ESPEYB19 2. Antenatal and Neonatal Endocrinology Gestational Diabetes Mellitus: Neonatal and Long-term Consequences (4 abstracts)
2.18. Novel epigenetic link between gestational diabetes mellitus and macrosomia
Joyce BT , Liu H , Wang L , Wang J , Zheng Y , Nannini D , Drong A , Shiau S , Li W , Leng J , Shen Y , Gao R , Baccarelli A , Hu G & Hou L
Epigenomics. 2021 Aug;13(15):1221-1230. doi: 10.2217/epi-2021-0096. PMID: 34337972.
Brief Summary: This case cohort study assessed whether epigenetic factors explain the link between gestational diabetes mellitus (GDM) and macrosomia. Epigenetic changes in the MEST gene were associated with both GDM and macrosomia.
GDM leads to neonatal macrosomia and in the long-term to the metabolic syndrome. The underlying mechanisms of the macrosomia and metabolic syndrome are unknown but epigenetic changes might be involved. GDM has been associated with placental DNA methylation changes in some epigenome-wide association studies. It remains unclear which genes or pathways are affected, and whether any placental differential gene methylations are correlated to fetal growth or circulating metabolic health biomarkers
The authors selected 8 genes (IGF1, IGF2, H19, ARHGRF11, MEST, NR3C1, Adiponectin, and RETN) which were known to be involved in GDM and obesogenic pathways and assessed the methylation status of these in GDM mothers and their macrosomic offspring. Epigenetic changes were found mainly in the MEST gene (Mesoderm-specific transcript) which is paternally imprinted and highly expressed in fetal and placental tissue and is believed to play an important role in fetal development.
There is now increasing evidence that downstream pathologies of obesity are amplified or even initiated by molecular changes within the white adipose tissue (WAT). Such changes are the result of an excessive expansion of individual white adipocytes and could potentially be ameliorated via an increase in de novo adipocyte recruitment (adipogenesis). MEST is a protein with a putative yet unidentified enzymatic function and has previously been shown to correlate with adiposity and adipocyte size in mice. MEST expression is upregulated during human adipocyte differentiation, increased in human white adipose tissue in the obese state and significantly correlated with adipocyte volume. Thus, epigenetic changes in MEST may lead to macrosomia in mothers with GDM.
Volume 19
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ESPE Yearbook of Paediatric Endocrinology
ISSN 1662-4009 (Online)
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