Insulin-Like Growth Factors
Jason Kelley in Cytokines of the Lung, 2022
The IGF-I transcripts are found in greater abundance postnatally and, with the exception of brain, are present at a higher level than IGF-II in all postnatal tissues. Either growth hormone deficiency or malnutrition will result in decreased IGF-I gene expression. The reduction in expression is seen as decreased IGF-I transcript and peptide concentrations in numerous organs and is reflected by decreased serum concentrations of IGF-I peptide. Administration of growth hormone or correction of malnutrition results in normalized IGF-I tissue and serum concentrations. Effects on IGF-I expression by other hormones within specific tissues have been described. For example, estrogen enhances IGF-I gene expression in the uterus (Murphy and Friesen, 1988) and parathyroid hormone (as well as growth hormone) stimulates IGF-I gene expression in cartilage (Canalis et al., 1989). Placental lactogen likely affects IGF-I gene expression in the fetus, acting as a growth hormone homologue (Hill et al., 1986, 1988).
Insulin Resistance in Pregnancy
Emilio Herrera, Robert H. Knopp in Perinatal Biochemistry, 2020
Placental lactogen rises to very high levels during pregnancy.34,38 In humans, placental lactogen is secreted as a peptide (hPL) closely related to growth hormone (hGH); whereas in the rat there are two species of placental lactogen: rPLI and rPLII.38 The rPLI form is only secreted between days 11 and 13 of pregnancy, whereas the rPLII form is secreted from day 12 of pregnancy and its circulating levels increase until term. This last form (rPLII) is more related to prolactin than to growth hormone, and it has already been cloned and sequenced.41 In any event, only human placental lactogen has been investigated in regard to its role in insulin resistance, and its effect is clearly diabetogenic.42 These results suggest placental lactogen could play an important role in insulin resistance during pregnancy.
Regulation of Reproduction by Dopamine
Nira Ben-Jonathan in Dopamine, 2020
The maternal endocrine system undergoes significant changes during pregnancy. The profile of several important hormones in the maternal plasma during gestation is shown in Figure 10.16A. Of total plasma estrogens, the most abundant is estriol, and the least abundant is estradiol. Human placental lactogen (hPL), also called human chorionic somatomammotropin (hCS), is produced by the syncytiotrophoblast and has both growth hormone (GH)-like and PRL-like activities [86]. hCG, made by the trophoblast, maintains progesterone production by the corpus luteum during the first trimester, until the placenta takes over progesterone production by 10 weeks of gestation and its levels are then reduced. The detection of hCG in the woman’s urine is used as an early test for pregnancy.
The effect of gestational diabetes mellitus on occurrence of the pelvic girdle pain and symptom severity in pregnant women
Published in Journal of Obstetrics and Gynaecology, 2022
Nilüfer Kablan, Habibe Ayvacı, Merve Can, Yaşar Tatar, Pınar Kumru, Sadık Şahin
A sequence of adaptations related to systemic and biomechanical changes occurs in pregnancy, which is a natural process; however, these changes may lead to the development of secondary pathologies in some cases. Gestational diabetes mellitus (GDM), is one of the most common metabolic disorders during pregnancy and affects 9%–26% of all pregnancies (Sacks et al. 2012). It has been defined as glucose intolerance with onset (Dirar and Doupis 2017) or first recognition during pregnancy (Challis et al. 2009). GDM results from insulin resistance developing despite the increasing insulin demand that occurs as the foetus grows (Dirar and Doupis 2017). It has been reported that, in addition to increased diabetogenic hormone secretion from the placenta, decreased adipokine secretion in parallel with maternal weight gain and increased secretion of adipocytokines, such as tumour necrosis factor α (TNF-α), play a role in the development of insulin resistance (Dirar and Doupis 2017). Moreover, it was determined that, along with the increased insulin resistance in most pregnant women with GDM, the pancreatic β cells are unable to secrete sufficient amounts of insulin, and thus contribute to the development of hyperglycaemia (Challis et al. 2009). This condition is usually diagnosed at 24–28 weeks of gestation during which placental lactogen secretion rises (Woodside and Bradford 2021) and it has been observed that glucose intolerance returns to normal postpartum in the majority of the cases (Coustan et al. 2010).
Impact of pregnancy on voice: a prospective observational study
Published in Logopedics Phoniatrics Vocology, 2022
Burak Ulkumen, Burcu Artunc-Ulkumen, Onur Celik
Pregnancy is characterized by major physiological changes which alter the metabolism and anatomy of women [11]. These changes are primarily orchestrated by sex hormones (gonadocorticoids) which are also known to affect the human larynx. Human placental lactogen, placental growth hormone, human chorionic gonadotropin, estrogen and progesterone are the main hormones which increase during pregnancy [18]. Progesterone and estrogen stand out in some respects. The influence of progesterone and estrogen on the larynx has been studied both in relation to pregnancy and different gonadocorticoid related disorders. It has been shown that fluctuation of serum progesterone and estrogen levels due to various conditions cause significant voice changes [6–9]. The effect of estrogen and progesterone on the laryngeal mucosa has also been demonstrated from a histological and biomolecular perspective [10,19]. It has been shown that estrogen leads to hypertrophy of vocal cord mucosa while progesterone leads to thickened mucosal secretions [19]. In our previous study, we revealed pregnancy related increase of MUC5AC levels in vocal cord mucosa, which was expected to affect voice [10]. Hereby, in the current study, we revealed pregnancy related voice changes regarding objective and subjective voice parameters.
Human placental lactogen mRNA in maternal plasma play a role in prenatal diagnosis of abnormally invasive placenta: yes or no?
Published in Gynecological Endocrinology, 2019
Jing Li, Ning Zhang, Yan Zhang, Xiaoyu Hu, Guoqiang Gao, Yuanhua Ye, Wei Peng, Jun Zhou
Recent efforts have been focused on the identification of biochemical and/or biological markers that can be used to improve the accuracy of antenatal diagnosis of abnormally invasive placenta. It is intuitively appealing to investigate whether measuring maternal plasma placenta mRNA levels might yield information on abnormal placental development. Some biomarkers such as concentrations of maternal serum creatinine kinase and α-fetoprotein, which are elevated in maternal plasma, have been suggested to serve as biological markers of abnormally invasive placenta [4,5]. Nevertheless, the diagnostic accuracy of these predictive tests remains unsatisfactory. Circulating cell-free placental mRNAs in maternal plasma, which could be stably isolated and quantified, have been investigated as potential markers for placental function and placental-related disorders [6–9]. Several cell-free placental mRNAs, including human placental lactogen (hPL), have been proposed as markers for the prenatal diagnosis of abnormally invasive placenta [10–13]. Yet, these studies have been limited by their small sample size, making it difficult to draw a definitive conclusion. Therefore, we measured the cell-free hPL mRNA concentration from maternal plasma of women with prior Cesarean deliveries to verify its usefulness as an antenatal predictor of abnormally invasive placenta compared with placenta previa alone or normal placentation.
Related Knowledge Centers
- Fetus
- Peptide
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