Pregnancy and maternal iron deficiency stimulate hepatic CRBPII expression in rats

Sarah C Cottin; Lorraine Gambling; Helen E Hayes; Valerie J Stevens; Harry J McArdle

doi:10.1016/j.jnutbio.2016.02.005

Pregnancy and maternal iron deficiency stimulate hepatic CRBPII expression in rats

Sarah C Cottin, Lorraine Gambling, Helen E Hayes, Valerie J Stevens, Harry J McArdle

The Rowett Institute of Nutrition and Health

Research output: Contribution to journal › Article › peer-review

21 Citations (Scopus)

Abstract

Iron deficiency impairs vitamin A (VA) metabolism in the rat but the mechanisms involved are unknown and the effect during development has not been investigated. We investigated the effect of pregnancy and maternal iron deficiency on VA metabolism in the mother and fetus. 54 rats were fed either a control or iron deficient diet for 2weeks prior to mating and throughout pregnancy. Another 15 female rats followed the same diet and were used as non-pregnant controls. Maternal liver, placenta and fetal liver were collected at d21 for total VA, retinol and retinyl ester (RE) measurement and VA metabolic gene expression analysis. Iron deficiency increased maternal hepatic RE (P<.05) and total VA (P<.0001), fetal liver RE (P<.05), and decreased placenta total VA (P<.05). Pregnancy increased Cellular Retinol Binding Protein (CRBP)-II gene expression by 7 fold (P=.001), decreased VA levels (P=.0004) and VA metabolic gene expression (P<.0001) in the liver. Iron deficiency increased hepatic CRBPII expression by a further 2 fold (P=.044) and RBP4 by~20% (P=.005), increased RBPR2 and decreased CRBPII, LRAT, and TTR in fetal liver, while it had no effect on VA metabolic gene expression in the placenta. Hepatic CRBPII expression is increased by pregnancy and further increased by iron deficiency, which may play an important role in VA metabolism and homeostasis. Maternal iron deficiency also alters VA metabolism in the fetus, which is likely to have consequences for development.

Original language	English
Pages (from-to)	55-63
Number of pages	9
Journal	The Journal of Nutritional Biochemistry
Volume	32
Early online date	10 Mar 2016
DOIs	https://doi.org/10.1016/j.jnutbio.2016.02.005
Publication status	Published - Jun 2016

Bibliographical note

Acknowledgements
HJM and SCC designed the research; LG, HEH, VJS and SCC conducted the research; SCC analyzed the data and wrote the manuscript; HJM reviewed the manuscript. HJM and SCC take responsibility of data interpretation and presentation. All authors read and approved the final manuscript. We are grateful for the technical assistance of Gill Campbell (ICPMS analysis) and Lynn Pirie (retinol analysis), the Biomedical Research facility staff and Dr. Bill Rees for his critical reading of the manuscript. This work was supported by Scottish Government (Rural and Environment Science and Analytical Services).

Keywords

iron deficiency
vitamin A
pregnancy
retinol
retinylester
cellular retinol binding protein (CRBP)-II

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title = "Pregnancy and maternal iron deficiency stimulate hepatic CRBPII expression in rats",

abstract = "Iron deficiency impairs vitamin A (VA) metabolism in the rat but the mechanisms involved are unknown and the effect during development has not been investigated. We investigated the effect of pregnancy and maternal iron deficiency on VA metabolism in the mother and fetus. 54 rats were fed either a control or iron deficient diet for 2weeks prior to mating and throughout pregnancy. Another 15 female rats followed the same diet and were used as non-pregnant controls. Maternal liver, placenta and fetal liver were collected at d21 for total VA, retinol and retinyl ester (RE) measurement and VA metabolic gene expression analysis. Iron deficiency increased maternal hepatic RE (P<.05) and total VA (P<.0001), fetal liver RE (P<.05), and decreased placenta total VA (P<.05). Pregnancy increased Cellular Retinol Binding Protein (CRBP)-II gene expression by 7 fold (P=.001), decreased VA levels (P=.0004) and VA metabolic gene expression (P<.0001) in the liver. Iron deficiency increased hepatic CRBPII expression by a further 2 fold (P=.044) and RBP4 by~20% (P=.005), increased RBPR2 and decreased CRBPII, LRAT, and TTR in fetal liver, while it had no effect on VA metabolic gene expression in the placenta. Hepatic CRBPII expression is increased by pregnancy and further increased by iron deficiency, which may play an important role in VA metabolism and homeostasis. Maternal iron deficiency also alters VA metabolism in the fetus, which is likely to have consequences for development.",

keywords = "iron deficiency, vitamin A, pregnancy, retinol, retinylester, cellular retinol binding protein (CRBP)-II",

author = "Cottin, {Sarah C} and Lorraine Gambling and Hayes, {Helen E} and Stevens, {Valerie J} and McArdle, {Harry J}",

note = "Acknowledgements HJM and SCC designed the research; LG, HEH, VJS and SCC conducted the research; SCC analyzed the data and wrote the manuscript; HJM reviewed the manuscript. HJM and SCC take responsibility of data interpretation and presentation. All authors read and approved the final manuscript. We are grateful for the technical assistance of Gill Campbell (ICPMS analysis) and Lynn Pirie (retinol analysis), the Biomedical Research facility staff and Dr. Bill Rees for his critical reading of the manuscript. This work was supported by Scottish Government (Rural and Environment Science and Analytical Services).",

year = "2016",

month = jun,

doi = "10.1016/j.jnutbio.2016.02.005",

language = "English",

volume = "32",

pages = "55--63",

journal = "The Journal of Nutritional Biochemistry",

issn = "0955-2863",

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T1 - Pregnancy and maternal iron deficiency stimulate hepatic CRBPII expression in rats

AU - Cottin, Sarah C

AU - Gambling, Lorraine

AU - Hayes, Helen E

AU - Stevens, Valerie J

AU - McArdle, Harry J

N1 - Acknowledgements HJM and SCC designed the research; LG, HEH, VJS and SCC conducted the research; SCC analyzed the data and wrote the manuscript; HJM reviewed the manuscript. HJM and SCC take responsibility of data interpretation and presentation. All authors read and approved the final manuscript. We are grateful for the technical assistance of Gill Campbell (ICPMS analysis) and Lynn Pirie (retinol analysis), the Biomedical Research facility staff and Dr. Bill Rees for his critical reading of the manuscript. This work was supported by Scottish Government (Rural and Environment Science and Analytical Services).

PY - 2016/6

Y1 - 2016/6

N2 - Iron deficiency impairs vitamin A (VA) metabolism in the rat but the mechanisms involved are unknown and the effect during development has not been investigated. We investigated the effect of pregnancy and maternal iron deficiency on VA metabolism in the mother and fetus. 54 rats were fed either a control or iron deficient diet for 2weeks prior to mating and throughout pregnancy. Another 15 female rats followed the same diet and were used as non-pregnant controls. Maternal liver, placenta and fetal liver were collected at d21 for total VA, retinol and retinyl ester (RE) measurement and VA metabolic gene expression analysis. Iron deficiency increased maternal hepatic RE (P<.05) and total VA (P<.0001), fetal liver RE (P<.05), and decreased placenta total VA (P<.05). Pregnancy increased Cellular Retinol Binding Protein (CRBP)-II gene expression by 7 fold (P=.001), decreased VA levels (P=.0004) and VA metabolic gene expression (P<.0001) in the liver. Iron deficiency increased hepatic CRBPII expression by a further 2 fold (P=.044) and RBP4 by~20% (P=.005), increased RBPR2 and decreased CRBPII, LRAT, and TTR in fetal liver, while it had no effect on VA metabolic gene expression in the placenta. Hepatic CRBPII expression is increased by pregnancy and further increased by iron deficiency, which may play an important role in VA metabolism and homeostasis. Maternal iron deficiency also alters VA metabolism in the fetus, which is likely to have consequences for development.

AB - Iron deficiency impairs vitamin A (VA) metabolism in the rat but the mechanisms involved are unknown and the effect during development has not been investigated. We investigated the effect of pregnancy and maternal iron deficiency on VA metabolism in the mother and fetus. 54 rats were fed either a control or iron deficient diet for 2weeks prior to mating and throughout pregnancy. Another 15 female rats followed the same diet and were used as non-pregnant controls. Maternal liver, placenta and fetal liver were collected at d21 for total VA, retinol and retinyl ester (RE) measurement and VA metabolic gene expression analysis. Iron deficiency increased maternal hepatic RE (P<.05) and total VA (P<.0001), fetal liver RE (P<.05), and decreased placenta total VA (P<.05). Pregnancy increased Cellular Retinol Binding Protein (CRBP)-II gene expression by 7 fold (P=.001), decreased VA levels (P=.0004) and VA metabolic gene expression (P<.0001) in the liver. Iron deficiency increased hepatic CRBPII expression by a further 2 fold (P=.044) and RBP4 by~20% (P=.005), increased RBPR2 and decreased CRBPII, LRAT, and TTR in fetal liver, while it had no effect on VA metabolic gene expression in the placenta. Hepatic CRBPII expression is increased by pregnancy and further increased by iron deficiency, which may play an important role in VA metabolism and homeostasis. Maternal iron deficiency also alters VA metabolism in the fetus, which is likely to have consequences for development.

KW - iron deficiency

KW - vitamin A

KW - pregnancy

KW - retinol

KW - retinylester

KW - cellular retinol binding protein (CRBP)-II

U2 - 10.1016/j.jnutbio.2016.02.005

DO - 10.1016/j.jnutbio.2016.02.005

M3 - Article

C2 - 27142737

SN - 0955-2863

VL - 32

SP - 55

EP - 63

JO - The Journal of Nutritional Biochemistry

JF - The Journal of Nutritional Biochemistry

ER -

Pregnancy and maternal iron deficiency stimulate hepatic CRBPII expression in rats

Abstract

Bibliographical note

Keywords

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