ESPE2021 ePoster Category 2 Fetal, neonatal endocrinology and metabolism (to include hypoglycaemia) (16 abstracts)
Hypomethylation of the Prader-Willi imprinting control region associates with postnatal growth and visceral adiposity in healthy children
Gemma Carreras-Badosa 1 , Berta Mas-Parés 1 , Ariadna Gómez-Vilarrubla 1 , Sílvia Xargay-Torrent 1 , Elsa Puerto-Carranza 2 , Antonio de Arriba Muñoz 3 , Anna Prats-Puig 4 , Francis de Zegher 5 , Lourdes Ibañez 6 , Judit Bassols 1 & Abel López-Bermejo 1
1Pediatrics, Girona Biomedical Research Institute, Girona, Spain; 2Pediatrics, Dr. Josep Trueta Hospital, Girona, Spain; 3Pediatric Endocrinology Unit, Miguel Servet Hospital, Zaragoza, Spain; 4University School of Health and Sport (EUSES), University of Girona, Girona, Spain; 5Department of Development & Regeneration, University of Leuven, Leuven, Belgium; 6Endocrinology, Sant Joan de Déu Children’s Hospital Pediatric Institute, University of Barcelona, Barcelona, Spain
Introduction: Children with Prader-Willi syndrome present with short stature and obesity. However, very little is known about the role of this imprinted control region in the general population. This study aims to analyze the methylation status of the PWS imprinting control region (ICR) in placenta and its association with postnatal growth and obesity parameters in healthy children.
Methodology: The methylation percentages of the PWS-ICR were determined by EpytyperTM technology in placentas from 118 healthy newborns included in a cohort of mother-newborn pairs in Girona, a region in Northeastern Spain. Methylation values for the different studied cytosine-guanine nucleotides (CpG) within the PWS-ICR were correlated with anthropometric parameters (weight, height and body composition) in the offspring from birth to 6 years of age.
Results: The methylation status of the PWS-ICR was inversely and independently correlated to weight and height at birth, height during the first month of life, and with height and visceral fat mass at 6 years of age. All inverse associations between PWS-ICR methylation and growth and visceral adiposity parameters were more pronounced in children who had been heavier at birth (those with birthweight above the median; adjusted multivariate models 0.40 ˃ R2 ˃ 0.30).
Conclusion: In conclusion, placental PWS-ICR methylation status associates with growth parameters in healthy children from birth to school age as well as with higher visceral adiposity at 6 years of age. As shown for PWS patients, PWS-ICR methylation could similarly be involved in postnatal growth and visceral obesity in healthy infants.
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