CoChat
Sign Up
Cited by 104Birth, Development, and HealthEpigenetics and DNA MethylationGestational Diabetes Research and Management

Maternal Obesity, Maternal Overnutrition and Fetal Programming: Effects of Epigenetic Mechanisms on the Development of Metabolic Disorders

Open access
Şanlı, Ezgi, Kabaran, Seray·2019·Current Genomics
DOI 10.2174/1389202920666191030092225PMC PMC7235386
Open this paper in CoChat — free accountOpen PDF

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. Method: 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.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.2174/1389202920666191030092225

Cites

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • DNA methylation, mediated by DNA methyltransferases (DNMTs), typically represses gene transcription when occurring in promoter regions.

    “DNA methylation, mediated by DNA methyltransferases (DNMTs), which typically repress gene transcription when occurring in promoter regions;”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [159]

    The DNA Methylation section describes methylation as an epigenetic mechanism, and the discussion of maternal high-fat diets mentions DNMT1 expression and altered methylation in promoter regions. Neither passage states that DNMTs mediate DNA methylation or that promoter methylation typically represses transcription. The copy provides related context but not the claim’s defining mechanism and effect; page numbers are unavailable. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • Maternal malnutrition, whether undernutrition, overnutrition, or obesity, can induce persistent epigenetic modifications that alter gene expression without changing the DNA sequence.

    “Maternal malnutrition (whether undernutrition, overnutrition, or obesity) can induce persistent epigenetic modifications that alter gene expression without changing the DNA sequence.”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [159]

    The Introduction’s epigenetic-mechanisms section (page unavailable) says maternal nutrition may permanently affect fetal gene expression through epigenetic mechanisms, and that deficient or excess dietary methyl donors can alter epigenetic patterns. The copy also discusses maternal undernutrition, but does not clearly establish persistent epigenetic modifications from undernutrition generally. It describes DNA methylation, histone modifications and microRNAs, without explicitly stating that the DNA sequence remains unchanged. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • Histone modifications such as acetylation, methylation, and phosphorylation influence chromatin structure and the accessibility of transcriptional machinery.

    “histone modifications (e.g., acetylation, methylation, phosphorylation) that influence chromatin structure and the accessibility of transcriptional machinery;”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [159]

    The Introduction section on epigenetic mechanisms describes histone acetylation and methylation, links histone modifications to altered chromatin structure, and discusses transcription-factor binding. It does not mention histone phosphorylation or explicitly address accessibility of transcriptional machinery. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Together, DNA methylation, histone modifications, and miRNA regulation form the molecular basis of fetal programming, through which maternal nutritional imbalance can imprint lasting effects on gene regulation, metabolism, and disease vulnerability in later life.

    “Together, these mechanisms form the molecular basis of fetal programming, through which maternal nutritional imbalance can imprint lasting effects on gene regulation, metabolism, and disease vulnerability in later life [157,158,159].”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [159]

  • microRNAs (miRNAs) are small non-coding RNAs that post-transcriptionally regulate gene expression.

    “regulation by microRNAs (miRNAs), small non-coding RNAs that post-transcriptionally regulate gene expression.”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [159]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

The citation lists haven’t been fetched yet

References 88 · Cited by 104

Research works printed but not linked: 86

  1. [1]Ng M. Fleming T. Robinson M. Thomson B. Graetz N. Margono C. Mullany E.C. Biryukov S. Abbafati C. Abera S.F. Abraham J.P. Abu-Rmeileh N.M. Achoki T. AlBuhairan F.S. Alemu Z.A. Alfonso R. Ali M.K. Ali R. Guzman N.A. Ammar W. Anwari P. Banerjee A. Barquera S. Basu S. Bennett D.A. Bhutta Z. Blore J. Cabral N. Nonato I.C. Chang J.C. Chowdhury R. Courville K.J. Criqui M.H. Cundiff D.K. Dabhadkar K.C. Dandona L. Davis A. Dayama A. Dharmaratne S.D. Ding E.L. Durrani A.M. Esteghamati A. Farzadfar F. Fay D.F. Feigin V.L. Flaxman A. Forouzanfar M.H. Goto A. Green M.A. Gupta R. Hafezi-Nejad N. Hankey G.J. Harewood H.C. Havmoeller R. Hay S. Hernandez L. Husseini A. Idrisov B.T. Ikeda N. Islami F. Jahangir E. Jassal S.K. Jee S.H. Jeffreys M. Jonas J.B. Kabagambe E.K. Khalifa S.E. Kengne A.P. Khader Y.S. Khang Y.H. Kim D. Kimokoti R.W. Kinge J.M. Kokubo Y. Kosen S. Kwan G. Lai T. Leinsalu M. Li Y. Liang X. Liu S. Logroscino G. Lotufo P.A. Lu Y. Ma J. Mainoo N.K. Mensah G.A. Merriman T.R. Mokdad A.H. Moschandreas J. Naghavi M. Naheed A. Nand D. Narayan K.M. Nelson E.L. Neuhouser M.L. Nisar M.I. Ohkubo T. Oti S.O. Pedroza A. Prabhakaran D. Roy N. Sampson U. Seo H. Sepanlou S.G. Shibuya K. Shiri R. Shiue I. Singh G.M. Singh J.A. Skirbekk V. Stapelberg N.J. Sturua L. Sykes B.L. Tobias M. Tran B.X. Trasande L. Toyoshima H. van de Vijver S. Vasankari T.J. Veerman J.L. Velasquez-Melendez G. Vlassov V.V. Vollset S.E. Vos T. Wang C. Wang X. Weiderpass E. Werdecker A. Wright J.L. Yang Y.C. Yatsuya H. Yoon J. Yoon S.J. Zhao Y. Zhou M. Zhu S. Lopez A.D. Murray C.J. Gakidou E. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: A systematic analysis for the Global Burden of Disease Study 2013. Lancet 2014 384 9945 766 781 10.1016/S0140-6736(14)60460-8 24880830 PMC4624264 · DOI · Paper page
  2. [2]Gaillard R. Durmuş B. Hofman A. Mackenbach J.P. Steegers E.A. Jaddoe V.W. Risk factors and outcomes of maternal obesity and excessive weight gain during pregnancy. Obesity (Silver Spring) 2013 21 5 1046 1055 10.1002/oby.20088 23784909 · DOI
  3. [3]Valsamakis G. Kyriazi E.L. Mouslech Z. Siristatidis C. Mastorakos G. Effect of maternal obesity on pregnancy outcomes and long-term metabolic consequences. Hormones (Athens) 2015 14 3 345 357 10.14310/horm.2002.1590 26188222 · DOI
  4. [4]Bouret S.G. Role of early hormonal and nutritional experiences in shaping feeding behavior and hypothalamic development. J. Nutr. 2010 140 3 653 657 10.3945/jn.109.112433 20107150 · DOI
  5. [5]Plagemann A. Harder T. Schellong K. Schulz S. Stupin J.H. Early postnatal life as a critical time window for determination of long-term metabolic health. Best Pract. Res. Clin. Endocrinol. Metab. 2012 26 5 641 653 10.1016/j.beem.2012.03.008 22980046 · DOI
  6. [6]Gicquel C. El-Osta A. Le Bouc Y. Epigenetic regulation and fetal programming. Best Pract. Res. Clin. Endocrinol. Metab. 2008 22 1 1 16 10.1016/j.beem.2007.07.009 18279777 · DOI
  7. [7]Waterland R.A. Jirtle R.L. Early nutrition, epigenetic changes at transposons and imprinted genes, and enhanced susceptibility to adult chronic diseases. Nutrition 2004 20 1 63 68 10.1016/j.nut.2003.09.011 14698016 · DOI
  8. [8]Nicholas L.M. Morrison J.L. Rattanatray L. Zhang S. Ozanne S.E. McMillen I.C. The early origins of obesity and insulin resistance: Timing, programming and mechanisms. Int. J. Obes. 2016 40 2 229 238 10.1038/ijo.2015.178 26367335 · DOI · Paper page
  9. [9]Kitsiou-Tzeli S. Tzetis M. Maternal epigenetics and fetal and neonatal growth. Curr. Opin. Endocrinol. Diabetes Obes. 2017 24 1 43 46 27898587
  10. [10]Desai M. Jellyman J.K. Ross M.G. Epigenomics, gestational programming and risk of metabolic syndrome. Int. J. Obes. 2015 39 4 633 641 10.1038/ijo.2015.13 25640766 · DOI
  11. [11]Elshenawy S. Simmons R. Maternal obesity and prenatal programming. Mol. Cell. Endocrinol. 2016 435 2 6 10.1016/j.mce.2016.07.002 27392495 · DOI
  12. [12]Nicholas L.M. Morrison J.L. Rattanatray L. Zhang S. Ozanne S.E. McMillen I.C. The early origins of obesity and insulin resistance: Timing, programming and mechanisms. Int. J. Obes. 2016 40 2 229 238 10.1038/ijo.2015.178 26367335 · DOI · Paper page
  13. [13]Montalvo-Martínez L. Maldonado-Ruiz R. Cárdenas-Tueme M. Reséndez-Pérez D. Camacho A. Maternal overnutrition programs central inflammation and addiction-like behavior in offspring. BioMed Res. Int. 2018 2018 8061389 10.1155/2018/8061389 30027100 PMC6031166 · DOI
  14. [14]Maffeis C. Morandi A. Effect of maternal obesity on foetal growth and metabolic health of the offspring. Obes. Facts 2017 10 2 112 117 10.1159/000456668 28384625 PMC5644955 · DOI
  15. [15]Padmanabhan V. Cardoso R.C. Puttabyatappa M. Developmental programming, a pathway to disease. Endocrinology 2016 157 4 1328 1340 10.1210/en.2016-1003 26859334 PMC4816734 · DOI
  16. [16]Alfaradhi M.Z. Ozanne S.E. Developmental programming in response to maternal overnutrition. Front. Genet. 2011 2 27 10.3389/fgene.2011.00027 22303323 PMC3268582 · DOI
  17. [17]Fernandez-Twinn D.S. Constância M. Ozanne S.E. Intergenerational epigenetic inheritance in models of developmental programming of adult disease. Semin. Cell Dev. Biol. 2015 43 85 95 10.1016/j.semcdb.2015.06.006 26135290 PMC5844462 · DOI
  18. [18]Fernandez-Twinn D.S. Ozanne S.E. Early life nutrition and metabolic programming. Ann. N. Y. Acad. Sci. 2010 1212 1 78 96 10.1111/j.1749-6632.2010.05798.x 21070247 · DOI
  19. [19]Roseboom T. de Rooij S. Painter R. The Dutch famine and its long-term consequences for adult health. Early Hum. Dev. 2006 82 8 485 491 10.1016/j.earlhumdev.2006.07.001 16876341 · DOI · Paper page
  20. [20]Barker D.J. Osmond C. Infant mortality, childhood nutrition, and ischaemic heart disease in England and Wales. Lancet 1986 1 8489 1077 1081 10.1016/S0140-6736(86)91340-1 2871345 · DOI · Paper page
  21. [21]Barker D.J. The fetal origins of coronary heart disease. Acta Paediatr. Suppl. 1997 422 S422 78 82 10.1111/j.1651-2227.1997.tb18351.x 9298799 · DOI
  22. [23]Stephenson S. Cunliffe A. Foetal developmental origins of adult onset non-insulin dependent diabetes mellitus. J. Nutr. Food Sci. 2018 8 5 1 11 10.4172/2155-9600.1000733 · DOI
  23. [24]Ravelli A.C. van der Meulen J.H. Michels R.P.J. Osmond C. Barker D.J. Hales C.N. Bleker O.P. Glucose tolerance in adults after prenatal exposure to famine. Lancet 1998 351 9097 173 177 10.1016/S0140-6736(97)07244-9 9449872 · DOI · Paper page
  24. [25]Hales C.N. Barker D.J. The thrifty phenotype hypothesis. Br. Med. Bull. 2001 60 1 5 20 10.1093/bmb/60.1.5 11809615 · DOI
  25. [26]Wells J.C. The thrifty phenotype hypothesis: Thrifty offspring or thrifty mother? J. Theor. Biol. 2003 221 1 143 161 10.1006/jtbi.2003.3183 12634051 · DOI
  26. [27]Armitage J.A. Poston L. Taylor P.D. Developmental origins of obesity and the metabolic syndrome: The role of maternal obesity. Front. Horm. Res. 2008 36 73 84 10.1159/000115355 18230895 · DOI
  27. [28]Smith N.H. Ozanne S.E. Intrauterine origins of metabolic disease. Rev. Gynaecol. Perinatal Practice 2006 6 3-4 211 217 10.1016/j.rigapp.2006.03.002 · DOI
  28. [29]Luo Z.C. Fraser W.D. Julien P. Deal C.L. Audibert F. Smith G.N. Xiong X. Walker M. Tracing the origins of “fetal origins” of adult diseases: Programming by oxidative stress? Med. Hypotheses 2006 66 1 38 44 10.1016/j.mehy.2005.08.020 16198060 · DOI
  29. [30]Catalano P.M. Shankar K. Obesity and pregnancy: Mechanisms of short term and long term adverse consequences for mother and child. BMJ 2017 356 j1 10.1136/bmj.j1 28179267 PMC6888512 · DOI · Paper page
  30. [31]McDowell M. Cain M.A. Brumley J. Excessive gestational weight gain. J. Midwifery Womens Health 2018 1 9 30548447
  31. [32]Goldstein R.F. Abell S.K. Ranasinha S. Misso M. Boyle J.A. Black M.H. Li N. Hu G. Corrado F. Rode L. Kim Y.J. Haugen M. Song W.O. Kim M.H. Bogaerts A. Devlieger R. Chung J.H. Teede H.J. Association of gestational weight gain with maternal and infant outcomes: A systematic review and meta-analysis. JAMA 2017 317 21 2207 2225 10.1001/jama.2017.3635 28586887 PMC5815056 · DOI
  32. [33]Yu Z. Han S. Zhu J. Sun X. Ji C. Guo X. Pre-pregnancy body mass index in relation to infant birth weight and offspring overweight/obesity: A systematic review and meta-analysis. PLoS One 2013 8 4 e61627 10.1371/journal.pone.0061627 23613888 PMC3628788 · DOI
  33. [34]Tie H.T. Xia Y.Y. Zeng Y.S. Zhang Y. Dai C.L. Guo J.J. Zhao Y. Risk of childhood overweight or obesity associated with excessive weight gain during pregnancy: A meta-analysis. Arch. Gynecol. Obstet. 2014 289 2 247 257 10.1007/s00404-013-3053-z 24141389 · DOI
  34. [35]Voerman E. Santos S. Patro Golab B. Amiano P. Ballester F. Barros H. Bergström A. Charles M.A. Chatzi L. Chevrier C. Chrousos G.P. Corpeleijn E. Costet N. Crozier S. Devereux G. Eggesbø M. Ekström S. Fantini M.P. Farchi S. Forastiere F. Georgiu V. Godfrey K.M. Gori D. Grote V. Hanke W. Hertz-Picciotto I. Heude B. Hryhorczuk D. Huang R.C. Inskip H. Iszatt N. Karvonen A.M. Kenny L.C. Koletzko B. Küpers L.K. Lagström H. Lehmann I. Magnus P. Majewska R. Mäkelä J. Manios Y. McAuliffe F.M. McDonald S.W. Mehegan J. Mommers M. Morgen C.S. Mori T.A. Moschonis G. Murray D. Chaoimh C.N. Nohr E.A. Nybo Andersen A.M. Oken E. Oostvogels A.J.J.M. Pac A. Papadopoulou E. Pekkanen J. Pizzi C. Polanska K. Porta D. Richiardi L. Rifas-Shiman S.L. Ronfani L. Santos A.C. Standl M. Stoltenberg C. Thiering E. Thijs C. Torrent M. Tough S.C. Trnovec T. Turner S. van Rossem L. von Berg A. Vrijheid M. Vrijkotte T.G.M. West J. Wijga A. Wright J. Zvinchuk O. Sørensen T.I.A. Lawlor D.A. Gaillard R. Jaddoe V.W.V. Maternal body mass index, gestational weight gain, and the risk of overweight and obesity across childhood: An individual participant data meta-analysis. PLoS Med. 2019 16 2 e1002744 10.1371/journal.pmed.1002744 30742624 PMC6370184 · DOI
  35. [36]Muhlhausler B.S. Ong Z.Y. The fetal origins of obesity: Early origins of altered food intake. Endocr. Metab. Immune Disord. Drug Targets 2011 11 3 189 197 10.2174/187153011796429835 21831032 · DOI
  36. [38]Muhlhausler B.S. Adam C.L. Findlay P.A. Duffield J.A. McMillen I.C. Increased maternal nutrition alters development of the appetite-regulating network in the brain. FASEB J. 2006 20 8 1257 1259 10.1096/fj.05-5241fje 16684802 · DOI
  37. [39]Brion M.J. Ness A.R. Rogers I. Emmett P. Cribb V. Davey Smith G. Lawlor D.A. Maternal macronutrient and energy intakes in pregnancy and offspring intake at 10 y: Exploring parental comparisons and prenatal effects. Am. J. Clin. Nutr. 2010 91 3 748 756 10.3945/ajcn.2009.28623 20053880 PMC2822901 · DOI
  38. [40]Lawlor D.A. Smith G.D. O’Callaghan M. Alati R. Mamun A.A. Williams G.M. Najman J.M. Epidemiologic evidence for the fetal overnutrition hypothesis: Findings from the mater-university study of pregnancy and its outcomes. Am. J. Epidemiol. 2007 165 4 418 424 10.1093/aje/kwk030 17158475 · DOI
  39. [41]Williams L. Seki Y. Vuguin P.M. Charron M.J. Animal models of in utero exposure to a high fat diet: A review. Biochimica et Biophysica Acta (BBA)-. Molecular Basis of Disease 2014 1842 3 507 519 10.1016/j.bbadis.2013.07.006 PMC3895417 23872578 · DOI
  40. [42]Fu G. Brkić J. Hayder H. Peng C. MicroRNAs in human placental development and pregnancy complications. Int. J. Mol. Sci. 2013 14 3 5519 5544 10.3390/ijms14035519 23528856 PMC3634453 · DOI
  41. [43]Nugent B.M. Bale T.L. The omniscient placenta: Metabolic and epigenetic regulation of fetal programming. Front. Neuroendocrinol. 2015 39 28 37 10.1016/j.yfrne.2015.09.001 26368654 PMC4681645 · DOI · Paper page
  42. [44]Upadhyay A. Anjum B. Godbole N.M. Rajak S. Shukla P. Tiwari S. Sinha R.A. Godbole M.M. Time-restricted feeding reduces high-fat diet associated placental inflammation and limits adverse effects on fetal organ development. Biochem. Biophys. Res. Commun. 2019 514 2 415 421 10.1016/j.bbrc.2019.04.154 31053302 · DOI
  43. [45]Heerwagen M.J. Miller M.R. Barbour L.A. Friedman J.E. Maternal obesity and fetal metabolic programming: A fertile epigenetic soil. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2010 299 3 R711 R722 10.1152/ajpregu.00310.2010 20631295 PMC2944425 · DOI
  44. [46]McCurdy C.E. Bishop J.M. Williams S.M. Grayson B.E. Smith M.S. Friedman J.E. Grove K.L. Maternal high-fat diet triggers lipotoxicity in the fetal livers of nonhuman primates. J. Clin. Invest. 2009 119 2 323 335 10.1172/JCI32661 19147984 PMC2631287 · DOI
  45. [47]Tarrade A. Panchenko P. Junien C. Gabory A. Placental contribution to nutritional programming of health and diseases: Epigenetics and sexual dimorphism. J. Exp. Biol. 2015 218 Pt 1 50 58 10.1242/jeb.110320 25568451 · DOI · Paper page
  46. [49]Alfaradhi M.Z. Ozanne S.E. Developmental programming in response to maternal overnutrition. Front. Genet. 2011 2 27 10.3389/fgene.2011.00027 22303323 PMC3268582 · DOI
  47. [50]Jang H. Serra C. Nutrition, epigenetics, and diseases. Clin. Nutr. Res. 2014 3 1 1 8 10.7762/cnr.2014.3.1.1 24527414 PMC3921290 · DOI
  48. [51]Chango A. Pogribny I.P. Considering maternal dietary modulators for epigenetic regulation and programming of the fetal epigenome. Nutrients 2015 7 4 2748 2770 10.3390/nu7042748 25875118 PMC4425171 · DOI · Paper page
  49. [52]Cheng Z. Zheng L. Almeida F.A. Epigenetic reprogramming in metabolic disorders: Nutritional factors and beyond. J. Nutr. Biochem. 2018 54 1 10 10.1016/j.jnutbio.2017.10.004 29154162 PMC5866737 · DOI
  50. [53]Freeman D.J. Effects of maternal obesity on fetal growth and body composition: Implications for programming and future health. Semin. Fetal Neonatal Med. 2010 15 2 113 118 10.1016/j.siny.2009.09.001 19853544 · DOI
  51. [54]Sen S. Carpenter A.H. Hochstadt J. Huddleston J.Y. Kustanovich V. Reynolds A.A. Roberts S. Nutrition, weight gain and eating behavior in pregnancy: A review of experimental evidence for long-term effects on the risk of obesity in offspring. Physiol. Behav. 2012 107 1 138 145 10.1016/j.physbeh.2012.04.014 22546810 · DOI
  52. [56]Muhlhausler B.S. Duffield J.A. McMillen I.C. Increased maternal nutrition stimulates peroxisome proliferator activated receptor-γ, adiponectin, and leptin messenger ribonucleic acid expression in adipose tissue before birth. Endocrinology 2007 148 2 878 885 10.1210/en.2006-1115 17068138 · DOI
  53. [57]MacLennan N.K. James S.J. Melnyk S. Piroozi A. Jernigan S. Hsu J.L. Janke S.M. Pham T.D. Lane R.H. Uteroplacental insufficiency alters DNA methylation, one-carbon metabolism, and histone acetylation in IUGR rats. Physiol. Genomics 2004 18 1 43 50 10.1152/physiolgenomics.00042.2004 15084713 · DOI
  54. [58]Panchenko P.E. Voisin S. Jouin M. Jouneau L. Prézelin A. Lecoutre S. Breton C. Jammes H. Junien C. Gabory A. Expression of epigenetic machinery genes is sensitive to maternal obesity and weight loss in relation to fetal growth in mice. Clin. Epigenetics 2016 8 1 22 10.1186/s13148-016-0188-3 26925174 PMC4769534 · DOI
  55. [59]Borengasser S.J. Zhong Y. Kang P. Lindsey F. Ronis M.J. Badger T.M. Gomez-Acevedo H. Shankar K. Maternal obesity enhances white adipose tissue differentiation and alters genome-scale DNA methylation in male rat offspring. Endocrinology 2013 154 11 4113 4125 10.1210/en.2012-2255 23959936 PMC3800750 · DOI · Paper page
  56. [60]Vucetic Z. Kimmel J. Totoki K. Hollenbeck E. Reyes T.M. Maternal high-fat diet alters methylation and gene expression of dopamine and opioid-related genes. Endocrinology 2010 151 10 4756 4764 10.1210/en.2010-0505 20685869 PMC2946145 · DOI
  57. [61]Godfrey K.M. Sheppard A. Gluckman P.D. Lillycrop K.A. Burdge G.C. McLean C. Rodford J. Slater-Jefferies J.L. Garratt E. Crozier S.R. Emerald B.S. Gale C.R. Inskip H.M. Cooper C. Hanson M.A. Epigenetic gene promoter methylation at birth is associated with child’s later adiposity. Diabetes 2011 60 5 1528 1534 10.2337/db10-0979 21471513 PMC3115550 · DOI
  58. [62]Gali Ramamoorthy T. Allen T.J. Davies A. Harno E. Sefton C. Murgatroyd C. White A. Maternal overnutrition programs epigenetic changes in the regulatory regions of hypothalamic Pomc in the offspring of rats. Int. J. Obes. 2018 42 8 1431 1444 10.1038/s41366-018-0094-1 29777232 PMC6113193 · DOI · Paper page
  59. [63]Chen H. Simar D. Lambert K. Mercier J. Morris M.J. Maternal and postnatal overnutrition differentially impact appetite regulators and fuel metabolism. Endocrinology 2008 149 11 5348 5356 10.1210/en.2008-0582 18635655 · DOI
  60. [64]Plagemann A. Harder T. Brunn M. Harder A. Roepke K. Wittrock-Staar M. Ziska T. Schellong K. Rodekamp E. Melchior K. Dudenhausen J.W. Hypothalamic proopiomelanocortin promoter methylation becomes altered by early overfeeding: An epigenetic model of obesity and the metabolic syndrome. J. Physiol. 2009 587 Pt 20 4963 4976 10.1113/jphysiol.2009.176156 19723777 PMC2770159 · DOI · Paper page
  61. [66]Sasson I.E. Vitins A.P. Mainigi M.A. Moley K.H. Simmons R.A. Pre-gestational vs gestational exposure to maternal obesity differentially programs the offspring in mice. Diabetologia 2015 58 3 615 624 10.1007/s00125-014-3466-7 25608625 PMC4452998 · DOI
  62. [67]Lecoutre S. Oger F. Pourpe C. Butruille L. Marousez L. Dickes-Coopman A. Laborie C. Guinez C. Lesage J. Vieau D. Junien C. Eberlé D. Gabory A. Eeckhoute J. Breton C. Maternal obesity programs increased leptin gene expression in rat male offspring via epigenetic modifications in a depot-specific manner. Mol. Metab. 2017 6 8 922 930 10.1016/j.molmet.2017.05.010 28752055 PMC5518658 · DOI · Paper page
  63. [68]Shankar K. Harrell A. Liu X. Gilchrist J.M. Ronis M.J. Badger T.M. Maternal obesity at conception programs obesity in the offspring. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2008 294 2 R528 R538 10.1152/ajpregu.00316.2007 18032473 · DOI
  64. [69]Seki Y. Suzuki M. Guo X. Glenn A.S. Vuguin P.M. Fiallo A. Du Q. Ko Y.A. Yu Y. Susztak K. Zheng D. Greally J.M. Katz E.B. Charron M.J. In utero exposure to a high-fat diet programs hepatic hypermethylation and gene dysregulation and development of metabolic syndrome in male mice. Endocrinology 2017 158 9 2860 2872 10.1210/en.2017-00334 28911167 PMC5659663 · DOI
  65. [70]Unal R. Yao-Borengasser A. Varma V. Rasouli N. Labbate C. Kern P.A. Ranganathan G. Matrix metalloproteinase-9 is increased in obese subjects and decreases in response to pioglitazone. J. Clin. Endocrinol. Metab. 2010 95 6 2993 3001 10.1210/jc.2009-2623 20392866 PMC2902064 · DOI
  66. [71]Cheng X. Blumenthal R.M. Coordinated chromatin control: Structural and functional linkage of DNA and histone methylation. Biochemistry 2010 49 14 2999 3008 10.1021/bi100213t 20210320 PMC2857722 · DOI
  67. [72]Kouzarides T. Chromatin modifications and their function. Cell 2007 128 4 693 705 10.1016/j.cell.2007.02.005 17320507 · DOI · Paper page
  68. [73]Dolinoy D.C. Das R. Weidman J.R. Jirtle R.L. Metastable epialleles, imprinting, and the fetal origins of adult diseases. Pediatr. Res. 2007 61 5 Pt 2 30R 37R 10.1203/pdr.0b013e31804575f7 17413847 · DOI
  69. [74]Geiman T.M. Robertson K.D. Chromatin remodeling, histone modifications, and DNA methylation-how does it all fit together? J. Cell. Biochem. 2002 87 2 117 125 10.1002/jcb.10286 12244565 · DOI
  70. [75]Gabory A. Attig L. Junien C. Developmental programming and epigenetics. Am. J. Clin. Nutr. 2011 94 Suppl. 6 1943S 1952S 10.3945/ajcn.110.000927 22049164 · DOI
  71. [76]Butler J.S. Koutelou E. Schibler A.C. Dent S.Y. Histone-modifying enzymes: Regulators of developmental decisions and drivers of human disease. Epigenomics 2012 4 2 163 177 10.2217/epi.12.3 22449188 PMC3382990 · DOI
  72. [77]Funato H. Oda S. Yokofujita J. Igarashi H. Kuroda M. Fasting and high-fat diet alter histone deacetylase expression in the medial hypothalamus. PLoS One 2011 6 4 e18950 10.1371/journal.pone.0018950 21526203 PMC3078138 · DOI
  73. [78]Gonçalves L.K. da Silva I.R.V. Cechinel L.R. Frusciante M.R. de Mello A.S. Elsner V.R. Funchal C. Dani C. Maternal consumption of high-fat diet and grape juice modulates global histone H4 acetylation levels in offspring hippocampus: A preliminary study. Neurosci. Lett. 2017 661 29 32 10.1016/j.neulet.2017.09.042 28951285 · DOI
  74. [79]Strakovsky R.S. Zhang X. Zhou D. Pan Y.X. The regulation of hepatic Pon1 by a maternal high-fat diet is gender specific and may occur through promoter histone modifications in neonatal rats. J. Nutr. Biochem. 2014 25 2 170 176 10.1016/j.jnutbio.2013.09.016 24445041 PMC6492273 · DOI
  75. [80]Aagaard-Tillery K.M. Grove K. Bishop J. Ke X. Fu Q. McKnight R. Lane R.H. Developmental origins of disease and determinants of chromatin structure: Maternal diet modifies the primate fetal epigenome. J. Mol. Endocrinol. 2008 41 2 91 102 10.1677/JME-08-0025 18515302 PMC2959100 · DOI
  76. [81]Suter M.A. Chen A. Burdine M.S. Choudhury M. Harris R.A. Lane R.H. Friedman J.E. Grove K.L. Tackett A.J. Aagaard K.M. A maternal high-fat diet modulates fetal SIRT1 histone and protein deacetylase activity in nonhuman primates. FASEB J. 2012 26 12 5106 5114 10.1096/fj.12-212878 22982377 PMC3509051 · DOI
  77. [82]Borengasser S.J. Kang P. Faske J. Gomez-Acevedo H. Blackburn M.L. Badger T.M. Shankar K. High fat diet and in utero exposure to maternal obesity disrupts circadian rhythm and leads to metabolic programming of liver in rat offspring. PLoS One 2014 9 1 e84209 10.1371/journal.pone.0084209 24416203 PMC3886966 · DOI
  78. [83]Aagaard-Tillery K.M. Grove K. Bishop J. Ke X. Fu Q. McKnight R. Lane R.H. Developmental origins of disease and determinants of chromatin structure: Maternal diet modifies the primate fetal epigenome. J. Mol. Endocrinol. 2008 41 2 91 102 10.1677/JME-08-0025 18515302 PMC2959100 · DOI
  79. [84]Vucetic Z. Kimmel J. Totoki K. Hollenbeck E. Reyes T.M. Maternal high-fat diet alters methylation and gene expression of dopamine and opioid-related genes. Endocrinology 2010 151 10 4756 4764 10.1210/en.2010-0505 20685869 PMC2946145 · DOI
  80. [85]Zamore P.D. Haley B. Ribo-gnome: The big world of small RNAs. Science 2005 309 5740 1519 1524 10.1126/science.1111444 16141061 · DOI
  81. [86]Neri C. Edlow A.G. Effects of maternal obesity on fetal programming: Molecular approaches. Cold Spring Harb. Perspect. Med. 2015 6 2 a026591 10.1101/cshperspect.a026591 26337113 PMC4743074 · DOI
  82. [87]Nakahara K. Carthew R.W. Expanding roles for miRNAs and siRNAs in cell regulation. Curr. Opin. Cell Biol. 2004 16 2 127 133 10.1016/j.ceb.2004.02.006 15196554 · DOI
  83. [89]Benatti R.O. Melo A.M. Borges F.O. Ignacio-Souza L.M. Simino L.A.P. Milanski M. Velloso L.A. Torsoni M.A. Torsoni A.S. Maternal high-fat diet consumption modulates hepatic lipid metabolism and microRNA-122 (miR-122) and microRNA-370 (miR-370) expression in offspring. Br. J. Nutr. 2014 111 12 2112 2122 10.1017/S0007114514000579 24666709 · DOI
  84. [90]Zhang J. Zhang F. Didelot X. Bruce K.D. Cagampang F.R. Vatish M. Hanson M. Lehnert H. Ceriello A. Byrne C.D. Maternal high fat diet during pregnancy and lactation alters hepatic expression of insulin like growth factor-2 and key microRNAs in the adult offspring. BMC Genomics 2009 10 1 478 10.1186/1471-2164-10-478 19835573 PMC2770530 · DOI
  85. [91]Enquobahrie D.A. Wander P.L. Tadesse M.G. Qiu C. Holzman C. Williams M.A. Maternal pre-pregnancy body mass index and circulating microRNAs in pregnancy. Obes. Res. Clin. Pract. 2017 11 4 464 474 10.1016/j.orcp.2016.10.287 27789200 PMC5403633 · DOI
  86. [92]Méndez-Mancilla A. Lima-Rogel V. Toro-Ortíz J.C. Escalante-Padrón F. Monsiváis-Urenda A.E. Noyola D.E. Salgado-Bustamante M. Differential expression profiles of circulating microRNAs in newborns associated to maternal pregestational overweight and obesity. Pediatr. Obes. 2018 13 3 168 174 10.1111/ijpo.12247 29045034 · DOI

Authors
Şanlı, E., & Kabaran, S.
Affiliations
Eastern Mediterranean University (CY)
Corresponding author
Kabaran, Seray
ORCID
Venue
Current Genomics
Publisher
Bentham Science Publishers Ltd.
Published
2019-01-02
Volume
20
Issue
6
Pages
419-427
ISSN
1389-2029 (ISSN-L)
DOI
10.2174/1389202920666191030092225
PMC
PMC7235386
OpenAlex
W2986784440
Cited by
104
References
88
Citations by year
2026: 16 · 2025: 22 · 2024: 15 · 2023: 18 · 2022: 10 · 2021: 16 · 2020: 6 · 2019: 1
FWCI
1.74
Type
journal article
Language
en
Open access
Locations
  • Current Genomics (publishedVersion)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • Eastern Mediterranean University Institutional Repository (Eastern Mediterranean University) (submittedVersion, cc-by-nc-nd)
Topics
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
  • Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
Keywords
maternal obesity, maternal overnutrition, fetal programming, epigenetic mechanisms, DNA methylation, histone modifications, microRNA, metabolic disorders, hypothalamic gene expression, energy intake, intergenerational effects, prenatal nutrition, maternal weight management

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review