Molecular mechanisms governing offspring metabolic programming in rodent models of in utero stress.
Animal models
DOHAD
Development
Fetal
Metabolism
Programming
Journal
Cellular and molecular life sciences : CMLS
ISSN: 1420-9071
Titre abrégé: Cell Mol Life Sci
Pays: Switzerland
ID NLM: 9705402
Informations de publication
Date de publication:
Dec 2020
Dec 2020
Historique:
received:
25
02
2020
accepted:
27
05
2020
revised:
23
05
2020
pubmed:
5
6
2020
medline:
24
11
2020
entrez:
5
6
2020
Statut:
ppublish
Résumé
The results of different human epidemiological datasets provided the impetus to introduce the now commonly accepted theory coined as 'developmental programming', whereby the presence of a stressor during gestation predisposes the growing fetus to develop diseases, such as metabolic dysfunction in later postnatal life. However, in a clinical setting, human lifespan and inaccessibility to tissue for analysis are major limitations to study the molecular mechanisms governing developmental programming. Subsequently, studies using animal models have proved indispensable to the identification of key molecular pathways and epigenetic mechanisms that are dysregulated in metabolic organs of the fetus and adult programmed due to an adverse gestational environment. Rodents such as mice and rats are the most used experimental animals in the study of developmental programming. This review summarises the molecular pathways and epigenetic mechanisms influencing alterations in metabolic tissues of rodent offspring exposed to in utero stress and subsequently programmed for metabolic dysfunction. By comparing molecular mechanisms in a variety of rodent models of in utero stress, we hope to summarise common themes and pathways governing later metabolic dysfunction in the offspring whilst identifying reasons for incongruencies between models so to inform future work. With the continued use and refinement of such models of developmental programming, the scientific community may gain the knowledge required for the targeted treatment of metabolic diseases that have intrauterine origins.
Identifiants
pubmed: 32494846
doi: 10.1007/s00018-020-03566-z
pii: 10.1007/s00018-020-03566-z
pmc: PMC7658077
doi:
Substances chimiques
Insulin
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
4861-4898Subventions
Organisme : Medical Research Council
ID : MR/R022690/1
Pays : United Kingdom
Organisme : Medical Research Council (UK)
ID : RG93186
Organisme : Royal Society
ID : RG74249
Organisme : Lister Institute of Preventive Medicine
ID : RG93692
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