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...
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| Veröffentlicht in: | Scientific reports 2016-04, Vol.6 (1), p.25091-25091, Article 25091 |
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| creator | Asghar, Zeenat A. Thompson, Alysha Chi, Maggie Cusumano, Andrew Scheaffer, Suzanne Al-Hammadi, Noor Saben, Jessica L. Moley, Kelle H. |
| 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. |
| doi_str_mv | 10.1038/srep25091 |
| format | Article |
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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.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep25091</identifier><identifier>PMID: 27125896</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/106 ; 13/51 ; 14/63 ; 631/136 ; 64/60 ; 692/163 ; 82/1 ; 82/58 ; 82/80 ; Acid production ; Allopurinol ; Allopurinol - administration & dosage ; Allopurinol - pharmacology ; AMP deaminase ; AMP Deaminase - metabolism ; Animals ; Disease Models, Animal ; Enzymes ; Female ; Fetal Growth Retardation - chemically induced ; Fetal Growth Retardation - prevention & control ; Fructose ; Fructose - adverse effects ; Fructose - blood ; Humanities and Social Sciences ; Lipids ; Low birth weight ; Metabolic disorders ; Metabolic syndrome ; Metabolism ; Mice ; multidisciplinary ; Offspring ; Oxidative Stress ; Placenta ; Placenta - metabolism ; Placental Insufficiency - chemically induced ; Placental Insufficiency - prevention & control ; Pregnancy ; Prenatal development ; Rodents ; Science ; Triglycerides ; Triglycerides - blood ; Uric acid ; Uric Acid - metabolism ; Xanthine oxidase ; Xanthine Oxidase - antagonists & inhibitors ; Xanthine Oxidase - metabolism</subject><ispartof>Scientific reports, 2016-04, Vol.6 (1), p.25091-25091, Article 25091</ispartof><rights>The Author(s) 2016</rights><rights>Copyright Nature Publishing Group Apr 2016</rights><rights>Copyright © 2016, Macmillan Publishers Limited 2016 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-57307f027c67b6845b90eda508d7c18d0525cfa0f3058a22e6bb7f3021875d73</citedby><cites>FETCH-LOGICAL-c504t-57307f027c67b6845b90eda508d7c18d0525cfa0f3058a22e6bb7f3021875d73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4850405/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4850405/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27125896$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Asghar, Zeenat A.</creatorcontrib><creatorcontrib>Thompson, Alysha</creatorcontrib><creatorcontrib>Chi, Maggie</creatorcontrib><creatorcontrib>Cusumano, Andrew</creatorcontrib><creatorcontrib>Scheaffer, Suzanne</creatorcontrib><creatorcontrib>Al-Hammadi, Noor</creatorcontrib><creatorcontrib>Saben, Jessica L.</creatorcontrib><creatorcontrib>Moley, Kelle H.</creatorcontrib><title>Maternal fructose drives placental uric acid production leading to adverse fetal outcomes</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><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.</description><subject>13/106</subject><subject>13/51</subject><subject>14/63</subject><subject>631/136</subject><subject>64/60</subject><subject>692/163</subject><subject>82/1</subject><subject>82/58</subject><subject>82/80</subject><subject>Acid production</subject><subject>Allopurinol</subject><subject>Allopurinol - administration & dosage</subject><subject>Allopurinol - pharmacology</subject><subject>AMP deaminase</subject><subject>AMP Deaminase - metabolism</subject><subject>Animals</subject><subject>Disease Models, Animal</subject><subject>Enzymes</subject><subject>Female</subject><subject>Fetal Growth Retardation - chemically induced</subject><subject>Fetal Growth Retardation - prevention & control</subject><subject>Fructose</subject><subject>Fructose - adverse effects</subject><subject>Fructose - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Asghar, Zeenat A.</au><au>Thompson, Alysha</au><au>Chi, Maggie</au><au>Cusumano, Andrew</au><au>Scheaffer, Suzanne</au><au>Al-Hammadi, Noor</au><au>Saben, Jessica L.</au><au>Moley, Kelle H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Maternal fructose drives placental uric acid production leading to adverse fetal outcomes</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2016-04-29</date><risdate>2016</risdate><volume>6</volume><issue>1</issue><spage>25091</spage><epage>25091</epage><pages>25091-25091</pages><artnum>25091</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>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.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>27125896</pmid><doi>10.1038/srep25091</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/106 13/51 14/63 631/136 64/60 692/163 82/1 82/58 82/80 Acid production Allopurinol Allopurinol - administration & dosage Allopurinol - pharmacology AMP deaminase AMP Deaminase - metabolism Animals Disease Models, Animal Enzymes Female Fetal Growth Retardation - chemically induced Fetal Growth Retardation - prevention & control Fructose Fructose - adverse effects Fructose - blood Humanities and Social Sciences Lipids Low birth weight Metabolic disorders Metabolic syndrome Metabolism Mice multidisciplinary Offspring Oxidative Stress Placenta Placenta - metabolism Placental Insufficiency - chemically induced Placental Insufficiency - prevention & control Pregnancy Prenatal development Rodents Science Triglycerides Triglycerides - blood Uric acid Uric Acid - metabolism Xanthine oxidase Xanthine Oxidase - antagonists & inhibitors Xanthine Oxidase - metabolism |
| title | Maternal fructose drives placental uric acid production leading to adverse fetal outcomes |
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