Endocrine Abstracts

Differential changes in placental or fetal growth can result from chronic alterations in the environment depending on their timing and duration. These include thermal stimulation and/or altered photoperiod whose effects may be mediated in part by increased maternal food intake and/or repartitioning of available nutrients across the placenta. Fetal growth can subsequently be enhanced due to increased abundance of fetal anabolic hormones including prolactin. In particular, fetal adipose tissue maturation (e.g. increased uncoupling protein-1 and prolactin receptor abundance) is promoted. As a consequence the resulting offspring are better adapted to respond to the cold challenge of birth.

Decreasing or increasing maternal nutrition (with respect to appetite) over the period of rapid placental compared with fetal growth can have pronounced effects on the fetal glucocorticoid axis (e.g. increased glucocorticoid receptor abundance in adrenal gland, kidney, liver and lung) in the absence of any gross effects on maternal metabolism or fetal weight. These effects are apparent at both the time of, and beyond, the period of nutritional manipulation. They are also closely associated with perturbed placental growth and increased glucose transport capacity. Although maternal cortisol status does not appear to be altered, placental capacity to inactivate cortisol may be decreased. One consequence of nutritionally mediated fetal reprogramming is that the resulting offspring exhibit altered blood pressure sensitivity later in juvenile life.

The support of the BBSRC, British Heart Foundation, Wellcome Trust and Special Trustees of Nottingham University Hospitals is gratefully acknowledged.