Human placental growth hormone

• Published in: American journal of obstetrics and gynecology 1997-12, Vol.177 (6), p.1526-1534
• Main Authors: Alsat, E., Guibourdenche, J., Luton, D., Frankenne, F., Evain-Brion, D.
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; fetal growth; Fundamental and applied biological sciences. Psychology; Growth hormone; Growth Hormone - genetics; Growth Hormone - metabolism; Growth Hormone - physiology; Hormone metabolism and regulation; Humans; Insulin-Like Growth Factor I - metabolism; intrauterine growth restriction; placenta; Placental Hormones - genetics; Placental Hormones - metabolism; Placental Hormones - physiology; Pregnancy. Parturition. Lactation; Receptors, Cell Surface - genetics; Receptors, Cell Surface - metabolism; Vertebrates: reproduction
• ISSN: 0002-9378; 1097-6868
• DOI: 10.1016/S0002-9378(97)70103-0

Placental growth hormone is the product of the GH-V gene specifically expressed in the syncytiotrophoblast layer of the human placenta. Placental growth hormone differs from pituitary growth hormone by 13 amino acids. It has high somatogenic and low lactogenic activities. Assays by specific monoclonal antibodies reveal that in the maternal circulation from 15 to 20 weeks up to term placental growth hormone gradually replaces pituitary growth hormone, which becomes undetectable. It is secreted by the placenta in a nonpulsatile manner. This continuous secretion appears to have important implications for physiologic adjustment to gestation and especially in the control of maternal insulin-like growth factor-I levels. Placental growth hormone secretion is inhibited by glucose in vitro and in vivo and is significantly decreased in the maternal circulation in pregnancies with intrauterine growth restriction. Placental growth hormone does not appear to have a direct effect on fetal growth because this hormone is not detectable in the fetal circulation. However, the physiologic role might also include a direct influence on placental development through an autocrine or paracrine mechanism, as suggested by the presence of specific growth hormone receptors in this tissue.(Am J Obstet Gynecol 1997;177:1526-34.)