Placental growth hormone (PGH), pituitary growth hormone (GH1), insulin-like growth factor (IGF-I) and ghrelin in pregnant women’s blood serum

Kędzia, Andrzej W.; Tarka, Agata; Petriczenko, Elżbieta; Pruski, Dominik; Iwaniec, Kinga

doi:10.17772/gp/1614

Cited by 6 publications

(5 citation statements)

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“…During pregnancy, the concentration of PGH and IGF-I increases proportionately and, following delivery, their concentration decreases. GH1 blockade appears to be released during labor and delivery, and its level increases three-fold, it then returns to normal postpartum ( 49 ). Pedersen et al ( 50 ) conducted a study to investigate whether maternal levels of PGH, IGF-I and hPL are associated with the growth rate of biparietal diameter during the first half of gestation.…”

Section: Pgh In Pregnancy and Fetal Growthmentioning

confidence: 99%

Human placental growth hormone in normal and abnormal fetal growth

2017

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Human placental growth hormone (PGH), encoded by the growth hormone (GH) variant gene on chromosome 17, is expressed in the syncytiotrophoblast and extravillous cytotrophoblast layers of the human placenta. Its maternal serum levels increase throughout pregnancy, and gradually replaces the pulsatile secreted pituitary GH. PGH is also detectable in cord blood and in the amniotic fluid. This placental-origin hormone stimulates glyconeogenesis, lipolysis and anabolism in maternal organs, and influences fetal growth, placental development and maternal adaptation to pregnancy. The majority of these actions are performed indirectly by regulating maternal insulin-like growth factor-I levels, while the extravillous trophoblast involvement indicates a direct effect on placental development, as it stimulates trophoblast invasiveness and function via a potential combination of autocrine and paracrine mechanisms. The current review focuses on the role of PGH in fetal growth. In addition, the association of PGH alterations in maternal circulation and placental expression in pregnancy complications associated with abnormal fetal growth is briefly reviewed.

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Section: Pgh In Pregnancy and Fetal Growthmentioning

confidence: 99%

Human placental growth hormone in normal and abnormal fetal growth

2017

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“…Circulating levels of ghrelin increase throughout normal gestation in both the human and rat and originate from maternal, placental, and fetal sources 29‐31 . Ghrelin and its receptor are present as early as the blastocyst stage of embryo development 31 .…”

Section: Introductionmentioning

confidence: 99%

“…28 Circulating levels of ghrelin increase throughout normal gestation in both the human and rat and originate from maternal, placental, and fetal sources. [29][30][31] Ghrelin and its receptor are present as early as the blastocyst stage of embryo development. 31 Maternal ghrelin levels are positively associated with neonatal waist circumference (ie, the higher the maternal ghrelin the larger the baby).…”

Section: Introductionmentioning

confidence: 99%

“…[29][30][31] Ghrelin and its receptor are present as early as the blastocyst stage of embryo development. 31 Maternal ghrelin levels are positively associated with neonatal waist circumference (ie, the higher the maternal ghrelin the larger the baby). 32 Likewise, exogenous ghrelin administration in pregnant rats increases the size of pups at birth, even when food intake is controlled in the dam.…”

Section: Introductionmentioning

confidence: 99%

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Ghrelin signalling is dysregulated in male but not female offspring in a rat model of maternal vertical sleeve gastrectomy

Spann

Welch

Grayson

2020

J Neuroendocrinology

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Bariatric surgery is the most effective and durable means of treating obesity and its comorbidities. Women make up 80% of those receiving weight loss surgery and they experience improvements in fertility. Unfortunately, bariatric surgery in the context of pregnancy is associated with complications, including growth restriction and small‐for‐gestational age offspring (SGA). SGA offspring have a greater risk for obesity in adulthood, although the mechanism for this SGA‐induced obesity is unknown. In a rat model of vertical sleeve gastrectomy (VSG), we previously identified reductions during pregnancy in ghrelin, a stomach‐derived hormone that increases appetite and induces growth hormone secretion. Here, we hypothesise that VSG offspring will have altered ghrelin signalling compared to offspring of Sham dams as a result of reduced in utero ghrelin. At postnatal day (PND)21, male and female offspring of dams that have previously received VSG have an increase in mRNA expression for the ghrelin receptor in the hypothalamus compared to Sham offspring, and the expression of GOAT is lower in females compared to males. Liver expression of endogenous ghrelin antagonist, LEAP2, is elevated at PND60 in VSG offspring. Expression of other genes in the growth hormone system (growth hormone‐releasing hormone and growth hormone) were not altered. Plasma levels of total ghrelin at PND21 are also not different between VSG and Sham pups. In adult pups, 1‐hour chow intake of male but not female VSG offspring given is less than Sham offspring when given 50 µg kg‐1 of exogenous ghrelin by i.p. injection. These results indicate that maternal VSG surgery has an impact on ghrelin signalling in offspring and that, as adults, male VSG offspring may be functionally less responsive to ghrelin than controls.

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“…Moreover, VEGF-A facilitates the initial glucose-induced injury in retinal endothelial cells [25]. Furthermore, during pregnancy, placental growth hormone assumes the role of growth hormone, modulating the secretion of insulin-like growth factor (IGF) [50][51][52]. IGF-I exerts a proangiogenic effect on retinal blood vessels [53].…”

Section: Growth Factorsmentioning

confidence: 99%

Pregnancy and diabetic retinopathy

Rashidian

2024

Med Hypothesis Discov Innov Optom

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Background: An increase in the worldwide prevalence of diabetes, especially among younger populations, has led to a higher prevalence of pre-existing diabetes among pregnant women. The precise mechanisms underlying the development or progression of diabetic retinopathy (DR) during pregnancy are not entirely understood. This narrative review incorporates all available data to offer fresh insights into the pathogenesis and mechanisms of the pregnancy-induced development and/or progression of DR. Moreover, the author aims to offer clinical recommendations for DR both before conception and during pregnancy to appropriately counsel these susceptible patients. Methods: A literature search was performed using various combinations of the following keywords: diabetes, pregnancy, diabetic retinopathy, ocular, eye, retina, microangiopathy, mechanism, pathophysiology, hyperglycemia, hypoxia, neovascularization, growth factors, immune system, blood flow, and recommendations. The search was conducted using PubMed/MEDLINE, ISI Web of Science, Scopus, and Google Scholar, and only English articles published from January 1, 2020, to December 31, 2023, involving human participants, were considered. The International Diabetes Federation Diabetes Atlas website was searched for clinical recommendations. Results: Pregnancy-induced hyperglycemia, blood flow changes, growth factors, and the immune system play important roles in the development and progression of DR. Hyperglycemia leads to significant stress on the capillary endothelium through increased glucose flux via the polyol and hexosamine pathways, activation of protein kinase C, and increased formation of advanced glycation end-products. These pathways act in several ways that may lead to increased oxidative stress, inflammation, and vascular blockage. Thus, eye examinations are crucial before, during, and up to 12 months after pregnancy. Individuals with severe non-proliferative and proliferative DR should gradually decrease their blood glucose levels to near-normal levels over a period of 6 months before conception. Statins and medications inhibiting the renin–angiotensin system should be discontinued before pregnancy or at the initial antenatal visit if they are still being used. Retinal examinations should be performed shortly after conception and during the first trimester using tropicamide eye drops and digital imaging. Subsequent examinations should be scheduled based on DR severity at the initial examination. Conclusions: While the precise mechanism underlying the progression of DR during pregnancy remains uncertain, the available literature suggests that pregnancy-induced hyperglycemia, blood flow changes, growth factors, and the immune system play important roles in its development and progression. Pregnant women with diabetic eye manifestations benefit from the expertise of multidisciplinary teams comprising ophthalmologists, diabetologists, and gynecologists to improve both maternal and perinatal outcomes. Moreover, postpartum follow-up requires special attention.

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Placental growth hormone (PGH), pituitary growth hormone (GH1), insulin-like growth factor (IGF-I) and ghrelin in pregnant women’s blood serum

Cited by 6 publications

References 0 publications

Human placental growth hormone in normal and abnormal fetal growth

Human placental growth hormone in normal and abnormal fetal growth

Ghrelin signalling is dysregulated in male but not female offspring in a rat model of maternal vertical sleeve gastrectomy

Pregnancy and diabetic retinopathy

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