Maternal alcohol intake around the time of conception causes glucose intolerance and insulin insensitivity in rat offspring, which is exacerbated by a postnatal high‐fat diet
ABSTRACT Alcohol consumption throughout pregnancy can cause metabolic dysregulation, including glucose intolerance in progeny. This study determined if periconceptional (PC) alcohol (12% v/v in a liquid diet) (PC:EtOH) consumed exclusively around conception results in similar outcomes in Sprague‐Daw...
Gespeichert in:
| Veröffentlicht in: | The FASEB journal 2015-07, Vol.29 (7), p.2690-2701 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2701 |
|---|---|
| container_issue | 7 |
| container_start_page | 2690 |
| container_title | The FASEB journal |
| container_volume | 29 |
| creator | Gårdebjer, Emelie M. Anderson, Stephen T. Pantaleon, Marie Wlodek, Mary E. Moritz, Karen M. |
| description | ABSTRACT
Alcohol consumption throughout pregnancy can cause metabolic dysregulation, including glucose intolerance in progeny. This study determined if periconceptional (PC) alcohol (12% v/v in a liquid diet) (PC:EtOH) consumed exclusively around conception results in similar outcomes in Sprague‐Dawley rats. Control (C) rats were given a liquid diet containing no alcohol but matched to ensure equal caloric intake. PC maternal alcohol intake (from 4 days before conception until day 4 of gestation), resulted in offspring with elevated fasting plasma glucose (~10–25%, P < 0.05), impaired glucose tolerance (P < 0.05), and decreased insulin sensitivity (P < 0.01) at 6 months of age. This was associated with increased hepatic gluconeogenesis and sex‐specific alterations in peripheral protein kinase B (AKT) signaling. These changes were accompanied by increased mRNA expression of DNA methyltransferases (DNMTs) 1, 3a, and 3b (1.5‐ to 1.9‐fold, P < 0.05) in fetal liver in late gestation, suggesting PC:EtOH may cause epigenetic changes that predispose offspring to metabolic dysfunction. Exposure to a postnatal (PN) high‐fat and cholesterol diet (HFD) from 3 months of age caused hyperinsulinemia (~2‐fold increase, P < 0.001) and exacerbated the metabolic dysfunction in male offspring exposed to PC:EtOH but had no additive effects in females. Given many women may drink alcohol while planning a pregnancy, it is crucial to increase public awareness regarding the effects of alcohol consumption around conception on offspring health.—Gårdebjer, E. M., Anderson, S. T., Pantaleon, M., Wlodek, M. E., Moritz, K. M. Maternal alcohol intake around the time of conception causes glucose intolerance and insulin insensitivity in rat offspring, which is exacerbated by a postnatal high‐fat diet. FASEB J. 29, 2690–2701 (2015). www.fasebj.org |
| doi_str_mv | 10.1096/fj.14-268979 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1808642516</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1808642516</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4119-1e8448097c07ec7fa135d2fed1e12161e16b29e92f15c5cc9c23f2afbc8713793</originalsourceid><addsrcrecordid>eNqFkbGOEzEURS0EYrMLHTVySbGz-HlmPHYJK7KAFlEA9cjxPGccHDuMPSzp-AQ-hW_iS3CUQAmNnyyfe_TkS8gTYFfAlHhuN1fQVFxI1al7ZAFtzSohBbtPFkwqXglRyzNyntKGMQYMxENyxtuurlvRLsjPdzrjFLSn2ps4Rk9dyPozUj3FOQw0j0iz2yKNlpoYDO6yi4EaPSdMdO1nExMeMtHjpMs71SXlQpq9C4eJIbnsvrq8Lzc66VxMNu0mF9aX9G50ZqQuUfymDU6rsstAV3uq6S6mHHQue41uPf76_sOW5OAwPyIPrPYJH5_mBfm0fPXx-nV1-_7mzfWL28o0AKoClE0jmeoM69B0VkPdDtziAAgcRDnFiitU3EJrWmOU4bXl2q6M7KDuVH1Bnh29uyl-mTHlfuuSQe91wDinHiSTouEtiP-jQtUg2xpYQS-PqJliShPavvzEVk_7Hlh_qLO3mx6a_lhnwZ-ezPNqi8Nf-E9_BZBH4M553P9T1i8_vOTLt9Cc3L8BB52wLw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1693185310</pqid></control><display><type>article</type><title>Maternal alcohol intake around the time of conception causes glucose intolerance and insulin insensitivity in rat offspring, which is exacerbated by a postnatal high‐fat diet</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><source>Alma/SFX Local Collection</source><creator>Gårdebjer, Emelie M. ; Anderson, Stephen T. ; Pantaleon, Marie ; Wlodek, Mary E. ; Moritz, Karen M.</creator><creatorcontrib>Gårdebjer, Emelie M. ; Anderson, Stephen T. ; Pantaleon, Marie ; Wlodek, Mary E. ; Moritz, Karen M.</creatorcontrib><description>ABSTRACT
Alcohol consumption throughout pregnancy can cause metabolic dysregulation, including glucose intolerance in progeny. This study determined if periconceptional (PC) alcohol (12% v/v in a liquid diet) (PC:EtOH) consumed exclusively around conception results in similar outcomes in Sprague‐Dawley rats. Control (C) rats were given a liquid diet containing no alcohol but matched to ensure equal caloric intake. PC maternal alcohol intake (from 4 days before conception until day 4 of gestation), resulted in offspring with elevated fasting plasma glucose (~10–25%, P < 0.05), impaired glucose tolerance (P < 0.05), and decreased insulin sensitivity (P < 0.01) at 6 months of age. This was associated with increased hepatic gluconeogenesis and sex‐specific alterations in peripheral protein kinase B (AKT) signaling. These changes were accompanied by increased mRNA expression of DNA methyltransferases (DNMTs) 1, 3a, and 3b (1.5‐ to 1.9‐fold, P < 0.05) in fetal liver in late gestation, suggesting PC:EtOH may cause epigenetic changes that predispose offspring to metabolic dysfunction. Exposure to a postnatal (PN) high‐fat and cholesterol diet (HFD) from 3 months of age caused hyperinsulinemia (~2‐fold increase, P < 0.001) and exacerbated the metabolic dysfunction in male offspring exposed to PC:EtOH but had no additive effects in females. Given many women may drink alcohol while planning a pregnancy, it is crucial to increase public awareness regarding the effects of alcohol consumption around conception on offspring health.—Gårdebjer, E. M., Anderson, S. T., Pantaleon, M., Wlodek, M. E., Moritz, K. M. Maternal alcohol intake around the time of conception causes glucose intolerance and insulin insensitivity in rat offspring, which is exacerbated by a postnatal high‐fat diet. FASEB J. 29, 2690–2701 (2015). www.fasebj.org</description><identifier>ISSN: 0892-6638</identifier><identifier>EISSN: 1530-6860</identifier><identifier>DOI: 10.1096/fj.14-268979</identifier><identifier>PMID: 25733565</identifier><language>eng</language><publisher>United States: Federation of American Societies for Experimental Biology</publisher><subject>Alcohol Drinking - adverse effects ; Animals ; Blood Glucose - metabolism ; developmental programming ; diabetes ; Diet, High-Fat - adverse effects ; DNA (Cytosine-5-)-Methyltransferases - genetics ; Female ; Fertilization ; Fetus - metabolism ; gene expression ; Gluconeogenesis ; Glucose Intolerance - etiology ; Glucose Intolerance - genetics ; Glucose Intolerance - metabolism ; Histone Deacetylases - genetics ; Humans ; Insulin Resistance ; Liver - metabolism ; Male ; metabolic pathways ; Models, Animal ; Pregnancy ; Prenatal Exposure Delayed Effects - etiology ; Prenatal Exposure Delayed Effects - genetics ; Prenatal Exposure Delayed Effects - metabolism ; Rats ; Rats, Sprague-Dawley ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Sex Characteristics ; Signal Transduction</subject><ispartof>The FASEB journal, 2015-07, Vol.29 (7), p.2690-2701</ispartof><rights>FASEB</rights><rights>FASEB.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4119-1e8448097c07ec7fa135d2fed1e12161e16b29e92f15c5cc9c23f2afbc8713793</citedby><cites>FETCH-LOGICAL-c4119-1e8448097c07ec7fa135d2fed1e12161e16b29e92f15c5cc9c23f2afbc8713793</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1096%2Ffj.14-268979$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1096%2Ffj.14-268979$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25733565$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gårdebjer, Emelie M.</creatorcontrib><creatorcontrib>Anderson, Stephen T.</creatorcontrib><creatorcontrib>Pantaleon, Marie</creatorcontrib><creatorcontrib>Wlodek, Mary E.</creatorcontrib><creatorcontrib>Moritz, Karen M.</creatorcontrib><title>Maternal alcohol intake around the time of conception causes glucose intolerance and insulin insensitivity in rat offspring, which is exacerbated by a postnatal high‐fat diet</title><title>The FASEB journal</title><addtitle>FASEB J</addtitle><description>ABSTRACT
Alcohol consumption throughout pregnancy can cause metabolic dysregulation, including glucose intolerance in progeny. This study determined if periconceptional (PC) alcohol (12% v/v in a liquid diet) (PC:EtOH) consumed exclusively around conception results in similar outcomes in Sprague‐Dawley rats. Control (C) rats were given a liquid diet containing no alcohol but matched to ensure equal caloric intake. PC maternal alcohol intake (from 4 days before conception until day 4 of gestation), resulted in offspring with elevated fasting plasma glucose (~10–25%, P < 0.05), impaired glucose tolerance (P < 0.05), and decreased insulin sensitivity (P < 0.01) at 6 months of age. This was associated with increased hepatic gluconeogenesis and sex‐specific alterations in peripheral protein kinase B (AKT) signaling. These changes were accompanied by increased mRNA expression of DNA methyltransferases (DNMTs) 1, 3a, and 3b (1.5‐ to 1.9‐fold, P < 0.05) in fetal liver in late gestation, suggesting PC:EtOH may cause epigenetic changes that predispose offspring to metabolic dysfunction. Exposure to a postnatal (PN) high‐fat and cholesterol diet (HFD) from 3 months of age caused hyperinsulinemia (~2‐fold increase, P < 0.001) and exacerbated the metabolic dysfunction in male offspring exposed to PC:EtOH but had no additive effects in females. Given many women may drink alcohol while planning a pregnancy, it is crucial to increase public awareness regarding the effects of alcohol consumption around conception on offspring health.—Gårdebjer, E. M., Anderson, S. T., Pantaleon, M., Wlodek, M. E., Moritz, K. M. Maternal alcohol intake around the time of conception causes glucose intolerance and insulin insensitivity in rat offspring, which is exacerbated by a postnatal high‐fat diet. FASEB J. 29, 2690–2701 (2015). www.fasebj.org</description><subject>Alcohol Drinking - adverse effects</subject><subject>Animals</subject><subject>Blood Glucose - metabolism</subject><subject>developmental programming</subject><subject>diabetes</subject><subject>Diet, High-Fat - adverse effects</subject><subject>DNA (Cytosine-5-)-Methyltransferases - genetics</subject><subject>Female</subject><subject>Fertilization</subject><subject>Fetus - metabolism</subject><subject>gene expression</subject><subject>Gluconeogenesis</subject><subject>Glucose Intolerance - etiology</subject><subject>Glucose Intolerance - genetics</subject><subject>Glucose Intolerance - metabolism</subject><subject>Histone Deacetylases - genetics</subject><subject>Humans</subject><subject>Insulin Resistance</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>metabolic pathways</subject><subject>Models, Animal</subject><subject>Pregnancy</subject><subject>Prenatal Exposure Delayed Effects - etiology</subject><subject>Prenatal Exposure Delayed Effects - genetics</subject><subject>Prenatal Exposure Delayed Effects - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Sex Characteristics</subject><subject>Signal Transduction</subject><issn>0892-6638</issn><issn>1530-6860</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkbGOEzEURS0EYrMLHTVySbGz-HlmPHYJK7KAFlEA9cjxPGccHDuMPSzp-AQ-hW_iS3CUQAmNnyyfe_TkS8gTYFfAlHhuN1fQVFxI1al7ZAFtzSohBbtPFkwqXglRyzNyntKGMQYMxENyxtuurlvRLsjPdzrjFLSn2ps4Rk9dyPozUj3FOQw0j0iz2yKNlpoYDO6yi4EaPSdMdO1nExMeMtHjpMs71SXlQpq9C4eJIbnsvrq8Lzc66VxMNu0mF9aX9G50ZqQuUfymDU6rsstAV3uq6S6mHHQue41uPf76_sOW5OAwPyIPrPYJH5_mBfm0fPXx-nV1-_7mzfWL28o0AKoClE0jmeoM69B0VkPdDtziAAgcRDnFiitU3EJrWmOU4bXl2q6M7KDuVH1Bnh29uyl-mTHlfuuSQe91wDinHiSTouEtiP-jQtUg2xpYQS-PqJliShPavvzEVk_7Hlh_qLO3mx6a_lhnwZ-ezPNqi8Nf-E9_BZBH4M553P9T1i8_vOTLt9Cc3L8BB52wLw</recordid><startdate>201507</startdate><enddate>201507</enddate><creator>Gårdebjer, Emelie M.</creator><creator>Anderson, Stephen T.</creator><creator>Pantaleon, Marie</creator><creator>Wlodek, Mary E.</creator><creator>Moritz, Karen M.</creator><general>Federation of American Societies for Experimental Biology</general><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><scope>7QG</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>201507</creationdate><title>Maternal alcohol intake around the time of conception causes glucose intolerance and insulin insensitivity in rat offspring, which is exacerbated by a postnatal high‐fat diet</title><author>Gårdebjer, Emelie M. ; Anderson, Stephen T. ; Pantaleon, Marie ; Wlodek, Mary E. ; Moritz, Karen M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4119-1e8448097c07ec7fa135d2fed1e12161e16b29e92f15c5cc9c23f2afbc8713793</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Alcohol Drinking - adverse effects</topic><topic>Animals</topic><topic>Blood Glucose - metabolism</topic><topic>developmental programming</topic><topic>diabetes</topic><topic>Diet, High-Fat - adverse effects</topic><topic>DNA (Cytosine-5-)-Methyltransferases - genetics</topic><topic>Female</topic><topic>Fertilization</topic><topic>Fetus - metabolism</topic><topic>gene expression</topic><topic>Gluconeogenesis</topic><topic>Glucose Intolerance - etiology</topic><topic>Glucose Intolerance - genetics</topic><topic>Glucose Intolerance - metabolism</topic><topic>Histone Deacetylases - genetics</topic><topic>Humans</topic><topic>Insulin Resistance</topic><topic>Liver - metabolism</topic><topic>Male</topic><topic>metabolic pathways</topic><topic>Models, Animal</topic><topic>Pregnancy</topic><topic>Prenatal Exposure Delayed Effects - etiology</topic><topic>Prenatal Exposure Delayed Effects - genetics</topic><topic>Prenatal Exposure Delayed Effects - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Sex Characteristics</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gårdebjer, Emelie M.</creatorcontrib><creatorcontrib>Anderson, Stephen T.</creatorcontrib><creatorcontrib>Pantaleon, Marie</creatorcontrib><creatorcontrib>Wlodek, Mary E.</creatorcontrib><creatorcontrib>Moritz, Karen M.</creatorcontrib><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><collection>Animal Behavior Abstracts</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>The FASEB journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gårdebjer, Emelie M.</au><au>Anderson, Stephen T.</au><au>Pantaleon, Marie</au><au>Wlodek, Mary E.</au><au>Moritz, Karen M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Maternal alcohol intake around the time of conception causes glucose intolerance and insulin insensitivity in rat offspring, which is exacerbated by a postnatal high‐fat diet</atitle><jtitle>The FASEB journal</jtitle><addtitle>FASEB J</addtitle><date>2015-07</date><risdate>2015</risdate><volume>29</volume><issue>7</issue><spage>2690</spage><epage>2701</epage><pages>2690-2701</pages><issn>0892-6638</issn><eissn>1530-6860</eissn><abstract>ABSTRACT
Alcohol consumption throughout pregnancy can cause metabolic dysregulation, including glucose intolerance in progeny. This study determined if periconceptional (PC) alcohol (12% v/v in a liquid diet) (PC:EtOH) consumed exclusively around conception results in similar outcomes in Sprague‐Dawley rats. Control (C) rats were given a liquid diet containing no alcohol but matched to ensure equal caloric intake. PC maternal alcohol intake (from 4 days before conception until day 4 of gestation), resulted in offspring with elevated fasting plasma glucose (~10–25%, P < 0.05), impaired glucose tolerance (P < 0.05), and decreased insulin sensitivity (P < 0.01) at 6 months of age. This was associated with increased hepatic gluconeogenesis and sex‐specific alterations in peripheral protein kinase B (AKT) signaling. These changes were accompanied by increased mRNA expression of DNA methyltransferases (DNMTs) 1, 3a, and 3b (1.5‐ to 1.9‐fold, P < 0.05) in fetal liver in late gestation, suggesting PC:EtOH may cause epigenetic changes that predispose offspring to metabolic dysfunction. Exposure to a postnatal (PN) high‐fat and cholesterol diet (HFD) from 3 months of age caused hyperinsulinemia (~2‐fold increase, P < 0.001) and exacerbated the metabolic dysfunction in male offspring exposed to PC:EtOH but had no additive effects in females. Given many women may drink alcohol while planning a pregnancy, it is crucial to increase public awareness regarding the effects of alcohol consumption around conception on offspring health.—Gårdebjer, E. M., Anderson, S. T., Pantaleon, M., Wlodek, M. E., Moritz, K. M. Maternal alcohol intake around the time of conception causes glucose intolerance and insulin insensitivity in rat offspring, which is exacerbated by a postnatal high‐fat diet. FASEB J. 29, 2690–2701 (2015). www.fasebj.org</abstract><cop>United States</cop><pub>Federation of American Societies for Experimental Biology</pub><pmid>25733565</pmid><doi>10.1096/fj.14-268979</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0892-6638 |
| ispartof | The FASEB journal, 2015-07, Vol.29 (7), p.2690-2701 |
| issn | 0892-6638 1530-6860 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1808642516 |
| source | MEDLINE; Access via Wiley Online Library; Alma/SFX Local Collection |
| subjects | Alcohol Drinking - adverse effects Animals Blood Glucose - metabolism developmental programming diabetes Diet, High-Fat - adverse effects DNA (Cytosine-5-)-Methyltransferases - genetics Female Fertilization Fetus - metabolism gene expression Gluconeogenesis Glucose Intolerance - etiology Glucose Intolerance - genetics Glucose Intolerance - metabolism Histone Deacetylases - genetics Humans Insulin Resistance Liver - metabolism Male metabolic pathways Models, Animal Pregnancy Prenatal Exposure Delayed Effects - etiology Prenatal Exposure Delayed Effects - genetics Prenatal Exposure Delayed Effects - metabolism Rats Rats, Sprague-Dawley RNA, Messenger - genetics RNA, Messenger - metabolism Sex Characteristics Signal Transduction |
| title | Maternal alcohol intake around the time of conception causes glucose intolerance and insulin insensitivity in rat offspring, which is exacerbated by a postnatal high‐fat diet |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-03T13%3A44%3A52IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Maternal%20alcohol%20intake%20around%20the%20time%20of%20conception%20causes%20glucose%20intolerance%20and%20insulin%20insensitivity%20in%20rat%20offspring,%20which%20is%20exacerbated%20by%20a%20postnatal%20high%E2%80%90fat%20diet&rft.jtitle=The%20FASEB%20journal&rft.au=G%C3%A5rdebjer,%20Emelie%20M.&rft.date=2015-07&rft.volume=29&rft.issue=7&rft.spage=2690&rft.epage=2701&rft.pages=2690-2701&rft.issn=0892-6638&rft.eissn=1530-6860&rft_id=info:doi/10.1096/fj.14-268979&rft_dat=%3Cproquest_cross%3E1808642516%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1693185310&rft_id=info:pmid/25733565&rfr_iscdi=true |