The role of growth hormone (GH) and the related placental lactogens in implantation and subsequent embryonic and fetal development is an enigma. Firstly, these peptides are abundant in both the fetal and maternal circulation. The variant growth hormone (hGH-V) is expressed by the placental syncytiotrophoblast and is released into the maternal circulation. It is not detectable in fetal blood. Fetal pituitary (GH) is abundant but is not a primary stimulus to human fetal musculoskeletal growth, since hypopituitary newborn infants have near-normal birth size. However, pituitary hGH has been shown to stimulate pancreatic islet growth and insulin release in vitro, and to be a mitogen for fetal hepatocytes obtained in late first trimester. This selectivity of action is confirmed by the immunohistochemical localization of hGH receptor in the human fetal kidney, endocrine pancreas, liver, skin and brain during the first and second trimester, and their absence from the musculoskeletal system, gut and lung. High-affinity human placental lactogen (hPL) receptors are abundant in animal and human fetal tissues, and hPL can attain concentrations of 10 nM in the human fetal circulation. In vitro data strongly suggest anabolic and mitogenic actions for PL on fetal tissues, including amino acid transport, hepatic glycogenesis, protein synthesis, and stimulation of insulin-like growth factor and insulin release. The PL axis in the fetus is influenced by maternal nutrition. Despite these findings, definitive evidence is still lacking that PL contributes to fetal growth and development in utero.