Keynote speech at the EliteOva Annual Meeting 2019
We are happy to invite you to watch this year’s keynote speech by Professor Mette Olaf Nielsen titled ‘Fetal programming and long-term implications for development and metabolic and endocrine function’. The presentation is part of the EliteOva Annual Meeting and is taking place inside the Swan Library, Grønnegårdsvej 7, 1st floor, at the UCPH Frederiksberg Campus on March 6, 2019 from 10.40 to 11.25 am. No prior registration is required.
Abstract
Mette Olaf Nielsen1, Prabhat Khanal2, Morteza Mansouryar1 and Sharmila Binti Ahmed1
1 Department of Veterinary and Animal Sciences, University of Copenhagen, Denmark
2 Faculty of Bioscience and Aquaculture, Nord University, Norway
In the early 1990’ies, reports based on human epidemiological research revolutionized the scientific view of the importance of foetal life development for body functions in postnatal life. Until then, it was believed that the genome received from the parents at conception in mammals would define the phenotype at birth and the ability of an individual to cope with the postnatal environment. Since then, it has been clearly demonstrated that malnourishment during fetal life can predispose to a wide range of developmental disorders later in life. This is due to a phenomenon termed foetal programming (FP), which alters the way the genome becomes phenotypically expressed. In our Copenhagen sheep model, we have demonstrated that FP induced by late gestation malnutrition in the form of either under- or overnutrition interferes with postnatal growth and development and functions of a wide range of metabolic and endocrine systems, which are key to farm animal productivity and animal aa well as human health. Birth appears to be a critical set point for when permanent programming effects are induced in precocial species such as sheep. Phenotypical manifestations of FP are not clearly observable at birth, but become increasingly manifested as the animal approaches adulthood. It alters the developmental trajectory resulting in smaller adult body size and induces permanent changes in the glucose-insulin-axis (but not glucagon) and all hypothalamic-pituitary-endocrine axis hitherto studies. The ability of adipose tissues to expand by healthy hyperplasic as compared to unhealthy hypertrophic growth is also negatively affected, but in a tissue specific way. Males appear to attain a more female phenotype in response to adverse pre- and postnatal nutritional exposures, whereas females are more resistant to long-term adverse outcomes in adipose tissue expandability.
The accumulating evidence suggest that the consequences of FP for both farm animal productivity and human health trajectory are so significant that we need to incorporate the foetal life history into future decision making tools and nutritional strategies, particularly because FP traits can be passed on to the next generations by epigenetic mechanisms.