Endocrine Regulation of Human Fetal Growth: The Role of the Mother, Placenta, and Fetus

Abstract

The environment in which the fetus develops is critical for its survival and long-term health. The regulation of normal human fetal growth involves many multidirectional interactions between the mother, placenta, and fetus. The mother supplies nutrients and oxygen to the fetus via the placenta. The fetus influences the provision of maternal nutrients via the placental production of hormones that regulate maternal metabolism. The placenta is the site of exchange between mother and fetus and regulates fetal growth via the production and metabolism of growth-regulating hormones such as IGFs and glucocorticoids. Adequate trophoblast invasion in early pregnancy and increased uteroplacental blood flow ensure sufficient growth of the uterus, placenta, and fetus. The placenta may respond to fetal endocrine signals to increase transport of maternal nutrients by growth of the placenta, by activation of transport systems, and by production of placental hormones to influence maternal physiology and even behavior. There are consequences of poor fetal growth both in the short term and long term, in the form of increased mortality and morbidity. Endocrine regulation of fetal growth involves interactions between the mother, placenta, and fetus, and these effects may program long-term physiology.

Litter-size-dependent intrauterine growth restriction in sheep

“…Placentomes are structures containing the uteroplacental complexes responsible for exchange of gases and micronutrients. The placenta is an autocrine, paracrine and endocrine organ that synthesises and secretes a broad range of steroid and peptide hormones which regulate foetal development, and directs maternal physiology to support this process (Anthony et al, 1998;Gootwine, 2004;Murphy et al, 2006).…”

“…Long-term effects IUGR and low BWT of human infants have received special attention because of their long-term effects on adult onset of various diseases (Gluckman and Pinal, 2003;Schwartz and Morrison, 2005;Bloomfield et al, 2006b;De Boo and Harding, 2006;Fowden et al, 2006a;Murphy et al, 2006). Similarly, low BWT was found to have long-term effects in sheep on glucose tolerance and blood pressure at 5 months but not at 30 months of age, and long-term effects at 30 months but not at 5 months of age on insulin tolerance and circulating levels of IGF1 (Oliver et al, 2002).…”

“…This reprogramming event may take place at mid gestation, after day 50 of pregnancy, as it was shown that conceptuses at that stage retain their full growth potential (Vatnick et al, 1991). Regulation of foetal growth involves multidirectional interactions between the mother, the placenta and the foetus (Murphy et al, 2006). Reprogramming patterns of conceptus growth by attenuating placental growth and function, i.e.…”

Timing of fetal exposure to stress hormones: Effects on newborn physical and neuromuscular maturation

“…Specifically, during the last trimester of pregnancy, exposure to cortisol is critical for the maturation of fetal physiological systems and organs, such as the cardiovascular system, the pulmonary system, renal systems, and overall fetal growth (Murphy, Smith, Giles, & Clifton, 2006;Trainer, 2002;Welberg, Seckl, & Holmes, 2001). Despite the necessity of cortisol for fetal maturation, it has been repeatedly demonstrated that women receiving synthetic corticosteroids (administration commencing typically around the 24th week gestation) were more likely to deliver infants with fetal growth restriction and low birth weight, even when controlling for length of gestation, suggesting that high levels of glucocorticoids may be detrimental to fetal growth (Bloom, Sheffield, McIntire, & Leveno, 2001;French, Hagan, Evans, Godfrey, & Newnham, 1999;Reinisch, Simon, Karow, & Gandelman, 1978).…”

Growth and development of adipose tissue and gut and related endocrine status during early growth in the pig: impact of low birth weight

“…In the pig, intrauterine growth retardation, leading to LBW, occurs naturally. The aetiology and underlying mechanisms of intrauterine growth retardation in livestock as well as in humans and rodents have been recently reviewed (McMillen and Robinson, 2005;Foxcroft et al, 2006;Murphy et al, 2006;Wu et al, 2006). It results from alteration in foetal substrate supply.…”