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MON-013 Effect of Poor Circumstance in Utero on Adiponectin Gene Expressions Through Epigenetic Changes in Offspring
Author(s) -
Hisashi Masuyama,
Takashi Mitsui,
Eriko Eto,
Kei Hayata
Publication year - 2020
Publication title -
journal of the endocrine society
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.046
H-Index - 20
ISSN - 2472-1972
DOI - 10.1210/jendso/bvaa046.107
Subject(s) - offspring , adiponectin , epigenetics , endocrinology , in utero , medicine , adipokine , metabolic syndrome , leptin , fetus , dna methylation , gestational diabetes , biology , pregnancy , gene expression , diabetes mellitus , obesity , gene , insulin resistance , gestation , genetics
The links between obesity and metabolic syndrome in parents and their offspring and the role of genes and a shared environment are not completely understood. Adipocytokines play important roles in glucose and lipid metabolism. We have already developed the model mice for transgenerational effect of obesity and metabolic syndrome and demonstrated that exposure to a high fat diet in utero might cause a metabolic syndrome-like phenomenon through epigenetic modifications of adipocytokine, adiponectin and leptin gene expressions in offspring of the model mice. In this study, we examined whether poor circumstance in utero affected the adiponectin gene expression and epigenetic changes of this gene using samples from umbilical cord in patients with hypertensive disorder of pregnancy (HDP) and fetal growth restriction (FGR) or gestational diabetes mellitus (GDM) and heavy for date fetus (HFD) compared with normal pregnant women without HDP, GDM and abnormal fetal growth. We observed that the poor circumstance under HDP with HGR or GDM with HFD caused significantly lower adiponectin gene expression and higher methylation level of histone H3 at lysine 9 of the promoter of adiponectin gene compared with normal control. Thus, poor circumstance in utero affected adiponectin gene expressions through epigenetic modifications, which might result in the increased risk for metabolic syndrome of offspring.

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