The effect of iron deficiency on the temporal changes in the expression of genes associated with fat metabolism in the pregnant rat

Susan M Hay, Harry J McArdle, Helen E Hayes, Valerie J Stevens, William D Rees

Research output: Contribution to journalArticle

6 Citations (Scopus)
4 Downloads (Pure)

Abstract

Iron is essential for the oxidative metabolism of lipids. Lipid metabolism changes during gestation to meet the requirements of the growing fetus and to prepare for lactation. The temporal effects of iron deficiency during gestation were studied in female rats fed complete or iron-deficient diets. Plasma triglycerides were elevated in the iron-deficient group throughout gestation. There were time-dependent changes in the triglyceride content of the maternal liver, falling at the midpoint of gestation and then increasing on d21.5. Compared to the control, triglycerides in the maternal liver were not different in the iron-deficient group prior to pregnancy and on d12.5, but were markedly reduced by d21.5. The abundance of mRNAs in the maternal liver suggests that lipogenesis is unchanged and beta-oxidation is reduced on d21.5 by iron deficiency. On d21.5 of gestation, the expression of placental lipase was unchanged by iron deficiency, however, the abundance of mRNAs for SREBP-1c, FABP4 were reduced, suggesting that there were changes in fatty acid handling. In the fetal liver, iron deficiency produced a marked decrease in the abundance of the L-CPT-1 mRNA, suggesting that beta-oxidation is reduced. This study shows that the major effect of iron deficiency on maternal lipid metabolism occurs late in gestation and that perturbed lipid metabolism may be a common feature of models of fetal programming.

Original languageEnglish
Article numbere12908
JournalPhysiological reports
Volume4
Issue number21
DOIs
Publication statusPublished - 15 Nov 2016

Fingerprint

Iron
Fats
Gene Expression
Pregnancy
Lipid Metabolism
Triglycerides
Liver
Mothers
Stored Messenger RNA
Sterol Regulatory Element Binding Protein 1
Messenger RNA
Lipogenesis
Fetal Development
Lipase
Lactation
Fetus
Fatty Acids
Diet

Keywords

  • development
  • fetal programming
  • iron
  • lipid metabolism
  • liver
  • mitochondria

Cite this

The effect of iron deficiency on the temporal changes in the expression of genes associated with fat metabolism in the pregnant rat. / Hay, Susan M; McArdle, Harry J; Hayes, Helen E; Stevens, Valerie J; Rees, William D.

In: Physiological reports, Vol. 4, No. 21, e12908, 15.11.2016.

Research output: Contribution to journalArticle

@article{99417ad5a7784ce8a4bc3c3a73fdca9d,
title = "The effect of iron deficiency on the temporal changes in the expression of genes associated with fat metabolism in the pregnant rat",
abstract = "Iron is essential for the oxidative metabolism of lipids. Lipid metabolism changes during gestation to meet the requirements of the growing fetus and to prepare for lactation. The temporal effects of iron deficiency during gestation were studied in female rats fed complete or iron-deficient diets. Plasma triglycerides were elevated in the iron-deficient group throughout gestation. There were time-dependent changes in the triglyceride content of the maternal liver, falling at the midpoint of gestation and then increasing on d21.5. Compared to the control, triglycerides in the maternal liver were not different in the iron-deficient group prior to pregnancy and on d12.5, but were markedly reduced by d21.5. The abundance of mRNAs in the maternal liver suggests that lipogenesis is unchanged and beta-oxidation is reduced on d21.5 by iron deficiency. On d21.5 of gestation, the expression of placental lipase was unchanged by iron deficiency, however, the abundance of mRNAs for SREBP-1c, FABP4 were reduced, suggesting that there were changes in fatty acid handling. In the fetal liver, iron deficiency produced a marked decrease in the abundance of the L-CPT-1 mRNA, suggesting that beta-oxidation is reduced. This study shows that the major effect of iron deficiency on maternal lipid metabolism occurs late in gestation and that perturbed lipid metabolism may be a common feature of models of fetal programming.",
keywords = "development, fetal programming, iron , lipid metabolism, liver, mitochondria",
author = "Hay, {Susan M} and McArdle, {Harry J} and Hayes, {Helen E} and Stevens, {Valerie J} and Rees, {William D}",
note = "Funding Information This work was funded as a part of the Scottish Government Rural and Environment Science and Analytical Services (RESAS) Strategic Research Program.",
year = "2016",
month = "11",
day = "15",
doi = "10.14814/phy2.12908",
language = "English",
volume = "4",
journal = "Physiological reports",
issn = "2051-817X",
publisher = "John Wiley and Sons Inc.",
number = "21",

}

TY - JOUR

T1 - The effect of iron deficiency on the temporal changes in the expression of genes associated with fat metabolism in the pregnant rat

AU - Hay, Susan M

AU - McArdle, Harry J

AU - Hayes, Helen E

AU - Stevens, Valerie J

AU - Rees, William D

N1 - Funding Information This work was funded as a part of the Scottish Government Rural and Environment Science and Analytical Services (RESAS) Strategic Research Program.

PY - 2016/11/15

Y1 - 2016/11/15

N2 - Iron is essential for the oxidative metabolism of lipids. Lipid metabolism changes during gestation to meet the requirements of the growing fetus and to prepare for lactation. The temporal effects of iron deficiency during gestation were studied in female rats fed complete or iron-deficient diets. Plasma triglycerides were elevated in the iron-deficient group throughout gestation. There were time-dependent changes in the triglyceride content of the maternal liver, falling at the midpoint of gestation and then increasing on d21.5. Compared to the control, triglycerides in the maternal liver were not different in the iron-deficient group prior to pregnancy and on d12.5, but were markedly reduced by d21.5. The abundance of mRNAs in the maternal liver suggests that lipogenesis is unchanged and beta-oxidation is reduced on d21.5 by iron deficiency. On d21.5 of gestation, the expression of placental lipase was unchanged by iron deficiency, however, the abundance of mRNAs for SREBP-1c, FABP4 were reduced, suggesting that there were changes in fatty acid handling. In the fetal liver, iron deficiency produced a marked decrease in the abundance of the L-CPT-1 mRNA, suggesting that beta-oxidation is reduced. This study shows that the major effect of iron deficiency on maternal lipid metabolism occurs late in gestation and that perturbed lipid metabolism may be a common feature of models of fetal programming.

AB - Iron is essential for the oxidative metabolism of lipids. Lipid metabolism changes during gestation to meet the requirements of the growing fetus and to prepare for lactation. The temporal effects of iron deficiency during gestation were studied in female rats fed complete or iron-deficient diets. Plasma triglycerides were elevated in the iron-deficient group throughout gestation. There were time-dependent changes in the triglyceride content of the maternal liver, falling at the midpoint of gestation and then increasing on d21.5. Compared to the control, triglycerides in the maternal liver were not different in the iron-deficient group prior to pregnancy and on d12.5, but were markedly reduced by d21.5. The abundance of mRNAs in the maternal liver suggests that lipogenesis is unchanged and beta-oxidation is reduced on d21.5 by iron deficiency. On d21.5 of gestation, the expression of placental lipase was unchanged by iron deficiency, however, the abundance of mRNAs for SREBP-1c, FABP4 were reduced, suggesting that there were changes in fatty acid handling. In the fetal liver, iron deficiency produced a marked decrease in the abundance of the L-CPT-1 mRNA, suggesting that beta-oxidation is reduced. This study shows that the major effect of iron deficiency on maternal lipid metabolism occurs late in gestation and that perturbed lipid metabolism may be a common feature of models of fetal programming.

KW - development

KW - fetal programming

KW - iron

KW - lipid metabolism

KW - liver

KW - mitochondria

U2 - 10.14814/phy2.12908

DO - 10.14814/phy2.12908

M3 - Article

VL - 4

JO - Physiological reports

JF - Physiological reports

SN - 2051-817X

IS - 21

M1 - e12908

ER -