Effects of maternal and fetal LEP common variants on maternal glycemic traits in pregnancy
Previous studies suggest that leptin (LEP) has an important role in glucose metabolism in the nonpregnant state. During pregnancy, circulating maternal concentrations of leptin rise significantly, mainly due to increased secretion of leptin from maternal adipose tissue and placenta. This study aimed...
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description | Previous studies suggest that leptin (LEP) has an important role in glucose metabolism in the nonpregnant state. During pregnancy, circulating maternal concentrations of leptin rise significantly, mainly due to increased secretion of leptin from maternal adipose tissue and placenta. This study aimed to analyze the impact of maternal and fetal common
LEP
variants on glucose homeostasis in the pregnant state. Several glycemic traits, including fasting plasma glucose, fasting plasma insulin (FPI), and plasma glucose 1 hour after a 50-g oral glucose load, were measured in 1,112 unrelated Chinese Han pregnant women at 24–28 weeks gestation. Homeostatic model assessment (HOMA) was used to assess beta cell function (HOMA1-β and HOMA2-β) and insulin resistance (HOMA1-IR and HOMA2-IR).The relationships between glycemic traits and 12
LEP
variants were determined. After applying the Bonferroni correction, we detected that (1) maternal rs10954173 and fetal rs10244329 were associated with maternal FPI although the effect of fetal rs10244329 may be not independent of maternal rs10244329, and (2) maternal rs12537573 was associated with maternal FPI and HOMA2-IR. This study provides genetic evidence that both maternal and fetal
LEP
polymorphisms may affect maternal glucose metabolism in pregnancy. |
doi_str_mv | 10.1038/s41598-017-18117-z |
format | Article |
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LEP
variants on glucose homeostasis in the pregnant state. Several glycemic traits, including fasting plasma glucose, fasting plasma insulin (FPI), and plasma glucose 1 hour after a 50-g oral glucose load, were measured in 1,112 unrelated Chinese Han pregnant women at 24–28 weeks gestation. Homeostatic model assessment (HOMA) was used to assess beta cell function (HOMA1-β and HOMA2-β) and insulin resistance (HOMA1-IR and HOMA2-IR).The relationships between glycemic traits and 12
LEP
variants were determined. After applying the Bonferroni correction, we detected that (1) maternal rs10954173 and fetal rs10244329 were associated with maternal FPI although the effect of fetal rs10244329 may be not independent of maternal rs10244329, and (2) maternal rs12537573 was associated with maternal FPI and HOMA2-IR. This study provides genetic evidence that both maternal and fetal
LEP
polymorphisms may affect maternal glucose metabolism in pregnancy.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-017-18117-z</identifier><identifier>PMID: 29255202</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>45 ; 45/22 ; 45/77 ; 631/208/205 ; 692/308/2056 ; 692/499 ; Adipose tissue ; Adult ; Asian Continental Ancestry Group - genetics ; Beta cells ; Blood Glucose - analysis ; Blood Glucose - metabolism ; China ; Ethnic Groups - genetics ; Fasting ; Female ; Fetus - metabolism ; Fetuses ; Gestation ; Glucose ; Glucose - metabolism ; Homeostasis ; Humanities and Social Sciences ; Humans ; Insulin ; Insulin - analysis ; Insulin - blood ; Insulin Resistance - genetics ; Insulin-Secreting Cells - metabolism ; Leptin ; Leptin - genetics ; Leptin - physiology ; Maternal-Fetal Exchange - genetics ; Metabolism ; multidisciplinary ; Phenotype ; Placenta ; Placenta - metabolism ; Pregnancy ; Prenatal Care ; Science ; Science (multidisciplinary) ; Secretion</subject><ispartof>Scientific reports, 2017-12, Vol.7 (1), p.17710-8, Article 17710</ispartof><rights>The Author(s) 2017</rights><rights>2017. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-bda544e32d804a9c9bcf989f317aff810a67abe2a6abfd65e74dc6cdcb63517d3</citedby><cites>FETCH-LOGICAL-c474t-bda544e32d804a9c9bcf989f317aff810a67abe2a6abfd65e74dc6cdcb63517d3</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/PMC5735190/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5735190/$$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/29255202$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, Rong</creatorcontrib><creatorcontrib>Ju, Hongfang</creatorcontrib><creatorcontrib>Yuan, Ziyu</creatorcontrib><creatorcontrib>Zhang, Caicai</creatorcontrib><creatorcontrib>Zeng, Liangliang</creatorcontrib><creatorcontrib>Sun, Yuantian</creatorcontrib><creatorcontrib>Su, Zhenyu</creatorcontrib><creatorcontrib>Jin, Li</creatorcontrib><title>Effects of maternal and fetal LEP common variants on maternal glycemic traits in pregnancy</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Previous studies suggest that leptin (LEP) has an important role in glucose metabolism in the nonpregnant state. During pregnancy, circulating maternal concentrations of leptin rise significantly, mainly due to increased secretion of leptin from maternal adipose tissue and placenta. This study aimed to analyze the impact of maternal and fetal common
LEP
variants on glucose homeostasis in the pregnant state. Several glycemic traits, including fasting plasma glucose, fasting plasma insulin (FPI), and plasma glucose 1 hour after a 50-g oral glucose load, were measured in 1,112 unrelated Chinese Han pregnant women at 24–28 weeks gestation. Homeostatic model assessment (HOMA) was used to assess beta cell function (HOMA1-β and HOMA2-β) and insulin resistance (HOMA1-IR and HOMA2-IR).The relationships between glycemic traits and 12
LEP
variants were determined. After applying the Bonferroni correction, we detected that (1) maternal rs10954173 and fetal rs10244329 were associated with maternal FPI although the effect of fetal rs10244329 may be not independent of maternal rs10244329, and (2) maternal rs12537573 was associated with maternal FPI and HOMA2-IR. This study provides genetic evidence that both maternal and fetal
LEP
polymorphisms may affect maternal glucose metabolism in pregnancy.</description><subject>45</subject><subject>45/22</subject><subject>45/77</subject><subject>631/208/205</subject><subject>692/308/2056</subject><subject>692/499</subject><subject>Adipose tissue</subject><subject>Adult</subject><subject>Asian Continental Ancestry Group - genetics</subject><subject>Beta cells</subject><subject>Blood Glucose - analysis</subject><subject>Blood Glucose - metabolism</subject><subject>China</subject><subject>Ethnic Groups - genetics</subject><subject>Fasting</subject><subject>Female</subject><subject>Fetus - metabolism</subject><subject>Fetuses</subject><subject>Gestation</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Homeostasis</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Insulin</subject><subject>Insulin - analysis</subject><subject>Insulin - blood</subject><subject>Insulin Resistance - genetics</subject><subject>Insulin-Secreting Cells - metabolism</subject><subject>Leptin</subject><subject>Leptin - genetics</subject><subject>Leptin - physiology</subject><subject>Maternal-Fetal Exchange - genetics</subject><subject>Metabolism</subject><subject>multidisciplinary</subject><subject>Phenotype</subject><subject>Placenta</subject><subject>Placenta - metabolism</subject><subject>Pregnancy</subject><subject>Prenatal Care</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Secretion</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kcFP2zAUxi0Egor1H-AwRdqFSzbbseP4MgmhwiZVYge4cLFeHLtLldidnSKVvx5nga5Dwgf7Sd_vfX72h9AFwV8JLqpvkREuqxwTkZOKpP35CM0oZjynBaXHB_UZmse4xmlxKhmRp-iMSso5xXSGHhfWGj3EzNush8EEB10GrsmsGVK1XPzKtO9777InCC24kXT_yFW306ZvdTYEaJPWumwTzMqB07tP6MRCF8389TxHDzeL--sf-fLu9uf11TLXTLAhrxvgjJmCNhVmILWstZWVtAURYG1FMJQCakOhhNo2JTeCNbrUja7LghPRFOfo--S72da9abRxaZhObULbQ9gpD636X3Htb7XyT4qLZCBxMrh8NQj-z9bEQfVt1KbrwBm_jYpIUQnKsSgT-uUduvbb8SdGqioYLUsyGtKJ0sHHGIzdD0OwGtNTU3oqpaf-pqeeU9Pnw2fsW96ySkAxATFJbmXCwd0f274AqzinsA</recordid><startdate>20171218</startdate><enddate>20171218</enddate><creator>Lin, Rong</creator><creator>Ju, Hongfang</creator><creator>Yuan, Ziyu</creator><creator>Zhang, Caicai</creator><creator>Zeng, Liangliang</creator><creator>Sun, Yuantian</creator><creator>Su, Zhenyu</creator><creator>Jin, Li</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20171218</creationdate><title>Effects of maternal and fetal LEP common variants on maternal glycemic traits in pregnancy</title><author>Lin, Rong ; Ju, Hongfang ; Yuan, Ziyu ; Zhang, Caicai ; Zeng, Liangliang ; Sun, Yuantian ; Su, Zhenyu ; Jin, Li</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-bda544e32d804a9c9bcf989f317aff810a67abe2a6abfd65e74dc6cdcb63517d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>45</topic><topic>45/22</topic><topic>45/77</topic><topic>631/208/205</topic><topic>692/308/2056</topic><topic>692/499</topic><topic>Adipose tissue</topic><topic>Adult</topic><topic>Asian Continental Ancestry Group - genetics</topic><topic>Beta cells</topic><topic>Blood Glucose - analysis</topic><topic>Blood Glucose - metabolism</topic><topic>China</topic><topic>Ethnic Groups - genetics</topic><topic>Fasting</topic><topic>Female</topic><topic>Fetus - metabolism</topic><topic>Fetuses</topic><topic>Gestation</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>Homeostasis</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Insulin</topic><topic>Insulin - analysis</topic><topic>Insulin - blood</topic><topic>Insulin Resistance - genetics</topic><topic>Insulin-Secreting Cells - metabolism</topic><topic>Leptin</topic><topic>Leptin - genetics</topic><topic>Leptin - physiology</topic><topic>Maternal-Fetal Exchange - genetics</topic><topic>Metabolism</topic><topic>multidisciplinary</topic><topic>Phenotype</topic><topic>Placenta</topic><topic>Placenta - metabolism</topic><topic>Pregnancy</topic><topic>Prenatal Care</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Secretion</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, Rong</creatorcontrib><creatorcontrib>Ju, Hongfang</creatorcontrib><creatorcontrib>Yuan, Ziyu</creatorcontrib><creatorcontrib>Zhang, Caicai</creatorcontrib><creatorcontrib>Zeng, Liangliang</creatorcontrib><creatorcontrib>Sun, Yuantian</creatorcontrib><creatorcontrib>Su, Zhenyu</creatorcontrib><creatorcontrib>Jin, Li</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - 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>Lin, Rong</au><au>Ju, Hongfang</au><au>Yuan, Ziyu</au><au>Zhang, Caicai</au><au>Zeng, Liangliang</au><au>Sun, Yuantian</au><au>Su, Zhenyu</au><au>Jin, Li</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of maternal and fetal LEP common variants on maternal glycemic traits in pregnancy</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2017-12-18</date><risdate>2017</risdate><volume>7</volume><issue>1</issue><spage>17710</spage><epage>8</epage><pages>17710-8</pages><artnum>17710</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Previous studies suggest that leptin (LEP) has an important role in glucose metabolism in the nonpregnant state. During pregnancy, circulating maternal concentrations of leptin rise significantly, mainly due to increased secretion of leptin from maternal adipose tissue and placenta. This study aimed to analyze the impact of maternal and fetal common
LEP
variants on glucose homeostasis in the pregnant state. Several glycemic traits, including fasting plasma glucose, fasting plasma insulin (FPI), and plasma glucose 1 hour after a 50-g oral glucose load, were measured in 1,112 unrelated Chinese Han pregnant women at 24–28 weeks gestation. Homeostatic model assessment (HOMA) was used to assess beta cell function (HOMA1-β and HOMA2-β) and insulin resistance (HOMA1-IR and HOMA2-IR).The relationships between glycemic traits and 12
LEP
variants were determined. After applying the Bonferroni correction, we detected that (1) maternal rs10954173 and fetal rs10244329 were associated with maternal FPI although the effect of fetal rs10244329 may be not independent of maternal rs10244329, and (2) maternal rs12537573 was associated with maternal FPI and HOMA2-IR. This study provides genetic evidence that both maternal and fetal
LEP
polymorphisms may affect maternal glucose metabolism in pregnancy.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29255202</pmid><doi>10.1038/s41598-017-18117-z</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 45 45/22 45/77 631/208/205 692/308/2056 692/499 Adipose tissue Adult Asian Continental Ancestry Group - genetics Beta cells Blood Glucose - analysis Blood Glucose - metabolism China Ethnic Groups - genetics Fasting Female Fetus - metabolism Fetuses Gestation Glucose Glucose - metabolism Homeostasis Humanities and Social Sciences Humans Insulin Insulin - analysis Insulin - blood Insulin Resistance - genetics Insulin-Secreting Cells - metabolism Leptin Leptin - genetics Leptin - physiology Maternal-Fetal Exchange - genetics Metabolism multidisciplinary Phenotype Placenta Placenta - metabolism Pregnancy Prenatal Care Science Science (multidisciplinary) Secretion |
title | Effects of maternal and fetal LEP common variants on maternal glycemic traits in pregnancy |
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