ESPE2021 ePoster Category 2 Fetal, neonatal endocrinology and metabolism (to include hypoglycaemia) (16 abstracts)
Placental FRAT-1 methylation in women with gestational obesity is associated with the body composition in the offspring at 6 years of age
Ariadna Gómez-Vilarrubla 1 , Berta Mas-Parés 1 , Gemma Carreras-Badosa 1 , Sílvia Xargay-Torrent 1 , Elsa Puerto-Carranza 2 , Anna Prats-Puig 3 , Francis de Zegher 4 , Lourdes Ibañez 5 , Abel López-Bermejo 1 & Judit Bassols 1
1Pediatrics, Girona Biomedical Research Institute (IDIBGI), Salt, Spain; 2Pediatrics, Dr. Josep Trueta Hospital, Girona, Spain; 3Department of Physical Therapy, EUSES University of Girona, Salt, Spain; 4Department of Development & Regeneration, University of Leuven, Leuven, Belgium; 5Endocrinology, Hospital Sant Joan de Déu, University of Barcelona, Barcelona, Spain
Background and Aims: Gestational obesity can cause metabolic programming in the offspring. Epigenetic modifications of DNA have been suggested as potential mechanisms underlying this programming. FRAT-1 is a gene involved in the WNT signaling pathway, which is an important regulator of adipose tissue development. The objective of this work was to study the methylation status of FRAT-1 in placentas of women with either normal weight or gestational obesity and its association with endocrine-metabolic parameters in the offspring at 6 years of age.
Methodology: A global methylation array (Infinium® Methylation EPIC BeadChip) was made in placental samples from 24 pregnant mothers with normal weight and gestational obesity. Two CpGs in FRAT-1 were significantly associated with increased maternal weight during gestation (FDR = 2.20x10-6 and OR = 0.91; FDR = 2.17x10-6 and OR = 0.94). The methylation status of these CpGs in FRAT-1 was validated by pyrosequencing in a cohort of 64 pregnant women (39 with normal weight and 24 with gestational obesity) and its association with endocrine-metabolic parameters [weight, height, body mass index (BMI) and body composition] in the offspring at 6 years of age was assessed.
Results: FRAT-1 methylation status was significantly associated with a lower percentage of total fat mass SDS (r = –0.274; p = 0.037) at 6 years of age. In women with gestational obesity, FRAT-1 methylation was negatively associated with weight-SDS, BMI-SDS, and visceral fat mass-SDS (r from –0.409 to –0.599; all P <0.05). In multivariate analysis, adjusted for confounding variables, the placental methylation status of FRAT-1 was a predictor of the percentage of fat mass-SDS at 6 years of age (β = –0.263; p = 0.041; R2 = 0.140); as well as of weight-SDS (β = –0.552; p = 0.030; R2 = 0.060), BMI-SDS (β = –0.713; p = 0.003; R2 = 0.232) and visceral fat-SDS (β = –0.452; p = 0.042; R2 = 0.319) in the offspring of mothers with gestational obesity.
Conclusions: Our results suggest that the methylation of the FRAT-1 may play a role in regulating the body composition of the offspring at 6 years of age. This methylation may explain, at least in part, the metabolic programming in the offspring caused by gestational obesity.
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