Maternal Obesity, Maternal Overnutrition and Fetal Programming: Effects of Epigenetic Mechanisms on the Development of Metabolic Disorders
Background: Maternal obesity and maternal overnutrition, can lead to epigenetic alterations during pregnancy and these alterations can influence fetal and neonatal phenotype which increase the risk of metabolic disorders in later stages of life. Objective: The effects of maternal obesity on fetal pr...
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Published in | Current genomics Vol. 20; no. 6; pp. 419 - 427 |
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Main Authors | , |
Format | Journal Article |
Language | English |
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United Arab Emirates
Bentham Science Publishers Ltd
01.09.2019
Benham Science Publishers Bentham Science Publishers |
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Abstract | Background: Maternal obesity and maternal overnutrition, can lead to epigenetic alterations during pregnancy and these alterations can influence fetal and neonatal phenotype which increase the risk of metabolic disorders in later stages of life.
Objective: The effects of maternal obesity on fetal programming and potential mechanisms of maternal epigenetic regulation of gene expression which have persistent effects on fetal health and development were investigated.
Methods: Review of the literature was carried out in order to discuss the effects of maternal obesity and epigenetic mechanisms in fetal programming of metabolic disorders. All abstracts and full-text articles were examined and the most relevant articles were included in this review.
Results: Maternal obesity and maternal overnutrition during fetal period has important overall effects on long-term health. Maternal metabolic alterations during early stages of fetal development can lead to permanent changes in organ structures, cell numbers and metabolism. Epigenetic modifications (DNA methylation, histone modifications, microRNAs) play an important role in disease susceptibility in the later stages of human life. Maternal nutrition alter expression of hypothalamic genes which can increase fetal and neonatal energy intake. Epigenetic modifications may affect the increasing rate of obesity and other metabolic disorders worldwide since the impact of these changes can be passed through generations.
Conclusion: Weight management before and during pregnancy, together with healthy nutritional intakes may improve the maternal metabolic environment, which can reduce the risks of fetal programming of metabolic diseases. Further evidence from long-term follow-up studies are needed in order to determine the role of maternal obesity on epigenetic mechanisms. |
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AbstractList | Background: Maternal obesity and maternal overnutrition, can lead to epigenetic alterations during pregnancy and these alterations can influence fetal and neonatal phenotype which increase the risk of metabolic disorders in later stages of life.
Objective: The effects of maternal obesity on fetal programming and potential mechanisms of maternal epigenetic regulation of gene expression which have persistent effects on fetal health and development were investigated.
Methods: Review of the literature was carried out in order to discuss the effects of maternal obesity and epigenetic mechanisms in fetal programming of metabolic disorders. All abstracts and full-text articles were examined and the most relevant articles were included in this review.
Results: Maternal obesity and maternal overnutrition during fetal period has important overall effects on long-term health. Maternal metabolic alterations during early stages of fetal development can lead to permanent changes in organ structures, cell numbers and metabolism. Epigenetic modifications (DNA methylation, histone modifications, microRNAs) play an important role in disease susceptibility in the later stages of human life. Maternal nutrition alter expression of hypothalamic genes which can increase fetal and neonatal energy intake. Epigenetic modifications may affect the increasing rate of obesity and other metabolic disorders worldwide since the impact of these changes can be passed through generations.
Conclusion: Weight management before and during pregnancy, together with healthy nutritional intakes may improve the maternal metabolic environment, which can reduce the risks of fetal programming of metabolic diseases. Further evidence from long-term follow-up studies are needed in order to determine the role of maternal obesity on epigenetic mechanisms. Maternal obesity and maternal overnutrition, can lead to epigenetic alterations during pregnancy and these alterations can influence fetal and neonatal phenotype which increase the risk of metabolic disorders in later stages of life.BACKGROUNDMaternal obesity and maternal overnutrition, can lead to epigenetic alterations during pregnancy and these alterations can influence fetal and neonatal phenotype which increase the risk of metabolic disorders in later stages of life.The effects of maternal obesity on fetal programming and potential mechanisms of maternal epigenetic regulation of gene expression which have persistent effects on fetal health and development were investigated.OBJECTIVEThe effects of maternal obesity on fetal programming and potential mechanisms of maternal epigenetic regulation of gene expression which have persistent effects on fetal health and development were investigated.Review of the literature was carried out in order to discuss the effects of maternal obesity and epigenetic mechanisms in fetal programming of metabolic disorders. All abstracts and full-text articles were examined and the most relevant articles were included in this review.METHODSReview of the literature was carried out in order to discuss the effects of maternal obesity and epigenetic mechanisms in fetal programming of metabolic disorders. All abstracts and full-text articles were examined and the most relevant articles were included in this review.Maternal obesity and maternal overnutrition during fetal period has important overall effects on long-term health. Maternal metabolic alterations during early stages of fetal development can lead to permanent changes in organ structures, cell numbers and metabolism. Epigenetic modifications (DNA methylation, histone modifications, microRNAs) play an important role in disease susceptibility in the later stages of human life. Maternal nutrition alter expression of hypothalamic genes which can increase fetal and neonatal energy intake. Epigenetic modifications may affect the increasing rate of obesity and other metabolic disorders worldwide since the impact of these changes can be passed through generations.RESULTSMaternal obesity and maternal overnutrition during fetal period has important overall effects on long-term health. Maternal metabolic alterations during early stages of fetal development can lead to permanent changes in organ structures, cell numbers and metabolism. Epigenetic modifications (DNA methylation, histone modifications, microRNAs) play an important role in disease susceptibility in the later stages of human life. Maternal nutrition alter expression of hypothalamic genes which can increase fetal and neonatal energy intake. Epigenetic modifications may affect the increasing rate of obesity and other metabolic disorders worldwide since the impact of these changes can be passed through generations.Weight management before and during pregnancy, together with healthy nutritional intakes may improve the maternal metabolic environment, which can reduce the risks of fetal programming of metabolic diseases. Further evidence from long-term follow-up studies are needed in order to determine the role of maternal obesity on epigenetic mechanisms.CONCLUSIONWeight management before and during pregnancy, together with healthy nutritional intakes may improve the maternal metabolic environment, which can reduce the risks of fetal programming of metabolic diseases. Further evidence from long-term follow-up studies are needed in order to determine the role of maternal obesity on epigenetic mechanisms. Maternal obesity and maternal overnutrition, can lead to epigenetic alterations during pregnancy and these alterations can influence fetal and neonatal phenotype which increase the risk of metabolic disorders in later stages of life. The effects of maternal obesity on fetal programming and potential mechanisms of maternal epigenetic regulation of gene expression which have persistent effects on fetal health and development were investigated. Review of the literature was carried out in order to discuss the effects of maternal obesity and epigenetic mechanisms in fetal programming of metabolic disorders. All abstracts and full-text articles were examined and the most relevant articles were included in this review. Maternal obesity and maternal overnutrition during fetal period has important overall effects on long-term health. Maternal metabolic alterations during early stages of fetal development can lead to permanent changes in organ structures, cell numbers and metabolism. Epigenetic modifications (DNA methylation, histone modifications, microRNAs) play an important role in disease susceptibility in the later stages of human life. Maternal nutrition alter expression of hypothalamic genes which can increase fetal and neonatal energy intake. Epigenetic modifications may affect the increasing rate of obesity and other metabolic disorders worldwide since the impact of these changes can be passed through generations. Weight management before and during pregnancy, together with healthy nutritional intakes may improve the maternal metabolic environment, which can reduce the risks of fetal programming of metabolic diseases. Further evidence from long-term follow-up studies are needed in order to determine the role of maternal obesity on epigenetic mechanisms. Background: Maternal obesity and maternal overnutrition, can lead to epigenetic alterations during pregnancy and these alterations can influence fetal and neonatal phenotype which increase the risk of metabolic disorders in later stages of life. Objective: The effects of maternal obesity on fetal programming and potential mechanisms of maternal epigenetic regulation of gene expression which have persistent effects on fetal health and development were investigated. Methods: Review of the literature was carried out in order to discuss the effects of maternal obesity and epigenetic mechanisms in fetal programming of metabolic disorders. All abstracts and full-text articles were examined and the most relevant articles were included in this review. Results: Maternal obesity and maternal overnutrition during fetal period has important overall effects on long-term health. Maternal metabolic alterations during early stages of fetal development can lead to permanent changes in organ structures, cell numbers and metabolism. Epigenetic modifications (DNA methylation, histone modifications, microRNAs) play an important role in disease susceptibility in the later stages of human life. Maternal nutrition alter expression of hypothalamic genes which can increase fetal and neonatal energy intake. Epigenetic modifications may affect the increasing rate of obesity and other metabolic disorders worldwide since the impact of these changes can be passed through generations. Conclusion: Weight management before and during pregnancy, together with healthy nutritional intakes may improve the maternal metabolic environment, which can reduce the risks of fetal programming of metabolic diseases. Further evidence from long-term follow-up studies are needed in order to determine the role of maternal obesity on epigenetic mechanisms. |
Author | Seray Kabaran Ezgi Şanlı |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32476999$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1111/j.1651-2227.2004.tb00236.x 10.1677/JME-08-0025 10.1016/j.semcdb.2015.06.006 10.1203/pdr.0b013e31804575f7 10.1111/j.1651-2227.1997.tb18351.x 10.1016/j.nut.2003.09.011 10.1210/en.2008-0582 10.3390/ijms14035519 10.1210/en.2016-1003 10.1113/jphysiol.2009.176156 10.1152/physrev.00053.2003 10.1152/physiolgenomics.00042.2004 10.1155/2018/8061389 10.1002/oby.20088 10.1186/s13148-016-0188-3 10.1016/S0140-6736(97)07244-9 10.1159/000115355 10.1016/S0140-6736(14)60460-8 10.1016/j.ejogrb.2013.02.003 10.2337/db10-0979 10.4172/2155-9600.1000733 10.1093/bmb/60.1.5 10.1016/j.beem.2012.03.008 10.1007/s00404-013-3053-z 10.2174/187153011796429835 10.3389/fgene.2011.00027 10.1093/aje/kwk030 10.1242/jeb.110320 10.1016/j.mehy.2005.08.020 10.1210/jc.2009-2623 10.1210/en.2017-00334 10.1007/s00125-014-3466-7 10.1111/j.1749-6632.2010.05798.x 10.1371/journal.pone.0061627 10.1097/MED.0000000000000305 10.14310/horm.2002.1590 10.1038/ijo.2015.178 10.3945/ajcn.110.000927 10.1096/fj.12-212878 10.1001/jama.2017.3635 10.1016/j.siny.2009.09.001 10.1016/j.cell.2007.02.005 10.1016/j.neulet.2017.09.042 10.3390/nu7042748 10.1016/j.jnutbio.2017.10.004 10.1371/journal.pone.0084209 10.1016/j.ceb.2004.02.006 10.1016/j.orcp.2016.10.287 10.1126/science.1111444 10.1210/en.2012-2255 10.1016/j.beem.2007.07.009 10.3945/ajcn.2009.28623 10.1016/j.earlhumdev.2006.07.001 10.1152/ajpregu.00316.2007 10.1371/journal.pone.0018950 10.1016/j.rigapp.2006.03.002 10.1006/jtbi.2003.3183 10.1159/000456668 10.1038/s41366-018-0094-1 10.1210/en.2006-1115 10.1021/bi100213t 10.2217/epi.12.3 10.1016/S0140-6736(86)91340-1 10.1172/JCI32661 10.1038/ijo.2008.240 10.1016/j.jnutbio.2013.09.016 10.1186/1471-2164-10-478 10.3945/jn.109.112433 10.1002/jcb.10286 10.1017/S0007114514000579 10.1210/en.2010-0505 10.1016/j.physbeh.2012.04.014 10.1016/j.bbrc.2019.04.154 10.1371/journal.pmed.1002744 10.7762/cnr.2014.3.1.1 10.1016/j.mce.2016.07.002 10.3390/nu7115467 10.1111/ijpo.12247 10.1016/j.bbadis.2013.07.006 10.1101/cshperspect.a026591 10.1016/j.yfrne.2015.09.001 10.1038/ijo.2015.13 10.1136/bmj.j1 10.1096/fj.05-5241fje 10.1152/ajpregu.00310.2010 10.1016/j.molmet.2017.05.010 |
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Keywords | maternal overnutrition Maternal obesity fetal programming maternal nutrition epigenetic mechanisms fetal metabolic disorders |
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References | Armitage J.A. (ref=27) 2008; 36 Muhlhausler B.S. (ref=38) 2006; 20 Gabory A. (ref=75) 2011; 94 Valsamakis G. (ref=3) 2015; 14 Elshenawy S. (ref=11) 2016; 435 Gaillard R. (ref=2) 2013; 21 Plagemann A. (ref=64) 2009; 587 Smith N.H. (ref=28) 2006; 6 Cheng X. (ref=71) 2010; 49 Fernandez-Twinn D.S. (ref=17) 2015; 43 Williams L. (ref=41) 2014; 1842 Freeman D.J. (ref=53) 2010; 15 Vucetic Z. (ref=60) 2010; 151 Goldstein R.F. (ref=32) 2017; 317 Chen H. (ref=63) 2008; 149 Wells J.C. (ref=26) 2003; 221 MacLennan N.K. (ref=57) 2004; 18 Sasson I.E. (ref=66) 2015; 58 Kitsiou-Tzeli S. (ref=9) 2017; 24 Unal R. (ref=70) 2010; 95 Padmanabhan V. (ref=15) 2016; 157 Lee H.S. (ref=88) 2015; 7 Hales C.N. (ref=25) 2001; 60 Nugent B.M. (ref=43) 2015; 39 McMillen I.C. (ref=55) 2005; 85 Aagaard-Tillery K.M. (ref=83) 2008; 41 Lawlor D.A. (ref=40) 2007; 165 Butler J.S. (ref=76) 2012; 4 Waterland R.A. (ref=7) 2004; 20 Borengasser S.J. (ref=82) 2014; 9 Ravelli A.C. (ref=24) 1998; 351 Brion M.J. (ref=39) 2010; 91 Upadhyay A. (ref=44) 2019; 514 Suter M.A. (ref=81) 2012; 26 Barker D.J. (ref=21) 1997; 422 Fu G. (ref=42) 2013; 14 Heerwagen M.J. (ref=45) 2010; 299 Muhlhausler B.S. (ref=36) 2011; 11 Shankar K. (ref=68) 2008; 294 Aagaard-Tillery K.M. (ref=80) 2008; 41 Godfrey K.M. (ref=61) 2011; 60 Strakovsky R.S. (ref=79) 2014; 25 Alfaradhi M.Z. (ref=49) 2011; 2 Desai M. (ref=10) 2015; 39 Luo Z.C. (ref=29) 2006; 66 Bouret S.G. (ref=4) 2010; 140 Tarrade A. (ref=37) 2015; 218 Tarrade A. (ref=47) 2015; 218 Catalano P.M. (ref=30) 2017; 356 Ng M. (ref=1) 2014; 384 Fernandez-Twinn D.S. (ref=18) 2010; 1212 Lecoutre S. (ref=67) 2017; 6 Neri C. (ref=86) 2015; 6 Plagemann A. (ref=5) 2012; 26 Nicholas L.M. (ref=12) 2016; 40 Barker D.J. (ref=20) 1986; 1 Kouzarides T. (ref=72) 2007; 128 Borengasser S.J. (ref=59) 2013; 154 Montalvo-Martínez L. (ref=13) 2018; 2018 Panchenko P.E. (ref=58) 2016; 8 Gonçalves L.K. (ref=78) 2017; 661 Funato H. (ref=77) 2011; 6 Zhang J. (ref=90) 2009; 10 McCurdy C.E. (ref=46) 2009; 119 Jang H. (ref=50) 2014; 3 Sen S. (ref=54) 2012; 107 Nakahara K. (ref=87) 2004; 16 Cheng Z. (ref=52) 2018; 54 Méndez-Mancilla A. (ref=92) 2018; 13 Maffeis C. (ref=14) 2017; 10 Stephenson S. (ref=23) 2018; 8 Seki Y. (ref=69) 2017; 158 Dolinoy D.C. (ref=73) 2007; 61 Benatti R.O. (ref=89) 2014; 111 Alfaradhi M.Z. (ref=16) 2011; 2 Gluckman P.D. (ref=65) 2008; 32 Vucetic Z. (ref=84) 2010; 151 Yu Z. (ref=33) 2013; 8 Tie H.T. (ref=34) 2014; 289 Voerman E. (ref=35) 2019; 16 Gicquel C. (ref=6) 2008; 22 Gali Ramamoorthy T. (ref=62) 2018; 42 Roseboom T. (ref=19) 2006; 82 Geiman T.M. (ref=74) 2002; 87 Enquobahrie D.A. (ref=91) 2017; 11 Muhlhausler B.S. (ref=56) 2007; 148 Zamore P.D. (ref=85) 2005; 309 Nicholas L.M. (ref=8) 2016; 40 McDowell M. (ref=31) 2018 Chango A. (ref=51) 2015; 7 Murabayashi N. (ref=48) 2013; 169 Barker D.J. (ref=22) 2004; 93 |
References_xml | – volume: 93 start-page: 26 year: 2004 ident: ref=22 publication-title: Acta Paediatr Suppl doi: 10.1111/j.1651-2227.2004.tb00236.x – volume: 41 start-page: 91 year: 2008 ident: ref=80 publication-title: J Mol Endocrinol doi: 10.1677/JME-08-0025 – volume: 43 start-page: 85 year: 2015 ident: ref=17 publication-title: Semin Cell Dev Biol doi: 10.1016/j.semcdb.2015.06.006 – volume: 61 start-page: 30R year: 2007 ident: ref=73 publication-title: Pediatr Res doi: 10.1203/pdr.0b013e31804575f7 – volume: 422 start-page: 78 year: 1997 ident: ref=21 publication-title: Acta Paediatr Suppl doi: 10.1111/j.1651-2227.1997.tb18351.x – volume: 20 start-page: 63 year: 2004 ident: ref=7 publication-title: Nutrition doi: 10.1016/j.nut.2003.09.011 – volume: 149 start-page: 5348 year: 2008 ident: ref=63 publication-title: Endocrinology doi: 10.1210/en.2008-0582 – volume: 41 start-page: 91 year: 2008 ident: ref=83 publication-title: J Mol Endocrinol doi: 10.1677/JME-08-0025 – volume: 14 start-page: 5519 year: 2013 ident: ref=42 publication-title: Int J Mol Sci doi: 10.3390/ijms14035519 – volume: 157 start-page: 1328 year: 2016 ident: ref=15 publication-title: Endocrinology doi: 10.1210/en.2016-1003 – volume: 587 start-page: 4963 year: 2009 ident: ref=64 publication-title: J Physiol doi: 10.1113/jphysiol.2009.176156 – volume: 85 start-page: 571 year: 2005 ident: ref=55 publication-title: Physiol Rev doi: 10.1152/physrev.00053.2003 – volume: 18 start-page: 43 year: 2004 ident: ref=57 publication-title: Physiol Genomics doi: 10.1152/physiolgenomics.00042.2004 – volume: 2018 year: 2018 ident: ref=13 publication-title: BioMed Res Int doi: 10.1155/2018/8061389 – volume: 21 start-page: 1046 year: 2013 ident: ref=2 publication-title: Obesity (Silver Spring) doi: 10.1002/oby.20088 – volume: 8 start-page: 22 year: 2016 ident: ref=58 publication-title: Clin Epigenetics doi: 10.1186/s13148-016-0188-3 – volume: 351 start-page: 173 year: 1998 ident: ref=24 publication-title: Lancet doi: 10.1016/S0140-6736(97)07244-9 – volume: 36 start-page: 73 year: 2008 ident: ref=27 publication-title: Front Horm Res doi: 10.1159/000115355 – volume: 384 start-page: 766 year: 2014 ident: ref=1 publication-title: Lancet doi: 10.1016/S0140-6736(14)60460-8 – volume: 169 start-page: 39 year: 2013 ident: ref=48 publication-title: Eur J Obstet Gynecol Reprod Biol doi: 10.1016/j.ejogrb.2013.02.003 – volume: 60 start-page: 1528 year: 2011 ident: ref=61 publication-title: Diabetes doi: 10.2337/db10-0979 – volume: 8 start-page: 1 year: 2018 ident: ref=23 publication-title: J Nutr Food Sci doi: 10.4172/2155-9600.1000733 – volume: 60 start-page: 5 year: 2001 ident: ref=25 publication-title: Br Med Bull doi: 10.1093/bmb/60.1.5 – volume: 26 start-page: 641 year: 2012 ident: ref=5 publication-title: Best Pract Res Clin Endocrinol Metab doi: 10.1016/j.beem.2012.03.008 – volume: 289 start-page: 247 year: 2014 ident: ref=34 publication-title: Arch Gynecol Obstet doi: 10.1007/s00404-013-3053-z – volume: 11 start-page: 189 year: 2011 ident: ref=36 publication-title: Endocr Metab Immune Disord Drug Targets doi: 10.2174/187153011796429835 – volume: 2 start-page: 27 year: 2011 ident: ref=49 publication-title: Front Genet doi: 10.3389/fgene.2011.00027 – volume: 165 start-page: 418 year: 2007 ident: ref=40 publication-title: Am J Epidemiol doi: 10.1093/aje/kwk030 – volume: 218 start-page: 50 year: 2015 ident: ref=37 publication-title: J Exp Biol doi: 10.1242/jeb.110320 – volume: 66 start-page: 38 year: 2006 ident: ref=29 publication-title: Med Hypotheses doi: 10.1016/j.mehy.2005.08.020 – volume: 95 start-page: 2993 year: 2010 ident: ref=70 publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2009-2623 – volume: 158 start-page: 2860 year: 2017 ident: ref=69 publication-title: Endocrinology doi: 10.1210/en.2017-00334 – volume: 58 start-page: 615 year: 2015 ident: ref=66 publication-title: Diabetologia doi: 10.1007/s00125-014-3466-7 – volume: 1212 start-page: 78 year: 2010 ident: ref=18 publication-title: Ann N Y Acad Sci doi: 10.1111/j.1749-6632.2010.05798.x – volume: 8 year: 2013 ident: ref=33 publication-title: PLoS One doi: 10.1371/journal.pone.0061627 – start-page: 1 year: 2018 ident: ref=31 publication-title: J Midwifery Womens Health – volume: 218 start-page: 50 year: 2015 ident: ref=47 publication-title: J Exp Biol doi: 10.1242/jeb.110320 – volume: 24 start-page: 43 year: 2017 ident: ref=9 publication-title: Curr Opin Endocrinol Diabetes Obes doi: 10.1097/MED.0000000000000305 – volume: 14 start-page: 345 year: 2015 ident: ref=3 publication-title: Hormones (Athens) doi: 10.14310/horm.2002.1590 – volume: 40 start-page: 229 year: 2016 ident: ref=12 publication-title: Int J Obes doi: 10.1038/ijo.2015.178 – volume: 94 start-page: 1943S year: 2011 ident: ref=75 publication-title: Am J Clin Nutr doi: 10.3945/ajcn.110.000927 – volume: 26 start-page: 5106 year: 2012 ident: ref=81 publication-title: FASEB J doi: 10.1096/fj.12-212878 – volume: 40 start-page: 229 year: 2016 ident: ref=8 publication-title: Int J Obes doi: 10.1038/ijo.2015.178 – volume: 317 start-page: 2207 year: 2017 ident: ref=32 publication-title: JAMA doi: 10.1001/jama.2017.3635 – volume: 15 start-page: 113 year: 2010 ident: ref=53 publication-title: Semin Fetal Neonatal Med doi: 10.1016/j.siny.2009.09.001 – volume: 128 start-page: 693 year: 2007 ident: ref=72 publication-title: Cell doi: 10.1016/j.cell.2007.02.005 – volume: 661 start-page: 29 year: 2017 ident: ref=78 publication-title: Neurosci Lett doi: 10.1016/j.neulet.2017.09.042 – volume: 7 start-page: 2748 year: 2015 ident: ref=51 publication-title: Nutrients doi: 10.3390/nu7042748 – volume: 54 start-page: 1 year: 2018 ident: ref=52 publication-title: J Nutr Biochem doi: 10.1016/j.jnutbio.2017.10.004 – volume: 9 year: 2014 ident: ref=82 publication-title: PLoS One doi: 10.1371/journal.pone.0084209 – volume: 16 start-page: 127 year: 2004 ident: ref=87 publication-title: Curr Opin Cell Biol doi: 10.1016/j.ceb.2004.02.006 – volume: 11 start-page: 464 year: 2017 ident: ref=91 publication-title: Obes Res Clin Pract doi: 10.1016/j.orcp.2016.10.287 – volume: 309 start-page: 1519 year: 2005 ident: ref=85 publication-title: Science doi: 10.1126/science.1111444 – volume: 154 start-page: 4113 year: 2013 ident: ref=59 publication-title: Endocrinology doi: 10.1210/en.2012-2255 – volume: 22 start-page: 1 year: 2008 ident: ref=6 publication-title: Best Pract Res Clin Endocrinol Metab doi: 10.1016/j.beem.2007.07.009 – volume: 91 start-page: 748 year: 2010 ident: ref=39 publication-title: Am J Clin Nutr doi: 10.3945/ajcn.2009.28623 – volume: 82 start-page: 485 year: 2006 ident: ref=19 publication-title: Early Hum Dev doi: 10.1016/j.earlhumdev.2006.07.001 – volume: 294 start-page: R528 year: 2008 ident: ref=68 publication-title: Am J Physiol Regul Integr Comp Physiol doi: 10.1152/ajpregu.00316.2007 – volume: 6 year: 2011 ident: ref=77 publication-title: PLoS One doi: 10.1371/journal.pone.0018950 – volume: 6 start-page: 211 year: 2006 ident: ref=28 publication-title: Rev Gynaecol Perinatal Practice doi: 10.1016/j.rigapp.2006.03.002 – volume: 221 start-page: 143 year: 2003 ident: ref=26 publication-title: J Theor Biol doi: 10.1006/jtbi.2003.3183 – volume: 10 start-page: 112 year: 2017 ident: ref=14 publication-title: Obes Facts doi: 10.1159/000456668 – volume: 42 start-page: 1431 year: 2018 ident: ref=62 publication-title: Int J Obes doi: 10.1038/s41366-018-0094-1 – volume: 148 start-page: 878 year: 2007 ident: ref=56 publication-title: Endocrinology doi: 10.1210/en.2006-1115 – volume: 49 start-page: 2999 year: 2010 ident: ref=71 publication-title: Biochemistry doi: 10.1021/bi100213t – volume: 4 start-page: 163 year: 2012 ident: ref=76 publication-title: Epigenomics doi: 10.2217/epi.12.3 – volume: 1 start-page: 1077 year: 1986 ident: ref=20 publication-title: Lancet doi: 10.1016/S0140-6736(86)91340-1 – volume: 119 start-page: 323 year: 2009 ident: ref=46 publication-title: J Clin Invest doi: 10.1172/JCI32661 – volume: 32 start-page: S62 year: 2008 ident: ref=65 publication-title: Int J Obes doi: 10.1038/ijo.2008.240 – volume: 25 start-page: 170 year: 2014 ident: ref=79 publication-title: J Nutr Biochem doi: 10.1016/j.jnutbio.2013.09.016 – volume: 10 start-page: 478 year: 2009 ident: ref=90 publication-title: BMC Genomics doi: 10.1186/1471-2164-10-478 – volume: 140 start-page: 653 year: 2010 ident: ref=4 publication-title: J Nutr doi: 10.3945/jn.109.112433 – volume: 87 start-page: 117 year: 2002 ident: ref=74 publication-title: J Cell Biochem doi: 10.1002/jcb.10286 – volume: 111 start-page: 2112 year: 2014 ident: ref=89 publication-title: Br J Nutr doi: 10.1017/S0007114514000579 – volume: 151 start-page: 4756 year: 2010 ident: ref=84 publication-title: Endocrinology doi: 10.1210/en.2010-0505 – volume: 107 start-page: 138 year: 2012 ident: ref=54 publication-title: Physiol Behav doi: 10.1016/j.physbeh.2012.04.014 – volume: 514 start-page: 415 year: 2019 ident: ref=44 publication-title: Biochem Biophys Res Commun doi: 10.1016/j.bbrc.2019.04.154 – volume: 2 start-page: 27 year: 2011 ident: ref=16 publication-title: Front Genet doi: 10.3389/fgene.2011.00027 – volume: 151 start-page: 4756 year: 2010 ident: ref=60 publication-title: Endocrinology doi: 10.1210/en.2010-0505 – volume: 16 year: 2019 ident: ref=35 publication-title: PLoS Med doi: 10.1371/journal.pmed.1002744 – volume: 3 start-page: 1 year: 2014 ident: ref=50 publication-title: Clin Nutr Res doi: 10.7762/cnr.2014.3.1.1 – volume: 435 start-page: 2 year: 2016 ident: ref=11 publication-title: Mol Cell Endocrinol doi: 10.1016/j.mce.2016.07.002 – volume: 7 start-page: 9492 year: 2015 ident: ref=88 publication-title: Nutrients doi: 10.3390/nu7115467 – volume: 13 start-page: 168 year: 2018 ident: ref=92 publication-title: Pediatr Obes doi: 10.1111/ijpo.12247 – volume: 1842 start-page: 507 year: 2014 ident: ref=41 publication-title: Molecular Basis of Disease doi: 10.1016/j.bbadis.2013.07.006 – volume: 6 year: 2015 ident: ref=86 publication-title: Cold Spring Harb Perspect Med doi: 10.1101/cshperspect.a026591 – volume: 39 start-page: 28 year: 2015 ident: ref=43 publication-title: Front Neuroendocrinol doi: 10.1016/j.yfrne.2015.09.001 – volume: 39 start-page: 633 year: 2015 ident: ref=10 publication-title: Int J Obes doi: 10.1038/ijo.2015.13 – volume: 356 start-page: j1 year: 2017 ident: ref=30 publication-title: BMJ doi: 10.1136/bmj.j1 – volume: 20 start-page: 1257 year: 2006 ident: ref=38 publication-title: FASEB J doi: 10.1096/fj.05-5241fje – volume: 299 start-page: R711 year: 2010 ident: ref=45 publication-title: Am J Physiol Regul Integr Comp Physiol doi: 10.1152/ajpregu.00310.2010 – volume: 6 start-page: 922 year: 2017 ident: ref=67 publication-title: Mol Metab doi: 10.1016/j.molmet.2017.05.010 |
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Snippet | Background: Maternal obesity and maternal overnutrition, can lead to epigenetic alterations during pregnancy and these alterations can influence fetal and... Maternal obesity and maternal overnutrition, can lead to epigenetic alterations during pregnancy and these alterations can influence fetal and neonatal... |
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SubjectTerms | Current Genomics Deoxyribonucleic acid Developmental stages Disorders DNA DNA methylation Energy intake Epigenetics Fetuses Gene expression Heredity Human nutrition Hypothalamus Literature reviews Metabolic disorders miRNA Neonates Nutrition Obesity Overnutrition Phenotypes Pregnancy Programming Weight control |
Title | Maternal Obesity, Maternal Overnutrition and Fetal Programming: Effects of Epigenetic Mechanisms on the Development of Metabolic Disorders |
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