期刊
NUTRIENTS
卷 11, 期 2, 页码 -出版社
MDPI
DOI: 10.3390/nu11020233
关键词
maternal and paternal metabolic imprinting; germ cell epigenome; sncRNAs; DOHaD; obesity; diabetes
资金
- CNRS
- ANR (programme Prograbeta) [ANR-06-PHYSIO-028-01]
- Institut Benjamin Delessert (prix Projets de Recherche 2014)
- Societe Francophone du Diabete
- Societe Francaise de Nutrition (prix SFN 2012)
- Societe Francaise de Nutrition (prix SFN 2015)
- ANR [ANR-12-ADAPT-0022]
- Fond Francais pour l'Alimentation et la Sante [12-A-52]
- Labex SIGNALIFE [ANR-11-LABX-0028-01]
- Societe Francaise de Nutrition (prix SFN 2017)
Extensive epidemiological and experimental evidence have shown that exposure to an adverse intrauterine environment as observed in offspring of pregnancies complicated by obesity or diabetes, can program susceptibility to metabolic, endocrine and cardiovascular disorders later in life. Although most studies have concentrated on the maternal environment, it is also becoming evident that paternal exposure to obesity or diabetes can result in the later development of metabolic disorders in the offspring. Such programmed effects might not be limited to the first directly exposed generation, but could be transmitted to subsequent generations. This suggests the existence of mechanisms by which metabolic changes in parental phenotype are transmissible to offspring. The mechanisms which underpin the transmission of the programmed effects across generations are still unclear. However, epigenetic regulation of transcription has emerged as a strong candidate for mediating the heritability of metabolic diseases. Here, we review the most relevant evidence from human and animal studies showing transmission of programming effects of obesity or diabetes across generations, and the current mechanisms underlying either maternal or paternal influences on the metabolic status of offspring.
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