Fetal stress, including inadequate nutrient supply and cessation of fetal growth, are major stimuli to the onset of parturition which acts to promote maturation of the hypothalamic-pituitary axis. These adaptations, together with rapid removal of lung liquid fluid and onset of endogenous heat production at birth, ensure oxygen supply is adequate and hypothermia prevented. A critical component of fetal organ maturation in preparation for life after birth is mitochondrial development. In adipose tissue, for example, the abundance of inner (e.g. uncoupling proteins) and outer (e.g. voltage dependent anion channel) mitochondrial protein peaks near to term. The parallel increases in fetal plasma hormone concentrations (e.g. leptin, prolactin, cortisol and thyroid hormones) and hormone receptor (e.g. prolactin receptor) abundance around the time of parturition act to promote mitochondrial protein synthesis. Hormonal manipulation of the fetus with individual or a combination of, these hormones act to promote both lung and adipose tissue development thereby preventing complications associated with prematurity.
After birth, as metabolic rate declines in conjunction with loss of hormone receptor populations the newborn adapts from being in a catabolic hormonal environment to one in which anabolic stimuli are dominant. The greatest increase in organ weight during postnatal life is that of adipose tissue which is important in preventing excess heat loss and possibly in resetting appetite as a consequence of changes in leptin secretion. At this time hormonal treatment may have the reverse effect to that observed prenatally. Endocrine strategies aimed at promoting fetal development can have very different effects after birth and could alleviate mitochondrial dysfunction associated with inadequate nutrition during different stages of fetal development.
08 - 11 Apr 2002
British Endocrine Societies