Document Detail

An unbalanced maternal diet in pregnancy associates with offspring epigenetic changes in genes controlling glucocorticoid action and foetal growth.
MedLine Citation:
PMID:  22642564     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: In epidemiological studies, adverse early-life conditions associate with subsequent cardiometabolic disease. Hypothesized causes include maternal malnutrition, foetal glucocorticoid overexposure and reduced growth factors. Animal studies suggest a role for epigenetic processes in maintaining early-life effects into adulthood, but human relevance is unknown. We aimed to investigate relationships between an unbalanced maternal diet in pregnancy, neonatal and adult anthropometric variables with methylation at key genes controlling tissue glucocorticoid action and foetal growth.
DESIGN: We studied 34 individuals aged 40 from the Motherwell cohort study whose mothers ate an unbalanced diet in pregnancy, previously linked with elevated blood pressure and cortisol in adult offspring.
MEASUREMENTS: DNA methylation at 11β-hydroxysteroid dehydrogenase type 2 (HSD2), glucocorticoid receptor (GR) and insulin-like growth factor 2 (IGF2) was measured by pyrosequencing on buffy coat DNA.
RESULTS: Methylation at specific CpGs in the HSD2 promoter and at one of the IGF2 differentially methylated regions (H19 ICR) correlated with neonatal anthropometric variables. CpG methylation within HSD2, GR and H19 ICR was positively associated with increased adiposity and blood pressure in adulthood. Methylation at GR (exon 1F) was increased in offspring of mothers with the most unbalanced diets in pregnancy.
CONCLUSIONS: Alterations in DNA methylation at genes important in regulating circulating cortisol levels, tissue glucocorticoid action, blood pressure and foetal growth are present in adulthood in association with both early-life parameters and cardiometabolic risk factors. The data indicate a persisting epigenetic link between early-life maternal diet and/or foetal growth and cardiovascular disease risk in humans.
Amanda J Drake; Rhoanne C McPherson; Keith M Godfrey; Cyrus Cooper; Karen A Lillycrop; Mark A Hanson; Richard R Meehan; Jonathan R Seckl; Rebecca M Reynolds
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical endocrinology     Volume:  77     ISSN:  1365-2265     ISO Abbreviation:  Clin. Endocrinol. (Oxf)     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-11-09     Completed Date:  2013-04-22     Revised Date:  2014-02-20    
Medline Journal Info:
Nlm Unique ID:  0346653     Medline TA:  Clin Endocrinol (Oxf)     Country:  England    
Other Details:
Languages:  eng     Pagination:  808-15     Citation Subset:  IM    
Copyright Information:
© 2012 Blackwell Publishing Ltd.
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MeSH Terms
11-beta-Hydroxysteroid Dehydrogenase Type 2 / genetics
Birth Weight
Blood Pressure / genetics
DNA / blood
DNA Methylation
Epigenesis, Genetic / genetics*
Fetal Development / genetics*
Glucocorticoids / pharmacology*
Hydrocortisone / blood,  genetics
Infant, Newborn
Insulin-Like Growth Factor II / genetics
Maternal Nutritional Physiological Phenomena / genetics*
Maternal-Fetal Exchange
Prenatal Exposure Delayed Effects
Receptors, Glucocorticoid / genetics
Grant Support
CZB/4/582//Chief Scientist Office; CZG/2/478//Chief Scientist Office; MC_PC_U127574433//Medical Research Council; MC_U127574433//Medical Research Council; MC_UP_A620_1014//Medical Research Council; MC_UP_A620_1017//Medical Research Council; SCD/09//Chief Scientist Office
Reg. No./Substance:
0/Glucocorticoids; 0/Receptors, Glucocorticoid; 67763-97-7/Insulin-Like Growth Factor II; 9007-49-2/DNA; EC Dehydrogenase Type 2; WI4X0X7BPJ/Hydrocortisone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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