EAR, except for the fortified rice cereal meal plans with high-iron or mixed PBFs. For infant-formula-based CFP, the iron intakes were close to or above the RNI regardless of types of PBF or rice cereal used. Conclusions: The inclusion of fortified rice cereal was important in maintaining adequate iron intake for infants, especially for breastfed infants. The replacement of home-cooked meals by low-iron PBFs could potentially put infants at risk of iron deficiency.


2017 ◽  
Vol 39 ◽  
pp. 100-107 ◽  
Author(s):  
Albert Friedrich Stättermayer ◽  
Stefan Traussnigg ◽  
Elmar Aigner ◽  
Christian Kienbacher ◽  
Ursula Huber-Schönauer ◽  
...  

1986 ◽  
Vol 20 (10) ◽  
pp. 1034-1034
Author(s):  
F Haschke ◽  
B Pietschnig ◽  
H Vanura ◽  
M Heil ◽  
I Steffan ◽  
...  

Hepatology ◽  
2015 ◽  
Vol 62 (6) ◽  
pp. 1731-1741 ◽  
Author(s):  
Xu Yang ◽  
Xiao‐peng Tang ◽  
Yong‐hong Zhang ◽  
Kai‐zhong Luo ◽  
Yong‐fang Jiang ◽  
...  

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 324-324
Author(s):  
Nicole Doan ◽  
Elaine Wang ◽  
Bo Lönnerdal ◽  
Peng Ji

Abstract Either iron excess or iron deficiency may adversely affect growth of pigs. This study assessed the effect of dose of iron supplement on growth and iron metabolism in nursing piglets born small (SGA) or appropriate for gestational age (AGA). Eight SGA piglets (BW=1.18 kg) and 16 AGA piglets (BW=1.73 kg) were enrolled on postnatal day (PD) 1. The SGA piglets orally received high iron supplementation (15 mg/kg·d; SGAH), and AGA piglets orally received either high (15 mg/kg·d; AGAH, n = 6) or low iron supplementation (1 mg/kg·d; AGAL, n = 6) from PD 2 to 21. Body weight was recorded every third day. Blood samples were collected on PD 1, 7, 14, and 21. Liver and duodenal mucosa samples were collected on PD 21 to analyze the mRNA and protein expressions of iron transporters and regulators. All data were analyzed as a randomized complete block design using the PROC MIXED of SAS. The SGA piglets had lower hematocrit and hemoglobin than AGA piglets on PD1 (P < 0.05). The dose of iron supplement did not affect the growth trajectory of nursing piglets. In comparison with AGAL group, high iron increased (P < 0.05) hematocrit, hemoglobin, plasma iron, transferrin saturation, and iron load in duodenal mucosa (DM) and liver on PD 21 regardless of birth BW. High iron reduced the DMT1 and TFRC and increased FTL in DM (P < 0.05). High iron decreased TFRC and increased HAMP in liver (P < 0.05). Hepatic expression of H-ferritin were increased (P < 0.05) by high iron. Despite drastic induction of HAMP in liver, protein expression of ferroportin in DM were unaffected by high iron intake. In conclusion, iron transporters and regulators in liver and gut were coordinately regulated to prevent iron overload, but the hepcidin-ferroportin axis was unresponsive to dietary iron intake.


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