-
Endocrinology May 2018Growth hormone (GH), an endocrine hormone, primarily secreted from the anterior pituitary, stimulates growth, cell reproduction, and regeneration and is a major... (Review)
Review
Growth hormone (GH), an endocrine hormone, primarily secreted from the anterior pituitary, stimulates growth, cell reproduction, and regeneration and is a major regulator of postnatal growth. Humans have two GH genes that encode two versions of GH proteins: a pituitary version (GH-N/GH1) and a placental GH-variant (GH-V/GH2), which are expressed in the syncytiotrophoblast and extravillous trophoblast cells of the placenta. During pregnancy, GH-V replaces GH-N in the maternal circulation at mid-late gestation as the major circulating form of GH. This remarkable change in spatial and temporal GH secretion patterns is proposed to play a role in mediating maternal adaptations to pregnancy. GH-V is associated with fetal growth, and its circulating concentrations have been investigated across a range of pregnancy complications. However, progress in this area has been hindered by a lack of readily accessible and reliable assays for measurement of GH-V. This review will discuss the potential roles of GH-V in normal and pathological pregnancies and will touch on the assays used to quantify this hormone.
Topics: Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Diabetes, Gestational; Down Syndrome; Female; Fetal Growth Retardation; Fetal Macrosomia; Gestational Trophoblastic Disease; Growth Hormone; Humans; Placental Hormones; Pregnancy; Pregnancy Complications; Pregnancy in Diabetics; Pregnancy, Ectopic; Protein Isoforms; Trisomy 18 Syndrome
PubMed: 29659791
DOI: 10.1210/en.2018-00037 -
Placenta Apr 2002Placental growth hormone (PGH) is the product of the GH-V gene, predominantly expressed in the syncytiotrophoblast layer of the human placenta. PGH differs from... (Review)
Review
Placental growth hormone (PGH) is the product of the GH-V gene, predominantly expressed in the syncytiotrophoblast layer of the human placenta. PGH differs from pituitary growth hormone by 13 amino acids and possesses one glycosylation site. It has high somatogenic and low lactogenic activities. In the maternal circulation from 12-20 weeks up to term, PGH gradually replaces pituitary growth hormone, which becomes undetectable. PGH is secreted by the placenta in a non-pulsatile manner. This continuous secretion appears to have important implications for physiological adjustment to gestation and especially in the control of maternal IGF1 levels. PGH secretion is regulated in vitro and in vivo by glucose. Lower maternal levels of PGH are observed in pregnancies with fetal growth retardation. PGH is one example of a trophoblast hormone, which allows maternal metabolic adaptation to pregnancy. In addition, our recent data on its expression in invasive extravillous trophoblasts suggest that the physiological role of PGH might also include a direct influence of this hormone on placental development via an autocrine or paracrine mechanism.
Topics: Adult; Female; Gestational Age; Growth Hormone; Humans; Maternal-Fetal Exchange; Organ Culture Techniques; Placental Hormones; Pregnancy; Trophoblasts
PubMed: 11978064
DOI: 10.1053/plac.2002.0811 -
American Journal of Obstetrics and... Dec 1997Placental growth hormone is the product of the GH-V gene specifically expressed in the syncytiotrophoblast layer of the human placenta. Placental growth hormone differs... (Review)
Review
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.
Topics: Growth Hormone; Humans; Insulin-Like Growth Factor I; Placental Hormones; Receptors, Cell Surface
PubMed: 9423763
DOI: 10.1016/s0002-9378(97)70103-0 -
Current Diabetes Reviews Aug 2009Gestational diabetes mellitus (GDM) and pre-gestational diabetes are known to pose risks to the mother and developing fetus, often related to abnormal fetal growth. One... (Review)
Review
Gestational diabetes mellitus (GDM) and pre-gestational diabetes are known to pose risks to the mother and developing fetus, often related to abnormal fetal growth. One potential mediator of maternal effects on fetal growth is Placental Growth Hormone (PGH). PGH is produced by the syncytiotrophoblast and found predominantly in the maternal circulation. It progressively replaces pituitary growth hormone (hGH) in the human maternal circulation from mid-gestation onwards, peaking towards term. PGH appears to be an important potential regulator of maternal insulin resistance in human pregnancy and may influence fetal growth both by modifying substrate availability and through paracrine actions in the placental bed. The details of PGH regulation remain relatively poorly understood, but current evidence does suggest a central role in growth restricted pregnancies. There is currently less evidence of a pathophysiologic role in production of the macrosomic fetal phenotype commonly seen in response to hyperglycaemia, although our recent in vitro studies do raise the possibility of feto-placental feedback as a mechanism of growth modulation.
Topics: Diabetes, Gestational; Female; Fetal Development; Gene Expression Regulation, Developmental; Growth Hormone; Humans; Insulin-Like Growth Factor I; Placental Hormones; Pregnancy; Trophoblasts
PubMed: 19689253
DOI: 10.2174/157339909788920947 -
Placenta Mar 2008The placentas of ruminants and muroid rodents express prolactin (PRL)-related genes whereas the placentas of anthropoid primates express growth hormone (GH)-related... (Review)
Review
The placentas of ruminants and muroid rodents express prolactin (PRL)-related genes whereas the placentas of anthropoid primates express growth hormone (GH)-related genes. The evolution of placental expression is associated with accelerated evolution of the corresponding pituitary hormone and destabilization of conserved endocrine systems. In particular, placental hormones often evolve novel interactions with new receptors. The adaptive functions of some placental hormones may be revealed only under conditions of physiological stress.
Topics: Animals; Endocrine System; Female; Growth Hormone; Humans; Placenta; Placental Hormones; Pregnancy; Prolactin
PubMed: 17981323
DOI: 10.1016/j.placenta.2007.09.010 -
Journal of Pediatric Endocrinology &... Apr 2000The human growth hormone (hGH)/human placental lactogen (hPL) gene family, which consists of two GH and three PL genes, is important in the regulation of maternal and... (Review)
Review
The human growth hormone (hGH)/human placental lactogen (hPL) gene family, which consists of two GH and three PL genes, is important in the regulation of maternal and fetal metabolism and the growth and development of the fetus. During pregnancy, pituitary GH (hGH-N) expression in the mother is suppressed; and hGH-V, a GH variant expressed by the placenta, becomes the predominant GH in the mother. hPL, which is the product of the hPL-A and hPL-B genes, is secreted into both the maternal and fetal circulations after the sixth week of pregnancy. hGH-V and hPL act in concert in the mother to stimulate insulin-like growth factor (IGF) production and modulate intermediary metabolism, resulting in an increase in the availability of glucose and amino acids to the fetus. In the fetus, hPL acts via lactogenic receptors and possibly a unique PL receptor to modulate embryonic development, regulate intermediary metabolism and stimulate the production of IGFs, insulin, adrenocortical hormones and pulmonary surfactant. hGH-N, which is expressed by the fetal pituitary, has little or no physiological actions in the fetus until late in pregnancy due to the lack of functional GH receptors on fetal tissues. hGH-V, which is also a potent somatogenic hormone, is not released into the fetus. Taken together, studies of the hGH/hPL gene family during pregnancy reveal a complex interaction of the hormones with one another and with other growth factors. Additional investigations are necessary to clarify the relative roles of the family members in the regulation of fetal growth and development and the factors that modulate the expression of the genes.
Topics: Embryonic and Fetal Development; Female; Gene Deletion; Growth Hormone; Human Growth Hormone; Humans; Pituitary Gland; Placental Hormones; Placental Lactogen; Pregnancy
PubMed: 10776988
DOI: 10.1515/jpem.2000.13.4.343 -
Biology of Reproduction Jul 2004Progesterone is unequivocally required for maternal support of conceptus (embryo/fetus and associated extraembryonic membranes) survival and development. In cyclic... (Review)
Review
Progesterone is unequivocally required for maternal support of conceptus (embryo/fetus and associated extraembryonic membranes) survival and development. In cyclic sheep, progesterone is paradoxically involved in suppressing and then initiating development of the endometrial luteolytic mechanism. In cyclic and pregnant sheep, progesterone negatively autoregulates progesterone receptor (PR) gene expression in the endometrial luminal (LE) and superficial glandular epithelium (GE). In cyclic sheep, PR loss is closely followed by increases in epithelial estrogen receptor (ERalpha) and then oxytocin receptor (OTR), allowing oxytocin to induce uterine release of luteolytic prostaglandin F2alpha pulses. In pregnant sheep, the conceptus produces interferon tau (IFNtau) that acts on the endometrium to inhibit transcription of the ERalpha gene and thus development of the endometrial luteolytic mechanism. After Day 13 of pregnancy, the endometrial epithelia do not express the PR, whereas the stroma and myometrium remain PR positive. The absence of PR in the endometrial GE is required for onset of differentiated function of the glands during pregnancy. The sequential, overlapping actions of progesterone, IFNtau, placental lactogen (PL), and growth hormone (GH) comprise a hormonal servomechanism that regulates endometrial gland morphogenesis and terminal differentiated function during gestation. In pigs, estrogen, the pregnancy-recognition signal, increases fibroblast growth factor 7 (FGF-7) expression in the endometrial LE that, in turn, stimulates proliferation and differentiated functions of the trophectoderm, which expresses the receptor for FGF-7. Strategic manipulation of these physiological mechanisms may offer therapeutic schemes to improve uterine capacity, conceptus survival, and reproductive health of domestic animals and humans.
Topics: Animals; Animals, Domestic; Female; Placental Hormones; Pregnancy; Pregnancy, Animal; Progesterone; Sheep; Swine; Uterus
PubMed: 14973264
DOI: 10.1095/biolreprod.103.024133 -
Journal of Diabetes Research 2019Insulin resistance changes over time during pregnancy, and in the last half of the pregnancy, insulin resistance increases considerably and can become severe, especially... (Review)
Review
Insulin resistance changes over time during pregnancy, and in the last half of the pregnancy, insulin resistance increases considerably and can become severe, especially in women with gestational diabetes and type 2 diabetes. Numerous factors such as placental hormones, obesity, inactivity, an unhealthy diet, and genetic and epigenetic contributions influence insulin resistance in pregnancy, but the causal mechanisms are complex and still not completely elucidated. In this review, we strive to give an overview of the many components that have been ascribed to contribute to the insulin resistance in pregnancy. Knowledge about the causes and consequences of insulin resistance is of extreme importance in order to establish the best possible treatment during pregnancy as severe insulin resistance can result in metabolic dysfunction in both mother and offspring on a short as well as long-term basis.
Topics: Adipokines; Chorionic Gonadotropin; Cytokines; Diabetes, Gestational; Diet; Epigenesis, Genetic; Estradiol; Exosomes; Female; Gastrointestinal Microbiome; Genetic Predisposition to Disease; Gestational Age; Growth Hormone; Humans; Hydrocortisone; Insulin Resistance; Obesity, Maternal; Placenta; Placental Hormones; Placental Lactogen; Polycystic Ovary Syndrome; Pregnancy; Progesterone; Prolactin; Sedentary Behavior
PubMed: 31828161
DOI: 10.1155/2019/5320156 -
Physiological Reviews Oct 2012Placenta has a wide range of functions. Some are supported by novel genes that have evolved following gene duplication events while others require acquisition of gene... (Review)
Review
Placenta has a wide range of functions. Some are supported by novel genes that have evolved following gene duplication events while others require acquisition of gene expression by the trophoblast. Although not expressed in the placenta, high-affinity fetal hemoglobins play a key role in placental gas exchange. They evolved following duplications within the beta-globin gene family with convergent evolution occurring in ruminants and primates. In primates there was also an interesting rearrangement of a cassette of genes in relation to an upstream locus control region. Substrate transfer from mother to fetus is maintained by expression of classic sugar and amino acid transporters at the trophoblast microvillous and basal membranes. In contrast, placental peptide hormones have arisen largely by gene duplication, yielding for example chorionic gonadotropins from the luteinizing hormone gene and placental lactogens from the growth hormone and prolactin genes. There has been a remarkable degree of convergent evolution with placental lactogens emerging separately in the ruminant, rodent, and primate lineages and chorionic gonadotropins evolving separately in equids and higher primates. Finally, coevolution in the primate lineage of killer immunoglobulin-like receptors and human leukocyte antigens can be linked to the deep invasion of the uterus by trophoblast that is a characteristic feature of human placentation.
Topics: Animals; Female; Humans; Maternal-Fetal Exchange; Placenta; Placental Hormones; Placentation; Pregnancy
PubMed: 23073626
DOI: 10.1152/physrev.00040.2011 -
Growth Hormone & IGF Research :... Apr 2006Placental growth hormone (PGH) has been known for 20 years. Nevertheless, its physiology is far from understood. In this review, basal aspects of PGH physiology are... (Review)
Review
Placental growth hormone (PGH) has been known for 20 years. Nevertheless, its physiology is far from understood. In this review, basal aspects of PGH physiology are summarised and put in relation to the highly homologous pituitary growth hormone (GH). During normal pregnancy, PGH progressively replaces GH and reach maximum serum concentrations in the third trimester. A close relationship to insulin-like growth factor (IGF)-I and -II levels is observed. Furthermore, PGH levels are positively associated to fetal growth. The potential importance of growth hormone receptors and binding protein for PGH effects is discussed. Finally, the review outlines current knowledge of PGH in pathological pregnancies.
Topics: Female; Growth Hormone; Humans; Placental Hormones; Pregnancy; Pregnancy Complications; Pregnancy Trimester, Third; Sequence Homology, Amino Acid
PubMed: 16632396
DOI: 10.1016/j.ghir.2006.03.010