ESPE2021 ePoster Category 1 Fetal Endocrinology and Multisystem Disorders B (10 abstracts)
Impact of gestational weight gain on methylation of imprinted genes in umbilical cord and its relationship with postnatal growth and metabolism
Berta Mas-Parés 1 , Gemma Carreras-Badosa 1 , Ariadna Gómez-Vilarrubla 1 , Sílvia Xargay-Torrent 1 , Anna Maroto 2 , Anna Prats-Puig 3 , Elsa Puerto-Carranza 2,1 , Francis de Zegher 4 , Lourdes Ibáñez 5 , Judit Bassols 1 & Abel López-Bermejo 2,1
1Girona Biomedical Research Institute (IDIBGI), Salt, Spain; 2Dr. Josep Trueta Hospital, Girona, Spain; 3EUSES University of Girona, Salt, Spain; 4University of Leuven, Leuven, Belgium; 5Sant Joan de Déu Hospital, Barcelona, Spain
Introduction: Imprinted genes are critical for placental function and normal fetal growth and development. Very little is known about the impact of maternal obesity on imprinted genes and their role in postnatal growth and metabolism.
Objectives: 1) To identify umbilical cord DNA methylation sites (CpG) associated with gestational weight gain (GWG); 2) to identify which of these CpGs lie within imprinting control regions (ICRs); and 3) to study the association of these CpGs with offspring’s growth and metabolism.
Materials and methods: A pilot study was conducted in 16 pregnant women with different degrees of GWG. The newborns were followed up from birth to 6 years of age. Umbilical cord DNA methylation was assessed using microarray Infinium Methylation EPICBeadChip (Illumina). Beta regression models (false discovery rate (FDR)<0.05 and odds ratio>1.5 or <0.67) were performed to identify the CpGs associated with GWG. The CpGs that lied within ICRs were selected and correlated with anthropometric and metabolic parameters of the offspring.
Results: 2773 differentially methylated CpG were identified, out of which 8 lied within ICRs. The top 5 CpGs, which annotated for KCNQ1OT1, GNAS A/B, MEST, PLAGL1 and FAM50B (FDR<0.001 and odds ratio>1.03), were chosen for the study. The methylation of all these CpGs was positively correlated with GWG (r from 0.603 to 0.826; all P < 0.02). The CpGs that annotated for KCNQ1OT1 and GNAS A/B were negatively associated with the levels of glycated haemoglobin (HbA1C) and glucose in the offspring at 6 years of age (r = -0.610, P = 0.016 and r=-0.705, P = 0.003, respectively). The CpGs that annotated for MEST and FAM5OB were negatively associated with visceral (renal) fat at 6 years of age (r = -0.627, P = 0.012 and r = -0.634, P = 0.011, respectively). Finally, the CpG annotated for PLAGL1 were associated with height and glucose at 6 years of age (r = -0.661 P = 0.005 and r = -0.714, P = 0.004, respectively).
Conclusions: This preliminary study suggests that excessive gestational weight gain can cause changes in DNA methylation of imprinted genes and thereby regulate postnatal growth and metabolism in the offspring.
Article tools
My recent searches
My recently viewed abstracts
Authors
ESPE Abstracts
© Bioscientifica 2024 |
Privacy policy |
Cookie settings
BiosciAbstracts
Bioscientifica Abstracts is the gateway to a series of products that provide a permanent, citable record of abstracts for biomedical and life science conferences.
Find out more