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Maternal-fetal hepatic and placental metabolome profiles are associated with reduced fetal growth in a rat model of maternal obesity

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journal contribution
posted on 03.01.2017, 15:50 by K. Mumme, C. Gray, C. M. Reynolds, M. H. Vickers, C. J. Harrison, J. L. Stanley, K. Ruggiero, S. G. Villas-Bôas, Philip N. Baker, K. Sulek
Introduction Maternal obesity is associated with a range of pregnancy complications, including fetal growth restriction (FGR), whereby a fetus fails to reach its genetically determined growth. Placental insufficiency and reduced nutrient transport play a role in the onset of FGR. Objectives Metabolomic profiling was used to reveal altered maternal and fetal metabolic pathways in a model of diet induced obesity during pregnancy, leading to reduced fetal growth. Methods We examined the metabolome of maternal and fetal livers, and placenta following a high fat and salt intake. Sprague–Dawley rats were assigned to (a) control diet (CD; 1 % salt, 10 % kcal from fat), (b) high salt diet (SD; 4 % salt, 10 % kcal from fat), (c) high fat diet (HF; 1 % salt, 45 % kcal from fat) or (d) high-fat high-salt diet (HFSD; 4 % salt, 45 % kcal from fat) 21 days prior to pregnancy and during gestation. Metabolites from maternal and fetal livers, and placenta were identified using gas and liquid chromatography combined with mass spectrometry. Results Maternal HF intake resulted in reduced fetal weight. Altered metabolite profiles were observed in the HF maternal and fetal liver, and placenta. Polyunsaturated fatty acid metabolism was significantly altered in maternal and fetal liver by maternal fat intake. Conclusion Excess of linoleic and α-linoleic acid (essential fatty acids) may be detrimental during placentation and associated with a reduction in fetal weight. Additionally, maternal, placental and fetal response to increased fat consumption seems likely to involve palmitoleic acid utilization as an adaptive response during maternal obesity.

Funding

The authors would like to express their gratitude for support provided by the Vernon Jansen Unit and the Centre for Genomics, Proteomics and Metabolomics. Technical assistance was provided by Rachna Patel, Angelica Bernal, Minglan Li, Elizabeth McKenzie and Margaret Coe. Financial assistance was provided by Gravida: National Centre for Growth and Development (project no. STF-13-24), Lotteries Health Research Fellowship, Faculty Development Research Funding (FDRF) and the Nutricia Research Foundation.

History

Citation

Metabolomics, (2016) 12: 83.

Author affiliation

/Organisation/COLLEGE OF MEDICINE, BIOLOGICAL SCIENCES AND PSYCHOLOGY

Version

AM (Accepted Manuscript)

Published in

Metabolomics

Publisher

Springer Verlag (Germany) for Metabolomics Society

issn

1573-3882

eissn

1573-3890

Acceptance date

18/02/2016

Available date

15/03/2017

Publisher version

http://link.springer.com/article/10.1007/s11306-016-1014-9

Notes

The online version of this article (doi:10.1007/s11306-016-1014-9) contains supplementary material, which is available to authorized users.

Language

en