Title :

Maternal obesity programs increased leptin gene expression in rat male offspring via epigenetic modifications in a depot-specific manner

Author(s) :

Lecoutre, Simon [Auteur]
Environnement périnatal et croissance - EA 4489 [EPS]
Oger, Frederik [Auteur]
Environnement périnatal et croissance - EA 4489 [EPS]
Pourpe, Charlène [Auteur]
Environnement périnatal et croissance - EA 4489 [EPS]
Butruille, Laura [Auteur]
Environnement périnatal et croissance - EA 4489 [EPS]
Marousez, Lucie [Auteur]
Environnement périnatal et croissance - EA 4489 [EPS]
Dickes-Coopman, Anne [Auteur]
Environnement périnatal et croissance - EA 4489 [EPS]
Laborie, Christine [Auteur]
Environnement périnatal et croissance - EA 4489 [EPS]
Guinez, Céline [Auteur]
Environnement périnatal et croissance - EA 4489 [EPS]
LESAGE, JEAN [Auteur]
Environnement périnatal et croissance - EA 4489 [EPS]
vieau, didier [Auteur]
Environnement périnatal et croissance - EA 4489 [EPS]
Junien, Claudine [Auteur]
Université de Versailles Saint-Quentin-en-Yvelines [UVSQ]
Université Paris-Saclay
Biologie du Développement et Reproduction [BDR]
Eberlé, Delphine [Auteur]
Environnement périnatal et croissance - EA 4489 [EPS]
Gabory, Anne [Auteur]
Université Paris-Saclay
Biologie du Développement et Reproduction [BDR]
Eeckhoute, Jérôme [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Breton, Christophe [Auteur]
Environnement périnatal et croissance - EA 4489 [EPS]

Journal title :

Molecular metabolism

Pages :

922-930

Publisher :

Elsevier

Publication date :

2017

ISSN :

2212-8778

Keyword(s) :

tissu adipeux
leptine
expression génique
obésité
épigénétique
immunoprécipitation
modification épigénique
chromatine

English keyword(s) :

Developmental origin of health and disease
Epigenetic mechanisms
Fat expansion
Perinatal programming
adipose tissue
gene expression
obesity
immunoprecipitation reaction
chromatin

HAL domain(s) :

Sciences du Vivant [q-bio]/Biologie du développement

English abstract : [en]

According to the Developmental Origin of Health and Disease (DOHaD) concept, maternal obesity and accelerated growth in neonates predispose offspring to white adipose tissue (WAT) accumulation. In rodents, adipogenesis ...
Show more >According to the Developmental Origin of Health and Disease (DOHaD) concept, maternal obesity and accelerated growth in neonates predispose offspring to white adipose tissue (WAT) accumulation. In rodents, adipogenesis mainly develops during lactation. The mechanisms underlying the phenomenon known as developmental programming remain elusive. We previously reported that adult rat offspring from high-fat diet-fed dams (called HF) exhibited hypertrophic adipocyte, hyperleptinemia and increased leptin mRNA levels in a depot-specific manner. We hypothesized that leptin upregulation occurs via epigenetic malprogramming, which takes place early during development of WAT.As a first step, we identified in silico two potential enhancers located upstream and downstream of the leptin transcription start site that exhibit strong dynamic epigenomic remodeling during adipocyte differentiation. We then focused on epigenetic modifications (methylation, hydroxymethylation, and histone modifications) of the promoter and the two potential enhancers regulating leptin gene expression in perirenal (pWAT) and inguinal (iWAT) fat pads of HF offspring during lactation (postnatal days 12 (PND12) and 21 (PND21)) and in adulthood.PND12 is an active period for epigenomic remodeling in both deposits especially in the upstream enhancer, consistent with leptin gene induction during adipogenesis. Unlike iWAT, some of these epigenetic marks were still observable in pWAT of weaned HF offspring. Retained marks were only visible in pWAT of 9-month-old HF rats that showed a persistent "expandable" phenotype.Consistent with the DOHaD hypothesis, persistent epigenetic remodeling occurs at regulatory regions especially within intergenic sequences, linked to higher leptin gene expression in adult HF offspring in a depot-specific manner.Show less >

Language :

Anglais

Peer reviewed article :

Oui

Audience :

Non spécifiée

Popular science :

Non

Collections :

• Récepteurs nucléaires, Maladies Cardiovasculaires et Diabète (EGID) - U1011

Source :

Harvested from HAL