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Maternal obesity is a serious health concern because it increases risks of neurological disorders, including anxiety and peripartum depression. In mice, a high fat diet (HFD) in pregnancy can negatively affect placental structure and function as well as maternal behavior reflected by impaired nest building and pup‐retrieval. In humans, maternal obesity in pregnancy is associated with reduced placental lactogen (PL) gene expression, which has been linked to a higher risk of depression. PL acting predominantly through the prolactin receptor maintains energy homeostasis and is a marker of placenta villous trophoblast differentiation during pregnancy. Impaired neurogenesis and low serum levels of brain‐derived neurotrophic factor (BDNF) have also been implicated in depression. Augmented neurogenesis in brain during pregnancy was reported in the subventricular zone (SVZ) of mice at gestation day 7 and linked to increased prolactin receptor signaling. Here, we used transgenic CD‐1 mice that express human (h) PL during pregnancy to investigate whether the negative effects of diet on maternal behavior are mitigated in these (CD‐1[hGH/PL]) mice. Specifically, we examined the effect of a HFD on nest building prepartum and pup retrieval postpartum, as well as on brain BDNF levels and neurogenesis. In contrast to wild‐type CD‐1[WT]mice, CD‐1[hGH/PL] mice displayed significantly less anxiety‐like behavior, and showed no impairment in prepartum nest building or postpartum pup‐retrieval when fed a HFD. Furthermore, the HFD decreased prepartum and increased postpartum BDNF levels in CD‐1[WT] but not CD‐1[hGH/PL] mice. Finally, neurogenesis in the SVZ as well as phosphorylated mitogen‐activated protein kinase, indicative of lactogenic signaling, appeared unaffected by pregnancy and diet at gestation day 7 in CD‐1[hGH/PL] mice. These observations indicate that CD‐1[hGH/PL] mice are resistant to the negative effects of HFD reported for CD‐1[WT] mice, including effects on maternal behaviors and BDNF levels, and potentially, neurogenesis. This difference probably reflects a direct or indirect effect of the products of the hGH/PL transgene. [ABSTRACT FROM AUTHOR]

The placenta secretes a prolactin (PRL)-like hormone PRL3B1 (placental lactogen II), a luteotropic hormone essential for maintaining pregnancy until labor in mice. A report from 1984 examined the secretion pattern of PRL3B1 in prepartum mice. In the current study, we found contradictory findings in the secretion pattern that invalidate the previous report. By measuring maternal plasma PRL3B1 and PRL every 4 hrs from gestational day 17 (G17), we newly discovered that maternal plasma PRL3B1 levels decrease rapidly in prepartum C57BL/6 mice. Interestingly, the onset of this decline coincided with the PRL surge at G18, demonstrating a plasma prolactin axis shift from placental to pituitary origin. We also found that maternal plasma progesterone regression precedes the onset of the PRL shift. The level of Prl3b1 mRNA was determined by RT-qPCR in the placenta and remained stable until parturition, implying that PRL3B1 peptide production or secretion was suppressed. We hypothesized that production of the PRL family, the 25 paralogous PRL proteins exclusively expressed in mice placenta, would decrease alongside PRL3B1 during this period. To investigate this hypothesis and to seek proteomic changes, we performed a shotgun proteome analysis of the placental tissue using data-independent acquisition mass spectrometry (DIA-MS). Up to 5,891 proteins were identified, including 17 PRL family members. Relative quantitative analysis between embryonic day 17 (E17) and E18 placentas showed no significant difference in the expression of PRL3B1 and most PRL family members except PRL7C1. These results suggest that PRL3B1 secretion from the placenta is suppressed at G18 (E18).

In this study, we examined the morphological features of the placentas from 3 species of rorqual whales (Balaenopteridae), namely Bryde's (Balaenoptera brydei), sei (B. borealis), and common minke (B. acutorostrata) whales, and verified the secretion of 2 placental-specific peptide hormones, placental lactogen (PL) and chorionic gonadotropin (CG). The placentas were collected in the second phase of the Japanese Whale Research Program under a special permit in the North Pacific (JARPN II) between 2009 and 2010. For all three species of rorqual whales, as the fetus grew, the interdigitation between the maternal endometrial folds and chorionic villi became more complicated, and many blood capillaries of chorionic villi and endometrium became larger and infiltrated the trophoblast cells and endometrial epithelial cells, respectively. In the immunohistochemical examination, the trophoblast cells (except for areolar trophoblast cells) showed immunoreactivities for the PL and luteinizing hormone (LH) antibodies, and this phenomenon was similar in the placentas of all 3 rorqual whale species. Our results suggest that PL and LH-like CG play roles in regulating pregnancy in the placenta of cetacean. [ABSTRACT FROM AUTHOR]

Obesity during pregnancy represents a significant health issue and can lead to increased complications during pregnancy and impairments with breastfeeding, along with long‐term negative health consequences for both mother and offspring. In rodent models, diet‐induced obesity (DIO) during pregnancy leads to poor outcomes for offspring. Using a DIO mouse model, consisting of feeding mice a high fat diet for 8 weeks before mating, we recapitulate the effect of high pup mortality within the first 3 days postpartum. To examine the activity of the dam around the time of birth, late pregnant control and DIO dams were recorded in their home cages and the behaviour of the dam immediately before and after birth was analysed. Prior to giving birth, DIO dams spent less time engaging in nesting behaviour, while after birth, DIO dams spent less time in the nest with their pups compared to control dams, indicating reduced pup‐engagement in the early postpartum period. We have previously reported that lactogenic hormone action, mediated by the prolactin receptor, in the medial preoptic area of the hypothalamus (MPOA) is critical for the onset of normal postpartum maternal behaviour. We hypothesized that DIO dams may have lower lactogenic hormone activity during late pregnancy, which would contribute to impaired onset of normal postpartum maternal behaviour. Day 16 lactogenic activity, transport of prolactin into the brain, and plasma prolactin concentrations around birth were all similar in control and DIO dams. Moreover, endogenous pSTAT5, a marker of prolactin receptor activity, in the MPOA was unaffected by DIO. Overall, these data indicate that lactogenic activity in late pregnancy of DIO dams is not different to controls and is unlikely to play a major role in impaired onset of normal postpartum maternal behaviour. [ABSTRACT FROM AUTHOR]

Hypoadiponectinemia is a risk factor of gestational diabetes mellitus (GDM). Our previous study reported that adiponectin gene knockout mice (Adipoq -/- ) develop GDM due to insulin insufficiency. The main objective of this study was to elucidate the underlying mechanism through which adiponectin controls islet expansion during pregnancy. A significant reduction in β-cell proliferation rates, β-cell areas, and blood insulin concentrations was detected in Adipoq -/- mice at midpregnancy. Surprisingly, conditionally knocking down adiponectin receptor 1 (AdipoR1) or AdipoR2 genes in β-cells during pregnancy did not reduce β-cell proliferation rates or blood insulin concentrations. In vitro adiponectin treatment also failed to show any effect on β-cell proliferation of isolated pancreatic islets. It was reported that placental lactogen (PL) plays a crucial role in pregnancy-induced maternal β-cell proliferation. A significant decrease in phosphorylation of signal transducer and activator of transcription 5, a downstream molecule of PL signaling, was observed in islets from Adipoq -/- dams. The mRNA levels of mouse PL genes were robustly decreased in the placentas of Adipoq -/- dams. In contrast, adiponectin treatment increased PL expression in human placenta explants and JEG3 trophoblast cells. Most importantly, bovine PL injection restored β-cell proliferation and blood insulin concentrations in Adipoq -/- dams. Together, these results demonstrate that adiponectin plays a vital role in pregnancy-induced β-cell proliferation by promoting PL expression in trophoblast cells.

Premature birth, despite the significant achievements of perinatal medicine in recent decades, remains an urgent global and national medical and social problem, as it is the leading cause of perinatal morbidity and mortality. According to modern views, placental dysfunction can be one of the causes of premature birth, and its frequency, according to randomized studies, can be from 78 to 91%, depending on the gestational age. At the same time, the research conducted to date does not provide a clear understanding of the role of timely diagnosis and prevention of placental dysfunction in preventing premature birth. The objective: to perform clinical evaluation of the prevalence of placental dysfunction in women at risk of preterm birth and with threat of preterm birth. Materials and methods. 180 pregnant women were took part in the study. To achieve the research aim, three research groups were formed. I group – 73 pregnant women with threat of premature birth; II group – 77 pregnant women with risk factors for premature birth. Women with risk factors for premature birth were included in the study at the stage of pregnancy planning (IIA subgroup, 39 women) or from the moment of applying to a women’s outpatient clinic to monitor the course of pregnancy (IIB subgroup, 38 pregnant women). The control group included 30 pregnant women with an uncomplicated course of pregnancy. Transabdominal ultrasound examination with color Doppler mapping, determination of free estriol, progesterone and placental lactogen levels in blood serum were performed at 18–21+6 and 28–30 weeks of gestation. Results. Analysis of the prevalence of risk factors for placental dysfunction and preterm birth in patients of the studied cohort showed that in pregnant women with preterm birth (I group), the combination of risk factors was 5.2; in pregnant women who received pre-gravid training (IIA subgroup) – 3.2; in pregnant women who were included in the study in the I trimester of pregnancy (IIB subgroup) – 4.7, while in pregnant women of the control group – only 0.8 (p<0.05). The threat of early spontaneous miscarriage with the formation of a retrochorial hematoma as a clinical manifestation of primary placental dysfunction was determined in 43.8% of pregnant women whose premature delivery was carried out for medical reasons. Placenta abruption in these patients can be considered as decompensation of the primary dysfunction of the placenta with the transition to acute placental insufficiency. The formation of chronic placental dysfunction, clinically manifested by the syndrome of fetal growth retardation, was most often observed in patients whose pregnancy ended in spontaneous premature birth at 34–36+6 weeks in the presence of an untouched amnion, – 68.6% compared to births at 28–33+6 weeks of gestation – 25.9% and with childbirth at 22–37+6 weeks – 13.3%. Conclusions. Clinical manifestations of placental dysfunction were detected in 30.6% of patients with premature birth, with morphological signs in 60.4% of cases, which indicates the hidden course of placental insufficiency before the development of premature birth. Morphological signs of placental dysfunction were determined in 87.5% of cases of premature births for medical reasons and in 100.0% of cases of spontaneous births at 22–27+6 weeks of gestation (with a combination of risk factors from 2.1 to 3.0), in 66.7% – with premature births at 28–33+6 weeks of pregnancy, in 40.0% – with premature births at 34–36+6 weeks of pregnancy and only in one (5.6%) case – with term births. The frequency of fixation of morphological characteristics of placental dysfunction correlates with the frequency of early pregnancy complications, primarily with the formation of retrochorial hematomas in the first half of pregnancy. [ABSTRACT FROM AUTHOR]

Premature birth (PB) is a polyetiological problem that depends on many factors, accompanied by violations of the placenta functional competence, changes in its metabolic, hormone-producing and protective functions. The objective: to establish the importance of placental factors in the development of PB in pregnant women with comorbid pathology. Materials and methods. The levels of fetal and placental proteins (placental alfa microglobulin-1, α2- microglobulin of fertility, trophoblastic β1 -glycoprotein) and hormones (estriol, placental lactogen, progesterone) were determined in 33 pregnant women with threat of PB at 26–34 weeks of gestation (main group), who had concomitant comorbid pathology in the stage of unstable remission. The control group included 26 healthy pregnant women who were representative for gestational age. Results. In pregnant women with comorbid pathology a decrease of the placenta protein-synthesizing function and the hormone-producing function of the trophoblast was found, which makes it difficult to launch the syntoxic adaptation programs of the mother’s organism, which are responsible for maintaining the pregnancy with the subsequent development of placental dysfunction, the result of which is PB. The markers of these disorders are a 3-fold decrease in the level of trophoblastic β1 -glycoprotein (p<0.0001) and a 1.7-fold decrease in the concentration of α2 -microglobulin of fertility (p<0.0001) with a simultaneous 4-fold increase of placental alfa microglobulin-1 concentration (p<0.0001) and a decrease in the levels of placental lactogen by 1.6 times (p<0.0001), estradiol by 40 % (p<0.0001) and progesterone by more than 2 times (p<0.0001) compared to healthy pregnant women. Conclusions. In patients with comorbid pathology there are disorders in the secretion of pregnancy proteins due to a decrease in the levels of trophoblastic β1 -glycoprotein and α2 -microglobulin of fertility and an increase in the level of placental alfa microglobulin-1 and disorders of the hormone-producing function of the trophoblast due to a decrease in the secretion of placental lactogen, progesterone, and estradiol. The disturbance of the secretion of the pregnancy zone proteins and hormones are the early markers for the initiation of premature birth caused by placental dysfunction in pregnant women with comorbid pathology. [ABSTRACT FROM AUTHOR]

Placental lactogen (hPL) is a key hormone of pregnancy responsible for inducing maternal adaptations critical for a successful pregnancy. Low levels of placental lactogen have been associated with lower birth weight as well as symptoms of maternal depression and anxiety. Lower placental lactogen has been reported in women with higher body mass index (BMI) but it is unclear whether prenatal health behaviours predict hPL levels or if hPL is associated with infant weight outcomes. This study utilised data from the longitudinal Grown in Wales cohort, based in South Wales. Participants were recruited at the pre-surgical appointment for an elective caesarean section. This study incorporates data from recruitment, post-delivery and a 12 month follow-up. Measures of maternal serum hPL were available for 248 participants. Analysis included unadjusted and adjusted linear and binary regression. Unadjusted, prenatal smoking and a Health Conscious dietary pattern were associated with hPL levels, however this was lost on adjustment for BMI at booking, Welsh Index of Multiple Deprivation (WIMD) score and placental weight. When stratified by maternal BMI at booking, a Health Conscious dietary pattern remained associated with increased hPL levels in women with a healthy BMI (p=.024, B=.59. 95% CI=.08,1.11) following adjustment for WIMD score and placental weight. When adjusted for a wide range of confounders, maternal hPL was also associated with increased custom birthweight centiles (CBWC) (p=.014, B=1.64. 95% CI=.33,2.94) and increased odds of large for gestational age deliveries (p=<.001, Exp(B)=1.42. 95% CI=1.17,1.72). This study identified that consuming a Health Conscious dietary pattern in pregnancy was associated with increased hPL, within women of a healthy BMI. Moreover, higher hPL levels were associated with increased CBWC and increased odds of delivering a large for gestational age infant. This improves the current limited evidence surrounding the nature of hPL in these areas. [ABSTRACT FROM AUTHOR]

Placental lactogen (hPL) is a key hormone of pregnancy responsible for inducing maternal adaptations critical for a successful pregnancy. Low levels of placental lactogen have been associated with lower birth weight as well as symptoms of maternal depression and anxiety. Lower placental lactogen has been reported in women with higher body mass index (BMI) but it is unclear whether prenatal health behaviours predict hPL levels or if hPL is associated with infant weight outcomes. This study utilised data from the longitudinal Grown in Wales cohort, based in South Wales. Participants were recruited at the pre-surgical appointment for an elective caesarean section. This study incorporates data from recruitment, post-delivery and a 12 month follow-up. Measures of maternal serum hPL were available for 248 participants. Analysis included unadjusted and adjusted linear and binary regression. Unadjusted, prenatal smoking and a Health Conscious dietary pattern were associated with hPL levels, however this was lost on adjustment for BMI at booking, Welsh Index of Multiple Deprivation (WIMD) score and placental weight. When stratified by maternal BMI at booking, a Health Conscious dietary pattern remained associated with increased hPL levels in women with a healthy BMI (p=.024, B=.59. 95% CI=.08,1.11) following adjustment for WIMD score and placental weight. When adjusted for a wide range of confounders, maternal hPL was also associated with increased custom birthweight centiles (CBWC) (p=.014, B=1.64. 95% CI=.33,2.94) and increased odds of large for gestational age deliveries (p=

Premature birth remains one of the most urgent problems of modern obstetrics. It is not possible to reliably establish the cause in 70–80% of premature births, so the search for risk factors and markers of premature termination of pregnancy is justified. According to many authors, 25–30% of women at risk of premature birth have placental dysfunction. The objective: was to assess the prevalence of placental dysfunction in women at risk of preterm birth and with preterm birth. Materials and methods. 80 pregnant women were under observation. The criteria for inclusion in the study were the presence of risk factors for premature birth – Group I (30 women) or the threat of premature birth – Group II (30 women). The control group consisted of 20 conditionally healthy pregnant women. Transabdominal ultrasound examination with color Doppler mapping, determination of free estriol, progesterone and placental lactogen levels in blood serum was performed at 18–21+6 and 28–30 weeks of gestation. Results. The average age of the patients was 31.4±2.5 years, there was no significant difference in age, life history, social status, somatic pathology between the formed groups. Pregnant women of groups I and II probably had a history of pelvic inflammatory disease more often than in controls; colpitis; sexually transmitted infections; pathology of the cervix and operations on the uterus and appendages. The course of this pregnancy in most of the women of the studied cohort was complicated by the threat of termination of pregnancy, 36.7% of pregnant women of the I group and 46.7% of the II group had premature births. Signs of premature ripening of the placenta were detected in 13 (43.3%) pregnant women of the experimental cohort and in 1 (5.0%) of the control group (Р<0.0001), which was accompanied by changes in parameters during dopplerometry of utero-placental blood flow. Clinical manifestations of placental dysfunction occurred in 36.7% of patients in the risk groupof premature birth and pregnant women with a threat of premature birth, and were manifested by a decrease in the level of progesterone, a plateau in the increase in the level of placental lactogen. Morphological signs of placental dysfunction were found in 43.3% of cases of premature birth, which correlates with the frequency of early complications of pregnancy, primarily with the formation of retrochorial hematoma. Conclusions. Clinical manifestations of placental dysfunction (fetal growth retardation, preeclampsia) occur in a third of patients of the risk group and pregnant women with a threat of premature birth, which correlates with changes in the hormoneproducing function of the placenta. [ABSTRACT FROM AUTHOR]

Hormonal factors affecting the vascular adaptions of the uteroplacental unit in noncomplicated and complicated pregnancies are of interest. Here, 4 human placentas from women with and without preeclampsia (PE) were investigated for the presence of placental lactogen (PL)-derived, antiangiogenic vasoinhibin. Western blotting and mass spectrometry of placental tissue revealed the presence of a 9-kDa PL-derived vasoinhibin, the normal 22-kDa full-length PL, and a 28-kDa immunoreactive protein of undetermined nature. The sequence of the 9-kDa vasoinhibin includes the antiangiogenic determinant of vasoinhibin and could constitute a relevant factor in normal pregnancy and PE. [ABSTRACT FROM AUTHOR]

The study of placental lactogen by immunohistochemistry in histological sections of the placenta during physiological pregnancy and on the background of iron deficiency anemia in the aspect of chronic placental insufficiency. It is established that during gestation against the background of iron deficiency anemia decreases the production of placental lactogen by syncytiotrophoblast of the chorionic villi and correlates with the state of the blood of the pregnant woman. The optical density of immunohistochemical staining for placental lactogen of the free trophoblast reflects the degree of maturation of the chorionic tree of the placenta in iron deficiency anemia in pregnant women. Chronic placental insufficiency caused by immaturity of the chorionic villi can be compensated at the level of metabolism.

In this article, we discover and demonstrate the way of immunohistochemical identification of extravillous cytotrophoblast in the structures of the uteroplacental area and myometrium, which can be used to study the uteroplacental form of placental insufficiency, in the morphogenesis of which the key reason is a violation of the gestational changes of the spiral arteries of the uterus.

Pregnancy in placental mammals places unique demands on the insulin-producing β-cells in the pancreatic islets of Langerhans. The pancreas anticipates the increase in insulin resistance that occurs late in pregnancy by increasing β-cell numbers and function earlier in pregnancy. In rodents, this β-cell expansion depends on secreted placental lactogens that signal through the prolactin receptor. Then at the end of pregnancy, the β-cell population contracts back to its pre-pregnancy size. In the current review, we focus on how glucose metabolism changes during pregnancy, how β-cells anticipate these changes through their response to lactogens and what molecular mechanisms guide the adaptive compensation. In addition, we summarize current knowledge of β-cell adaptation during human pregnancy and what happens when adaptation fails and gestational diabetes ensues. A better understanding of human β-cell adaptation to pregnancy would benefit efforts to predict, prevent and treat gestational diabetes.

Hypothyroidism increases the incidence of gestational diabetes mellitus (GDM) but the mechanisms responsible are unknown. This study aimed to assess the pathophysiological mechanisms by which hypothyroidism leads to glucose intolerance in pregnancy. Hypothyroidism was induced in female Sprague-Dawley rats by adding methimazole (MMI) to drinking water at moderate (MOD, MMI at 0.005% w/v) and severe (SEV, MMI at 0.02% w/v) doses from 1 week before pregnancy and throughout gestation. A nonpregnant cohort received the same dose for the same duration but were not mated. On gestational day 16 (GD16), or nonpregnant day 16 (NP16), animals were subjected to an intraperitoneal glucose tolerance test. Tissues and blood samples were collected 4 days later. Hypothyroidism induced a diabetic-like phenotype by GD16 in pregnant females only. Pregnant MOD and SEV females had reduced fasting plasma insulin, less insulin following a glucose load, and altered expression of genes involved in insulin signaling within skeletal muscle and adipose tissue. Hypothyroidism reduced rat placental lactogen concentrations, which was accompanied by reduced percentage β-cell cross-sectional area (CSA) relative to total pancreas CSA, and a reduced number of large β-cell clusters in the SEV hypothyroid group. Plasma triglycerides and free fatty acids were reduced by hypothyroidism in pregnant rats, as was the expression of genes that regulate lipid homeostasis. Hypothyroidism in pregnant rats results in a diabetic-like phenotype that is likely mediated by impaired β-cell expansion in pregnancy. This pregnancy-specific phenomenon is likely due to reduced placental lactogen secretion. [ABSTRACT FROM AUTHOR]

The article focuses on study of metabolic transcriptone perturbed by chorionic somatomammotropin (CSH) deficiency in ruminant placenta. Topics discussed include association of CSH with intrauterine growth restriction (IUGR) in sheep, investigation of transcriptomic changes with employed RNA sequencing and transcriptomic alterations to genes in both IUGR.

The placenta secretes a prolactin (PRL)-like hormone PRL3B1 (placental lactogen II), a luteotropic hormone essential for maintaining pregnancy until labor in mice. A report from 1984 examined the secretion pattern of PRL3B1 in prepartum mice. In the current study, we found contradictory findings in the secretion pattern that invalidate the previous report. By measuring maternal plasma PRL3B1 and PRL every 4 hrs from gestational day 17 (G17), we newly discovered that maternal plasma PRL3B1 levels decrease rapidly in prepartum C57BL/6 mice. Interestingly, the onset of this decline coincided with the PRL surge at G18, demonstrating a plasma prolactin axis shift from placental to pituitary origin. We also found that maternal plasma progesterone regression precedes the onset of the PRL shift. The level of Prl3b1 mRNA was determined by RT-qPCR in the placenta and remained stable until parturition, implying that PRL3B1 peptide production or secretion was suppressed. We hypothesized that production of the PRL family, the 25 paralogous PRL proteins exclusively expressed in mice placenta, would decrease alongside PRL3B1 during this period. To investigate this hypothesis and to seek proteomic changes, we performed a shotgun proteome analysis of the placental tissue using data-independent acquisition mass spectrometry (DIA-MS). Up to 5,891 proteins were identified, including 17 PRL family members. Relative quantitative analysis between embryonic day 17 (E17) and E18 placentas showed no significant difference in the expression of PRL3B1 and most PRL family members except PRL7C1. These results suggest that PRL3B1 secretion from the placenta is suppressed at G18 (E18).

The liver increases its size during pregnancy to adapt to metabolic demand associated with pregnancy. Our previous study showed that proliferation of maternal hepatocytes are increased during pregnancy in mice and that estradiol (E2) is one of the candidate hormones responsible for maternal hepatocyte proliferation. Here, we discovered that chorionic gonadotropin (CG) induces maternal hepatocyte proliferation during pregnancy. CG administration was sufficient to stimulate hepatocyte proliferation in non-pregnant mice as well as in cell culture system. We conclude that CG stimulates proliferation in the early pregnancy of maternal hepatocytes. In contrast, estrogen stimulates hepatocyte proliferation in the late pregnancy. [Display omitted] • CG is the major maternal hepatocyte proliferator during pregnancy. • CG binds to LH/CGR for maternal proliferation. • Impaired CG-induced hepatocyte proliferation in aged mice. [ABSTRACT FROM AUTHOR]

GDM determine the condition as a passing maternal condition that affected the fetal outcomes negatively and that abated after birth. Sex of the fetus could be associated with the risk of post-partum progression toT2DM and with the likelihood of having GDM in a second pregnancy, Pregnancy cases complicated by GDM are attached with increases at the both maternal and neonatal illness, including an increased need for cesarean birth duo to increased rates growth of fetal causing macrosomia, and an increased incidence of birth trauma. This study was conducted through the duration from November of the year 2020. and continued until January of the year 2021. The pregnant women was divided into 40-control sample there ages range between (15-40) years, and 40- patient (with gestational diabetes) sample there ages range between (18-43) years. It has been carried out at the following main location, Bint- AL- Huda Hospital, Nasiriya province, Iraq; Mohammed AL-Mousawi Children’s Hospital, Nasiriya province, Iraq. The results of our current study showed that there was an inverse significant difference in the relationship between HPL, BMI, BP, at a significant level (p<0.05). In addition, show a significant inverse correlation in (p<0.01) between HPL & IR in non-GDM with female and show the female fetus is more influential that than the male fetus. Also indicated in BMI their increase significant (p<0.05) in GDM with female compared with other study groups. While showed in SBP decrease significant (p<0.05) in non-GDM with female compared to other study groups. Nevertheless, in DBP indicated to increase significant (p<0.05) in GDM with male and decrease significant (p<0.05) in non-GDM with female compared with other two-group non-GDM with male and GDM with female. [ABSTRACT FROM AUTHOR]

The purpose of the study was TO analyze the fetoplacental complex hormone levels and changes in their dynamics in pregnant women with miscarriage and the impact of these features on the subsequent course of pregnancy. Hormone levels were determined at different stages of gestation in 50 healthy women with a physiological course of pregnancy (control group) and 50 pregnant women with a history of miscarriage (main group). The women of the main group had a significantly slower rate of increase in hormones and a lag in quantitative indicators than the control group. The estradiol level indicators were 4.1 times (76.0%) and 2.89 times (65.5%) lower in women with miscarriage in the embryonic and late fetal period, respectively, compared to healthy women. Indicators of the level of placental lactogen and chorionic gonadotropin in the embryonic period in women with miscarriage were lower by 39.1% and 50.9%, respectively, compared to healthy women. In the late fetal period, the level of these hormones was lower by 72.9% and 35.4%, respectively. In the embryonic and late fetal periods, progesterone levels were lower by 67.4% and 68.4%, respectively, compared to the control group. The data obtained are evidence of a pronounced hormonal abnormality of the placenta, and hence a marker of fetoplacental dysfunction, which on the background of miscarriage develops at the early stages and continues to progress with the course of pregnancy. [ABSTRACT FROM AUTHOR]

Pregnancy in women with adenomyosis has an increased risk of multiple obstetric complications, especially early pregnancy losses. The purpose of the study was to conduct a comparative analysis of the impact of different methods of curation of pregnant women on the development of early gestational complications. Material and methods. There were 89 pregnant women with a pre-radiologically diagnosed adenomyosis. The main group (n = 45) included women receiving 10 mg twice daily hydrochloride per os from the time of pregnancy to 20 weeks of gestation; folic acid per os at 400 mcg once a day from the moment of establishment of pregnancy to 12 weeks of pregnancy; solution of L-arginine aspartate per os 5 ml four times daily from 8th to 10th and from 14th to 16th week of pregnancy. The comparison group (n = 44) was comprised of women receiving folic acid 400 μg once daily from the time of pregnancy until 12 weeks of gestation. In the instrumental examination of women, ultrasound was performed with Doppler. To evaluate the function of the yellow body of pregnancy, chorion and placenta it were determined such hormones of peripheral blood as placental lactogen, human β-chorionic gonadotropin, progesterone, free estriol and PAPP-A. Serum concentrations of total nitrite anions (NO2-) and free L-arginine were studied in serum. Early pregnancy complications were assessed. Results. Carrying out medical support for early gestation in pregnant women with adenomyosis according to the developed scheme has led to a decrease in the number of presence of pain syndrome in 12 weeks of gestation by 2.67 times (OR 0.17; 95% CI 0.06-0.47; p

The molecular evolution of pituitary growth hormone and prolactin in mammals shows two unusual features: episodes of markedly accelerated evolution and, in some species, complex families of related proteins expressed in placenta and resulting from multiple gene duplications. Explanations of these phenomena in terms of physiological adaptations seem unconvincing. Here, I propose an alternative explanation, namely that these evolutionary features reflect the use of the hormones (and their receptors) as viral receptors. Episodes of rapid evolution can then be explained as due to "arms races" in which changes in the hormone lead to reduced interaction with the virus, and subsequent changes in the virus counteract this. Placental paralogues of the hormones could provide decoys that bind viruses, and protect the foetus against infection. The hypothesis implies that the extensive changes introduced into growth hormone, prolactin and their receptors during the course of mammalian evolution reflect viral interactions, not endocrine adaptations. [ABSTRACT FROM AUTHOR]

In this study, we examined the morphological features of the placentas from 3 species of rorqual whales (Balaenopteridae), namely Bryde's (Balaenoptera brydei), sei (B. borealis), and common minke (B. acutorostrata) whales, and verified the secretion of 2 placental-specific peptide hormones, placental lactogen (PL) and chorionic gonadotropin (CG). The placentas were collected in the second phase of the Japanese Whale Research Program under a special permit in the North Pacific (JARPN II) between 2009 and 2010. For all three species of rorqual whales, as the fetus grew, the interdigitation between the maternal endometrial folds and chorionic villi became more complicated, and many blood capillaries of chorionic villi and endometrium became larger and infiltrated the trophoblast cells and endometrial epithelial cells, respectively. In the immunohistochemical examination, the trophoblast cells (except for areolar trophoblast cells) showed immunoreactivities for the PL and luteinizing hormone (LH) antibodies, and this phenomenon was similar in the placentas of all 3 rorqual whale species. Our results suggest that PL and LH-like CG play roles in regulating pregnancy in the placenta of cetacean.

During pregnancy, the energy requirements of the fetus impose changes in maternal metabolism. Increasing insulin resistance in the mother maintains nutrient flow to the growing fetus, whereas prolactin and placental lactogen counterbalance this resistance and prevent maternal hyperglycemia by driving expansion of the maternal population of insulin-producing beta cells. However, the exact mechanisms by which the lactogenic hormones drive beta cell expansion remain uncertain. Here we show that serotonin acts downstream of lactogen signaling to stimulate beta cell proliferation. Expression of serotonin synthetic enzyme tryptophan hydroxylase-1 (Tph1) and serotonin production rose sharply in beta cells during pregnancy or after treatment with lactogens in vitro. Inhibition of serotonin synthesis by dietary tryptophan restriction or Tph inhibition blocked beta cell expansion and induced glucose intolerance in pregnant mice without affecting insulin sensitivity. Expression of the G alpha(q)-linked serotonin receptor 5-hydroxytryptamine receptor-2b (Htr2b) in maternal islets increased during pregnancy and normalized just before parturition, whereas expression of the G alpha(i)-linked receptor Htr1d increased at the end of pregnancy and postpartum. Blocking Htr2b signaling in pregnant mice also blocked beta cell expansion and caused glucose intolerance. These studies reveal an integrated signaling pathway linking beta cell mass to anticipated insulin need during pregnancy. Modulators of this pathway, including medications and diet, may affect the risk of gestational diabetes.

Pregnancy represents a period of remarkable adaptive physiology throughout the body, with many of these important adaptations mediated by changes in gene transcription in the brain. A marked activation of the transcription factor signal transducer and activator of transcription 5 (STAT5) has been described in the brain during pregnancy and likely drives some of these changes. We aimed to investigate the physiological mechanism causing this increase in phosphorylated STAT5 (pSTAT5) during pregnancy. In various tissues, STAT5 is known to be activated by a number of different cytokines, including erythropoietin, growth hormone and prolactin. Because the lactogenic hormones that act through the prolactin receptor (PRLR), prolactin and its closely‐related placental analogue placental lactogen, are significantly increased during pregnancy, we hypothesised that this receptor was primarily responsible for the pregnancy‐induced increase in pSTAT5 in the brain. By examining temporal changes in plasma prolactin levels and the pattern of pSTAT5 immunoreactivity in the hypothalamus during early pregnancy, we found that the level of pSTAT5 was sensitive to circulating levels of endogenous prolactin. Using a transgenic model to conditionally delete PRLRs from forebrain neurones (Prlrlox/lox/CamK‐Cre), we assessed the relative contribution of the PRLR to the up‐regulation of pSTAT5 in the brain of pregnant mice. In the absence of PRLRs on most forebrain neurones, a significant reduction in pSTAT5 was observed throughout the hypothalamus and amygdala in late pregnancy, confirming that PRLR is key in mediating this response. The exception to this was the hypothalamic paraventricular nucleus, where only 17% of pSTAT5 immunoreactivity during pregnancy was in PRLR‐expressing cells. Taken together, these data indicate that, although there are region‐specific mechanisms involved, lactogenic activity through the PRLR is the primary signal activating STAT5 in the brain during pregnancy. [ABSTRACT FROM AUTHOR]

The four genes coding for placental members of the human (h) growth hormone (GH) family include two that code independently for placental lactogen (PL), also known as chorionic somatomammotrophin hormone, one that codes for placental growth hormone (PGH) and a pseudogene for which RNA but no protein product is reported. These genes are expressed preferentially in the villus syncytiotrophoblast of the placenta in pregnancy. In higher primates, the placental members, including hPL and PGH, are the result of multiple duplication events of the GH gene. This contrasts with rodents and ruminants, where PLs result from duplication of the prolactin (PRL) gene. Thus, unlike their mouse counterparts, the hPL and PGH hormones bind both lactogenic and somatogenic receptors with varying affinity. Roles influenced by nutrient availability in both metabolic control in pregnancy and maternal behaviour are supported. However, the effect maternal obesity has on the activation of placental members of the hGH gene family, particularly the expression and function of those genes, is poorly understood. Evidence from partially humanised hGH/PL transgenic mice indicates that both the remote upstream hPL locus control region (LCR) and more gene‐related regulatory regions are required for placental expression in vivo. Furthermore, a specific pattern of interactions between the LCR and hPL gene promoter regions is detected in term placenta chromatin from women with a normal body mass index (BMI) in the range 18.5–25 kg m‐2 by chromosome conformation capture assay. This pattern is disrupted with maternal obesity (class II BMI > 35 kg m‐2) and associated with a > 40% decrease in term hPL RNA levels, as well as serum hPL but not PRL levels, during pregnancy. The relative importance of the chromosomal architecture and predicted properties for transcription factor participation in terms of hPL production and response to obesity are considered, based on comparison with components required for efficient human pituitary GH gene expression. [ABSTRACT FROM AUTHOR]

The frequency of post-term pregnancy ranges from 3.5 to 16%. Compared to full-term newborns perinatal morbidity was in the post-term pregnancy group 1.7 times higher and mortality - in 5.5 times. The aim. To study the features of feto-placental complex functioning in the post-term pregnancy; to detect relationship between complications of the gestational period and perinatal outcomes based on the feto-placental complex violations. Materials and Methods. To study the features of delayed delivery and perinatal outcomes in this case 96 pregnant women with prolonged delivery were analyzed for 2013-2015, who gave birth in the term of 41-42 weeks. As a control group we examined 41 pregnant women, who did not differ from the comparison group by clinical and demographic characteristics, but with delivery in term of 37-40 weeks. Results. In women with term pregnancy placental lactogen was 14.64 mg / ml and it was higher than the same indicator of post-term pregnancy (10.31 mg / ml). Reducing placental lactogen leads to a decrease in biosynthetic processes and growth retardation. In women of term pregnancy we found increased levels of estriol – 12.11 ng / ml at the end of gestational period, compared with prolonged pregnancy group (7.16 ng / ml), which corresponds to our concepts of the post-term pregnancy pathogenic features formation – lack of estriol level increasing before the start of delivery. The examination of the control group women showed a strong increase of progesterone – 158.79 ng / ml, while in the group of post-term pregnancy this index was almost 2 times less – 85.83 ng / ml. In women of term pregnancy group marked increase cortisol level before delivery was observed to 36.11 nmol / ml, more than the same indicator of post-term pregnancy (29.25 nmol / ml). Increased stress hormone cortisol indicates the hypothalamus-pituitary- adrenal cortex system activation for childbirth preparation. Conclusions. There is a statistically significant decrease in hormones of the fetoplacental complex in prolonged pregnancy compared to the control group: cortisol - 19 % (р

True placenta accreta is the attachment of chorionic villi to the myometrium, possibly penetrating into the thickness of the myometrium and its outside, including through the serous tunic. The main current diagnostic techniques are considered to be ultrasonography, laboratory diagnosis (elevated human chorionic gonadotropin and placental lactogen levels), and clinical data (pain and vaginal discharge). Magnetic resonance imaging is deemed to be an adjuvant technique. By using a clinical example, this paper considers the capabilities of magnetic resonance imaging to diagnose this abnormality and to choose a right treatment policy. The abnormality is compared with the conditions (trophoblastic tumor and myoma with lysis) that are similar in their diagnosis and magnetic resonance pattern). The disorder in question is rather rare and its detailed consideration, determination of the capabilities of various techniques, and comparison with externally similar cases areimportant for the development of diagnostic opportunities.

As pregnancy progresses the placental syncytiotrophoblast increasingly assumes control of maternal glucose homeostasis through the release and counter-balancing effects of placental lactogen (PL) and placental variant growth hormone (GH-V). While local actions of these hormones on placental growth and function are likely to exist, each also exerts indirect actions to ensure fetal nutritional availability through modulation of the maternal insulin/insulin-like growth factor axis. Peripheral insulin resistance results from the increasing levels of GH-V in the maternal circulation and is counter-balanced by an increase in insulin availability through an expansion of maternal pancreatic β-cell mass. GH-V also increases maternal IGF-1 synthesis leading to enhanced placental growth and nutrient transporter activity. Maternal obesity and the presence of diabetes in pregnancy is associated with a disrupted balance in the placental expression of PL and GH-V. Several parallel mechanisms are likely to contribute to the increasing maternal β-cell mass as gestation progresses, including a reactivation of β-cell proliferation, an expansion of subsequent differentiation of resident β-cell progenitors, and α-to β-cell trans-differentiation. Each of these pathways could potentially be modulated during pregnancy to increase β-cell mass and prevent the onset of gestational diabetes. [ABSTRACT FROM AUTHOR]