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Diet during Pregnancy is Implicated in the Regulation of Hypothalamic RNA Methylation and Risk of Obesity in Offspring
Author(s) -
Kaspi Antony,
Khurana Ishant,
Ziemann Mark,
Connor Timothy,
Spolding Briana,
Zimmet Paul,
Walder Ken,
ElOsta Assam
Publication year - 2018
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201800134
Subject(s) - offspring , biology , endocrinology , medicine , epigenetics , obesity , pregnancy , type 2 diabetes , phenotype , diabetes mellitus , gene , genetics
Scope Early life nutrition has long‐lasting influence in adults through key mediators that modulate epigenetic states, although the determinants involved that underlie this response remain controversial. Because of the similarities between metabolic, physiological, and endocrine changes and those occurring in human type 2 diabetes, we studied the interaction of diet during pregnancy regulating RNA adenosine methylation (N6‐methyladenosine [m6A]) and the transcriptome in Psammomys obesus . Methods and results Breeding pairs were randomly allocated standard diet (total digestible energy 18 MJ kg −1 ) or low‐fat diet (15 MJ kg −1 ). Offspring were weaned onto the low‐fat diet at 4 weeks of age and given ad libitum access, resulting in two experimental groups: 1) male offspring of animals fed a low‐fat diet and weaned onto the low‐fat diet and 2) male offspring of animals fed a standard diet and weaned onto the low‐fat diet. Hypothalamic RNA was used to assess m6A by immunoprecipitation. Parental low‐fat diet alters the metabolic phenotype in offspring. An association between parental diet and hypothalamic m6A was observed in regulating the expression of FTO and METTL3 in the offspring. Conclusions We propose the regulatory capacity is now broadened for the first time to include m6A in developmental programming and obesity phenotype.