Hyperhomocysteinemia is not sufficient to cause preeclampsia in an animal model: the importance of folate intake
Objective The objective of our study was to determine whether methylenetetrahydrofolate reductase (Mthfr)-deficient mice develop preeclampsia (PE). Study Design Mice were placed on a normal or low-folate/high-methionine (LF/HM) diet to assess the impact of mild and severe homocysteinemia. Blood pres...
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| Veröffentlicht in: | American journal of obstetrics and gynecology 2009-02, Vol.200 (2), p.198.e1-198.e5 |
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| container_title | American journal of obstetrics and gynecology |
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| creator | Falcao, Stéphanie, MSc Bisotto, Sandra, MSc Gutkowska, Jolanta, PhD Lavoie, Julie L., PhD |
| description | Objective The objective of our study was to determine whether methylenetetrahydrofolate reductase (Mthfr)-deficient mice develop preeclampsia (PE). Study Design Mice were placed on a normal or low-folate/high-methionine (LF/HM) diet to assess the impact of mild and severe homocysteinemia. Blood pressure and proteinuria were measured throughout gestation in Mthfr-deficient and control mice on both diets, by radiotelemetry and by determining the urinary albumin/creatinine ratio by enzyme-linked immunosorbent assay, respectively. Results Although Mthfr-deficient mice have endothelial dysfunction, they do not develop hypertension or proteinuria during gestation. The LF/HM diet induced proteinuria, growth restriction, and a decrease in the number of pups per litter in all mice without any effect on the placenta. Conclusion Our study clearly demonstrates that hyperhomocysteinemia is not sufficient to cause PE in this animal model. Furthermore, it confirms the importance of folate intake on pregnancy outcomes. |
| doi_str_mv | 10.1016/j.ajog.2008.10.003 |
| format | Article |
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Study Design Mice were placed on a normal or low-folate/high-methionine (LF/HM) diet to assess the impact of mild and severe homocysteinemia. Blood pressure and proteinuria were measured throughout gestation in Mthfr-deficient and control mice on both diets, by radiotelemetry and by determining the urinary albumin/creatinine ratio by enzyme-linked immunosorbent assay, respectively. Results Although Mthfr-deficient mice have endothelial dysfunction, they do not develop hypertension or proteinuria during gestation. The LF/HM diet induced proteinuria, growth restriction, and a decrease in the number of pups per litter in all mice without any effect on the placenta. Conclusion Our study clearly demonstrates that hyperhomocysteinemia is not sufficient to cause PE in this animal model. Furthermore, it confirms the importance of folate intake on pregnancy outcomes.</description><identifier>ISSN: 0002-9378</identifier><identifier>EISSN: 1097-6868</identifier><identifier>DOI: 10.1016/j.ajog.2008.10.003</identifier><identifier>PMID: 19110222</identifier><identifier>CODEN: AJOGAH</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>Animals ; Biological and medical sciences ; Disease Models, Animal ; Diseases of mother, fetus and pregnancy ; Endothelium, Vascular - physiopathology ; Female ; Folate deficiency ; Folic Acid - administration & dosage ; Gynecology. Andrology. Obstetrics ; hyperhomocysteinemia ; Hyperhomocysteinemia - complications ; Medical sciences ; Methylenetetrahydrofolate Reductase (NADPH2) - deficiency ; Mice ; Mice, Knockout ; mouse models ; Obstetrics and Gynecology ; Pre-Eclampsia - etiology ; preeclampsia ; Pregnancy ; pregnancy outcomes ; Pregnancy. Fetus. Placenta</subject><ispartof>American journal of obstetrics and gynecology, 2009-02, Vol.200 (2), p.198.e1-198.e5</ispartof><rights>Mosby, Inc.</rights><rights>2009 Mosby, Inc.</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c439t-f444eef663af67ad28725544fd5f8296c619f0743db3be2d54bd29b1a87db4633</citedby><cites>FETCH-LOGICAL-c439t-f444eef663af67ad28725544fd5f8296c619f0743db3be2d54bd29b1a87db4633</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ajog.2008.10.003$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21093077$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19110222$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Falcao, Stéphanie, MSc</creatorcontrib><creatorcontrib>Bisotto, Sandra, MSc</creatorcontrib><creatorcontrib>Gutkowska, Jolanta, PhD</creatorcontrib><creatorcontrib>Lavoie, Julie L., PhD</creatorcontrib><title>Hyperhomocysteinemia is not sufficient to cause preeclampsia in an animal model: the importance of folate intake</title><title>American journal of obstetrics and gynecology</title><addtitle>Am J Obstet Gynecol</addtitle><description>Objective The objective of our study was to determine whether methylenetetrahydrofolate reductase (Mthfr)-deficient mice develop preeclampsia (PE). Study Design Mice were placed on a normal or low-folate/high-methionine (LF/HM) diet to assess the impact of mild and severe homocysteinemia. Blood pressure and proteinuria were measured throughout gestation in Mthfr-deficient and control mice on both diets, by radiotelemetry and by determining the urinary albumin/creatinine ratio by enzyme-linked immunosorbent assay, respectively. Results Although Mthfr-deficient mice have endothelial dysfunction, they do not develop hypertension or proteinuria during gestation. The LF/HM diet induced proteinuria, growth restriction, and a decrease in the number of pups per litter in all mice without any effect on the placenta. Conclusion Our study clearly demonstrates that hyperhomocysteinemia is not sufficient to cause PE in this animal model. Furthermore, it confirms the importance of folate intake on pregnancy outcomes.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Disease Models, Animal</subject><subject>Diseases of mother, fetus and pregnancy</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Female</subject><subject>Folate deficiency</subject><subject>Folic Acid - administration & dosage</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>hyperhomocysteinemia</subject><subject>Hyperhomocysteinemia - complications</subject><subject>Medical sciences</subject><subject>Methylenetetrahydrofolate Reductase (NADPH2) - deficiency</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>mouse models</subject><subject>Obstetrics and Gynecology</subject><subject>Pre-Eclampsia - etiology</subject><subject>preeclampsia</subject><subject>Pregnancy</subject><subject>pregnancy outcomes</subject><subject>Pregnancy. Fetus. Placenta</subject><issn>0002-9378</issn><issn>1097-6868</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kt-LFSEUgCWK9rb1D_QQvtTb3Pwx15mJCGJp22Chh-pZHD22zs7opE5w__uUe2mhh0BQD9856udB6CUle0qoeDvt1RR-7hkhfQnsCeGP0I6SoWtEL_rHaEcIYc3Au_4CPUtpqls2sKfogg6UljXbofXmuEK8C0vQx5TBeVicwi5hHzJOm7VOO_AZ54C12hLgNQLoWS1rqpzHqg63qBkvwcD8Duc7wG5ZQ8zKa8DBYhtmlUvQZ3UPz9ETq-YEL87zJfpx_en71U1z-_Xzl6uPt41u-ZAb27YtgBWCKys6ZVjfscOhba052J4NQgs6WNK13Ix8BGYO7WjYMFLVd2ZsBeeX6M2p7hrDrw1SlotLGuZZeQhbkkKUioT1BWQnUMeQUgQr11jeE4-SElk9y0lWz7J6rrHiuSS9OlffxgXMQ8pZbAFenwGVtJptLDJc-sux8k2cdF3h3p84KC5-O4gyVeEajIugszTB_f8eH_5J17Pzrpx4D0dIU9iiL5YllYlJIr_VFqgNQXpSynSc_wF1rbG6</recordid><startdate>20090201</startdate><enddate>20090201</enddate><creator>Falcao, Stéphanie, MSc</creator><creator>Bisotto, Sandra, MSc</creator><creator>Gutkowska, Jolanta, PhD</creator><creator>Lavoie, Julie L., PhD</creator><general>Mosby, Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20090201</creationdate><title>Hyperhomocysteinemia is not sufficient to cause preeclampsia in an animal model: the importance of folate intake</title><author>Falcao, Stéphanie, MSc ; Bisotto, Sandra, MSc ; Gutkowska, Jolanta, PhD ; Lavoie, Julie L., PhD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c439t-f444eef663af67ad28725544fd5f8296c619f0743db3be2d54bd29b1a87db4633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Disease Models, Animal</topic><topic>Diseases of mother, fetus and pregnancy</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Female</topic><topic>Folate deficiency</topic><topic>Folic Acid - administration & dosage</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>hyperhomocysteinemia</topic><topic>Hyperhomocysteinemia - complications</topic><topic>Medical sciences</topic><topic>Methylenetetrahydrofolate Reductase (NADPH2) - deficiency</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>mouse models</topic><topic>Obstetrics and Gynecology</topic><topic>Pre-Eclampsia - etiology</topic><topic>preeclampsia</topic><topic>Pregnancy</topic><topic>pregnancy outcomes</topic><topic>Pregnancy. Fetus. Placenta</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Falcao, Stéphanie, MSc</creatorcontrib><creatorcontrib>Bisotto, Sandra, MSc</creatorcontrib><creatorcontrib>Gutkowska, Jolanta, PhD</creatorcontrib><creatorcontrib>Lavoie, Julie L., PhD</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of obstetrics and gynecology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Falcao, Stéphanie, MSc</au><au>Bisotto, Sandra, MSc</au><au>Gutkowska, Jolanta, PhD</au><au>Lavoie, Julie L., PhD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperhomocysteinemia is not sufficient to cause preeclampsia in an animal model: the importance of folate intake</atitle><jtitle>American journal of obstetrics and gynecology</jtitle><addtitle>Am J Obstet Gynecol</addtitle><date>2009-02-01</date><risdate>2009</risdate><volume>200</volume><issue>2</issue><spage>198.e1</spage><epage>198.e5</epage><pages>198.e1-198.e5</pages><issn>0002-9378</issn><eissn>1097-6868</eissn><coden>AJOGAH</coden><abstract>Objective The objective of our study was to determine whether methylenetetrahydrofolate reductase (Mthfr)-deficient mice develop preeclampsia (PE). Study Design Mice were placed on a normal or low-folate/high-methionine (LF/HM) diet to assess the impact of mild and severe homocysteinemia. Blood pressure and proteinuria were measured throughout gestation in Mthfr-deficient and control mice on both diets, by radiotelemetry and by determining the urinary albumin/creatinine ratio by enzyme-linked immunosorbent assay, respectively. Results Although Mthfr-deficient mice have endothelial dysfunction, they do not develop hypertension or proteinuria during gestation. The LF/HM diet induced proteinuria, growth restriction, and a decrease in the number of pups per litter in all mice without any effect on the placenta. Conclusion Our study clearly demonstrates that hyperhomocysteinemia is not sufficient to cause PE in this animal model. Furthermore, it confirms the importance of folate intake on pregnancy outcomes.</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>19110222</pmid><doi>10.1016/j.ajog.2008.10.003</doi><tpages>3</tpages></addata></record> |
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| subjects | Animals Biological and medical sciences Disease Models, Animal Diseases of mother, fetus and pregnancy Endothelium, Vascular - physiopathology Female Folate deficiency Folic Acid - administration & dosage Gynecology. Andrology. Obstetrics hyperhomocysteinemia Hyperhomocysteinemia - complications Medical sciences Methylenetetrahydrofolate Reductase (NADPH2) - deficiency Mice Mice, Knockout mouse models Obstetrics and Gynecology Pre-Eclampsia - etiology preeclampsia Pregnancy pregnancy outcomes Pregnancy. Fetus. Placenta |
| title | Hyperhomocysteinemia is not sufficient to cause preeclampsia in an animal model: the importance of folate intake |
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