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Maternal fructose drives placental uric acid production leading to adverse fetal outcomes
Maternal metabolic diseases increase offspring risk for low birth weight and cardiometabolic diseases in adulthood. Excess fructose consumption may confer metabolic risks for both women and their offspring. However, the direct consequences of fructose intake per se are unknown. We assessed the impac...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4850405/ https://www.ncbi.nlm.nih.gov/pubmed/27125896 http://dx.doi.org/10.1038/srep25091 |
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author | Asghar, Zeenat A. Thompson, Alysha Chi, Maggie Cusumano, Andrew Scheaffer, Suzanne Al-Hammadi, Noor Saben, Jessica L. Moley, Kelle H. |
author_facet | Asghar, Zeenat A. Thompson, Alysha Chi, Maggie Cusumano, Andrew Scheaffer, Suzanne Al-Hammadi, Noor Saben, Jessica L. Moley, Kelle H. |
author_sort | Asghar, Zeenat A. |
collection | PubMed |
description | Maternal metabolic diseases increase offspring risk for low birth weight and cardiometabolic diseases in adulthood. Excess fructose consumption may confer metabolic risks for both women and their offspring. However, the direct consequences of fructose intake per se are unknown. We assessed the impact of a maternal high-fructose diet on the fetal-placental unit in mice in the absence of metabolic syndrome and determined the association between maternal serum fructose and placental uric acid levels in humans. In mice, maternal fructose consumption led to placental inefficiency, fetal growth restriction, elevated fetal serum glucose and triglyceride levels. In the placenta, fructose induced de novo uric acid synthesis by activating the activities of the enzymes AMP deaminase and xanthine oxidase. Moreover, the placentas had increased lipids and altered expression of genes that control oxidative stress. Treatment of mothers with the xanthine oxidase inhibitor allopurinol reduced placental uric acid levels, prevented placental inefficiency, and improved fetal weights and serum triglycerides. Finally, in 18 women delivering at term, maternal serum fructose levels significantly correlated with placental uric acid levels. These findings suggest that in mice, excess maternal fructose consumption impairs placental function via a xanthine oxidase/uric acid-dependent mechanism, and similar effects may occur in humans. |
format | Online Article Text |
id | pubmed-4850405 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-48504052016-05-05 Maternal fructose drives placental uric acid production leading to adverse fetal outcomes Asghar, Zeenat A. Thompson, Alysha Chi, Maggie Cusumano, Andrew Scheaffer, Suzanne Al-Hammadi, Noor Saben, Jessica L. Moley, Kelle H. Sci Rep Article Maternal metabolic diseases increase offspring risk for low birth weight and cardiometabolic diseases in adulthood. Excess fructose consumption may confer metabolic risks for both women and their offspring. However, the direct consequences of fructose intake per se are unknown. We assessed the impact of a maternal high-fructose diet on the fetal-placental unit in mice in the absence of metabolic syndrome and determined the association between maternal serum fructose and placental uric acid levels in humans. In mice, maternal fructose consumption led to placental inefficiency, fetal growth restriction, elevated fetal serum glucose and triglyceride levels. In the placenta, fructose induced de novo uric acid synthesis by activating the activities of the enzymes AMP deaminase and xanthine oxidase. Moreover, the placentas had increased lipids and altered expression of genes that control oxidative stress. Treatment of mothers with the xanthine oxidase inhibitor allopurinol reduced placental uric acid levels, prevented placental inefficiency, and improved fetal weights and serum triglycerides. Finally, in 18 women delivering at term, maternal serum fructose levels significantly correlated with placental uric acid levels. These findings suggest that in mice, excess maternal fructose consumption impairs placental function via a xanthine oxidase/uric acid-dependent mechanism, and similar effects may occur in humans. Nature Publishing Group 2016-04-29 /pmc/articles/PMC4850405/ /pubmed/27125896 http://dx.doi.org/10.1038/srep25091 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Asghar, Zeenat A. Thompson, Alysha Chi, Maggie Cusumano, Andrew Scheaffer, Suzanne Al-Hammadi, Noor Saben, Jessica L. Moley, Kelle H. Maternal fructose drives placental uric acid production leading to adverse fetal outcomes |
title | Maternal fructose drives placental uric acid production leading to adverse fetal outcomes |
title_full | Maternal fructose drives placental uric acid production leading to adverse fetal outcomes |
title_fullStr | Maternal fructose drives placental uric acid production leading to adverse fetal outcomes |
title_full_unstemmed | Maternal fructose drives placental uric acid production leading to adverse fetal outcomes |
title_short | Maternal fructose drives placental uric acid production leading to adverse fetal outcomes |
title_sort | maternal fructose drives placental uric acid production leading to adverse fetal outcomes |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4850405/ https://www.ncbi.nlm.nih.gov/pubmed/27125896 http://dx.doi.org/10.1038/srep25091 |
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