AHRR Hypomethylation mediates the association between maternal smoking and metabolic profiles in children
Tobacco smoking during pregnancy is associated with metabolic dysfunction in children, but mechanistic insights remain limited. Hypomethylation of cg05575921 in the aryl hydrocarbon receptor repressor (AHRR) gene is associated with in utero tobacco smoke exposure. In this study, we evaluated whether...
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| Veröffentlicht in: | Hepatology communications 2023-10, Vol.7 (10) |
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| creator | Vidal, Adriana C Chandramouli, Shivram A Marchesoni, Joddy Brown, Nia Liu, Yukun Murphy, Susan K Maguire, Rachel Wang, Yaxu Abdelmalek, Manal F Mavis, Alisha M Bashir, Mustafa R Jima, Dereje Skaar, David A Hoyo, Cathrine Moylan, Cynthia A |
| description | Tobacco smoking during pregnancy is associated with metabolic dysfunction in children, but mechanistic insights remain limited. Hypomethylation of cg05575921 in the aryl hydrocarbon receptor repressor (AHRR) gene is associated with in utero tobacco smoke exposure. In this study, we evaluated whether AHRR hypomethylation mediates the association between maternal smoking and metabolic dysfunction in children.
We assessed metabolic dysfunction using liver fat content (LFC), serum, and clinical data in children aged 7-12 years (n=78) followed since birth. Maternal smoking was self-reported at 12 weeks gestation. Methylation was measured by means of pyrosequencing at 3 sequential CpG sites, including cg05575921, at birth and at ages 7-12. Regression models were used to evaluate whether AHRR methylation mediated the association between maternal smoking and child metabolic dysfunction.
Average AHRR methylation at birth was significantly higher among children of nonsmoking mothers compared with children of mothers who smoked (69.8% ± 4.4% vs. 63.5% ± 5.5, p=0.0006). AHRR hypomethylation at birth was associated with higher liver fat content (p=0.01), triglycerides (p=0.01), and alanine aminotransferase levels (p=0.03), and lower HDL cholesterol (p=0.01) in childhood. AHRR hypomethylation significantly mediated associations between maternal smoking and liver fat content (indirect effect=0.213, p=0.018), triglycerides (indirect effect=0.297, p=0.044), and HDL cholesterol (indirect effect = -0.413, p=0.007). AHRR methylation in childhood (n=78) was no longer significantly associated with prenatal smoke exposure or child metabolic parameters (p>0.05).
AHRR hypomethylation significantly mediates the association between prenatal tobacco smoke exposure and features of childhood metabolic dysfunction, despite the lack of persistent hypomethylation of AHRR into childhood. Further studies are needed to replicate these findings and to explore their causal and long-term significance. |
| doi_str_mv | 10.1097/HC9.0000000000000243 |
| format | Article |
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We assessed metabolic dysfunction using liver fat content (LFC), serum, and clinical data in children aged 7-12 years (n=78) followed since birth. Maternal smoking was self-reported at 12 weeks gestation. Methylation was measured by means of pyrosequencing at 3 sequential CpG sites, including cg05575921, at birth and at ages 7-12. Regression models were used to evaluate whether AHRR methylation mediated the association between maternal smoking and child metabolic dysfunction.
Average AHRR methylation at birth was significantly higher among children of nonsmoking mothers compared with children of mothers who smoked (69.8% ± 4.4% vs. 63.5% ± 5.5, p=0.0006). AHRR hypomethylation at birth was associated with higher liver fat content (p=0.01), triglycerides (p=0.01), and alanine aminotransferase levels (p=0.03), and lower HDL cholesterol (p=0.01) in childhood. AHRR hypomethylation significantly mediated associations between maternal smoking and liver fat content (indirect effect=0.213, p=0.018), triglycerides (indirect effect=0.297, p=0.044), and HDL cholesterol (indirect effect = -0.413, p=0.007). AHRR methylation in childhood (n=78) was no longer significantly associated with prenatal smoke exposure or child metabolic parameters (p>0.05).
AHRR hypomethylation significantly mediates the association between prenatal tobacco smoke exposure and features of childhood metabolic dysfunction, despite the lack of persistent hypomethylation of AHRR into childhood. Further studies are needed to replicate these findings and to explore their causal and long-term significance.</description><identifier>ISSN: 2471-254X</identifier><identifier>EISSN: 2471-254X</identifier><identifier>DOI: 10.1097/HC9.0000000000000243</identifier><identifier>PMID: 37755881</identifier><language>eng</language><publisher>United States: Lippincott Williams & Wilkins</publisher><subject>Basic Helix-Loop-Helix Transcription Factors - genetics ; Child ; Cholesterol, HDL ; Female ; Humans ; Infant, Newborn ; Metabolome ; Original ; Pregnancy ; Repressor Proteins - genetics ; Smoking - adverse effects ; Tobacco Smoke Pollution - adverse effects ; Tobacco Smoking</subject><ispartof>Hepatology communications, 2023-10, Vol.7 (10)</ispartof><rights>Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Association for the Study of Liver Diseases.</rights><rights>Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Association for the Study of Liver Diseases. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c358t-b27706e50c1d13d18a51c6b5768121250a9e314235840a33c5562ba87e66483</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/PMC10531191/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10531191/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37755881$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vidal, Adriana C</creatorcontrib><creatorcontrib>Chandramouli, Shivram A</creatorcontrib><creatorcontrib>Marchesoni, Joddy</creatorcontrib><creatorcontrib>Brown, Nia</creatorcontrib><creatorcontrib>Liu, Yukun</creatorcontrib><creatorcontrib>Murphy, Susan K</creatorcontrib><creatorcontrib>Maguire, Rachel</creatorcontrib><creatorcontrib>Wang, Yaxu</creatorcontrib><creatorcontrib>Abdelmalek, Manal F</creatorcontrib><creatorcontrib>Mavis, Alisha M</creatorcontrib><creatorcontrib>Bashir, Mustafa R</creatorcontrib><creatorcontrib>Jima, Dereje</creatorcontrib><creatorcontrib>Skaar, David A</creatorcontrib><creatorcontrib>Hoyo, Cathrine</creatorcontrib><creatorcontrib>Moylan, Cynthia A</creatorcontrib><title>AHRR Hypomethylation mediates the association between maternal smoking and metabolic profiles in children</title><title>Hepatology communications</title><addtitle>Hepatol Commun</addtitle><description>Tobacco smoking during pregnancy is associated with metabolic dysfunction in children, but mechanistic insights remain limited. Hypomethylation of cg05575921 in the aryl hydrocarbon receptor repressor (AHRR) gene is associated with in utero tobacco smoke exposure. In this study, we evaluated whether AHRR hypomethylation mediates the association between maternal smoking and metabolic dysfunction in children.
We assessed metabolic dysfunction using liver fat content (LFC), serum, and clinical data in children aged 7-12 years (n=78) followed since birth. Maternal smoking was self-reported at 12 weeks gestation. Methylation was measured by means of pyrosequencing at 3 sequential CpG sites, including cg05575921, at birth and at ages 7-12. Regression models were used to evaluate whether AHRR methylation mediated the association between maternal smoking and child metabolic dysfunction.
Average AHRR methylation at birth was significantly higher among children of nonsmoking mothers compared with children of mothers who smoked (69.8% ± 4.4% vs. 63.5% ± 5.5, p=0.0006). AHRR hypomethylation at birth was associated with higher liver fat content (p=0.01), triglycerides (p=0.01), and alanine aminotransferase levels (p=0.03), and lower HDL cholesterol (p=0.01) in childhood. AHRR hypomethylation significantly mediated associations between maternal smoking and liver fat content (indirect effect=0.213, p=0.018), triglycerides (indirect effect=0.297, p=0.044), and HDL cholesterol (indirect effect = -0.413, p=0.007). AHRR methylation in childhood (n=78) was no longer significantly associated with prenatal smoke exposure or child metabolic parameters (p>0.05).
AHRR hypomethylation significantly mediates the association between prenatal tobacco smoke exposure and features of childhood metabolic dysfunction, despite the lack of persistent hypomethylation of AHRR into childhood. Further studies are needed to replicate these findings and to explore their causal and long-term significance.</description><subject>Basic Helix-Loop-Helix Transcription Factors - genetics</subject><subject>Child</subject><subject>Cholesterol, HDL</subject><subject>Female</subject><subject>Humans</subject><subject>Infant, Newborn</subject><subject>Metabolome</subject><subject>Original</subject><subject>Pregnancy</subject><subject>Repressor Proteins - genetics</subject><subject>Smoking - adverse effects</subject><subject>Tobacco Smoke Pollution - adverse effects</subject><subject>Tobacco Smoking</subject><issn>2471-254X</issn><issn>2471-254X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1OAyEUhYnRqKm-gTGzdFPlwjA_K2MatSYmJurCHWGYW4syUIFq-vZiqqbKBpLznXOBQ8gR0FOgbX02nbSndHOxkm-RfVbWMGaifNreOO-RwxhfMgMtA2jpLtnjdS1E08A-MRfT-_tiulr4AdN8ZVUy3hUD9kYljEWaY6Fi9NqshQ7TB2IGshqcskUc_Ktxz4VyfXYl1XlrdLEIfmZs9htX6LmxfUB3QHZmykY8_N5H5OHq8nEyHd_eXd9MLm7HmosmjTtW17RCQTX0wHtolABddaKuGmDABFUtcihZhkuqONdCVKxTTY1VVTZ8RM7XqYtll1-h0aWgrFwEM6iwkl4Z-VdxZi6f_bsEKnj-HcgJJ98Jwb8tMSY5mKjRWuXQL6NkTdVWwEsmMlquUR18jAFnv3OAyq-eZO5J_u8p24437_hr-mmFfwJOjI7Q</recordid><startdate>20231001</startdate><enddate>20231001</enddate><creator>Vidal, Adriana C</creator><creator>Chandramouli, Shivram A</creator><creator>Marchesoni, Joddy</creator><creator>Brown, Nia</creator><creator>Liu, Yukun</creator><creator>Murphy, Susan K</creator><creator>Maguire, Rachel</creator><creator>Wang, Yaxu</creator><creator>Abdelmalek, Manal F</creator><creator>Mavis, Alisha M</creator><creator>Bashir, Mustafa R</creator><creator>Jima, Dereje</creator><creator>Skaar, David A</creator><creator>Hoyo, Cathrine</creator><creator>Moylan, Cynthia A</creator><general>Lippincott Williams & Wilkins</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>5PM</scope></search><sort><creationdate>20231001</creationdate><title>AHRR Hypomethylation mediates the association between maternal smoking and metabolic profiles in children</title><author>Vidal, Adriana C ; Chandramouli, Shivram A ; Marchesoni, Joddy ; Brown, Nia ; Liu, Yukun ; Murphy, Susan K ; Maguire, Rachel ; Wang, Yaxu ; Abdelmalek, Manal F ; Mavis, Alisha M ; Bashir, Mustafa R ; Jima, Dereje ; Skaar, David A ; Hoyo, Cathrine ; Moylan, Cynthia A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c358t-b27706e50c1d13d18a51c6b5768121250a9e314235840a33c5562ba87e66483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Basic Helix-Loop-Helix Transcription Factors - genetics</topic><topic>Child</topic><topic>Cholesterol, HDL</topic><topic>Female</topic><topic>Humans</topic><topic>Infant, Newborn</topic><topic>Metabolome</topic><topic>Original</topic><topic>Pregnancy</topic><topic>Repressor Proteins - genetics</topic><topic>Smoking - adverse effects</topic><topic>Tobacco Smoke Pollution - adverse effects</topic><topic>Tobacco Smoking</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vidal, Adriana C</creatorcontrib><creatorcontrib>Chandramouli, Shivram A</creatorcontrib><creatorcontrib>Marchesoni, Joddy</creatorcontrib><creatorcontrib>Brown, Nia</creatorcontrib><creatorcontrib>Liu, Yukun</creatorcontrib><creatorcontrib>Murphy, Susan K</creatorcontrib><creatorcontrib>Maguire, Rachel</creatorcontrib><creatorcontrib>Wang, Yaxu</creatorcontrib><creatorcontrib>Abdelmalek, Manal F</creatorcontrib><creatorcontrib>Mavis, Alisha M</creatorcontrib><creatorcontrib>Bashir, Mustafa R</creatorcontrib><creatorcontrib>Jima, Dereje</creatorcontrib><creatorcontrib>Skaar, David A</creatorcontrib><creatorcontrib>Hoyo, Cathrine</creatorcontrib><creatorcontrib>Moylan, Cynthia A</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>PubMed Central (Full Participant titles)</collection><jtitle>Hepatology communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vidal, Adriana C</au><au>Chandramouli, Shivram A</au><au>Marchesoni, Joddy</au><au>Brown, Nia</au><au>Liu, Yukun</au><au>Murphy, Susan K</au><au>Maguire, Rachel</au><au>Wang, Yaxu</au><au>Abdelmalek, Manal F</au><au>Mavis, Alisha M</au><au>Bashir, Mustafa R</au><au>Jima, Dereje</au><au>Skaar, David A</au><au>Hoyo, Cathrine</au><au>Moylan, Cynthia A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>AHRR Hypomethylation mediates the association between maternal smoking and metabolic profiles in children</atitle><jtitle>Hepatology communications</jtitle><addtitle>Hepatol Commun</addtitle><date>2023-10-01</date><risdate>2023</risdate><volume>7</volume><issue>10</issue><issn>2471-254X</issn><eissn>2471-254X</eissn><abstract>Tobacco smoking during pregnancy is associated with metabolic dysfunction in children, but mechanistic insights remain limited. Hypomethylation of cg05575921 in the aryl hydrocarbon receptor repressor (AHRR) gene is associated with in utero tobacco smoke exposure. In this study, we evaluated whether AHRR hypomethylation mediates the association between maternal smoking and metabolic dysfunction in children.
We assessed metabolic dysfunction using liver fat content (LFC), serum, and clinical data in children aged 7-12 years (n=78) followed since birth. Maternal smoking was self-reported at 12 weeks gestation. Methylation was measured by means of pyrosequencing at 3 sequential CpG sites, including cg05575921, at birth and at ages 7-12. Regression models were used to evaluate whether AHRR methylation mediated the association between maternal smoking and child metabolic dysfunction.
Average AHRR methylation at birth was significantly higher among children of nonsmoking mothers compared with children of mothers who smoked (69.8% ± 4.4% vs. 63.5% ± 5.5, p=0.0006). AHRR hypomethylation at birth was associated with higher liver fat content (p=0.01), triglycerides (p=0.01), and alanine aminotransferase levels (p=0.03), and lower HDL cholesterol (p=0.01) in childhood. AHRR hypomethylation significantly mediated associations between maternal smoking and liver fat content (indirect effect=0.213, p=0.018), triglycerides (indirect effect=0.297, p=0.044), and HDL cholesterol (indirect effect = -0.413, p=0.007). AHRR methylation in childhood (n=78) was no longer significantly associated with prenatal smoke exposure or child metabolic parameters (p>0.05).
AHRR hypomethylation significantly mediates the association between prenatal tobacco smoke exposure and features of childhood metabolic dysfunction, despite the lack of persistent hypomethylation of AHRR into childhood. Further studies are needed to replicate these findings and to explore their causal and long-term significance.</abstract><cop>United States</cop><pub>Lippincott Williams & Wilkins</pub><pmid>37755881</pmid><doi>10.1097/HC9.0000000000000243</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Basic Helix-Loop-Helix Transcription Factors - genetics Child Cholesterol, HDL Female Humans Infant, Newborn Metabolome Original Pregnancy Repressor Proteins - genetics Smoking - adverse effects Tobacco Smoke Pollution - adverse effects Tobacco Smoking |
| title | AHRR Hypomethylation mediates the association between maternal smoking and metabolic profiles in children |
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