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PubMed2000

Placental growth hormone and IGF-I in a pregnant woman with Pit-1 deficiency.

The respective contributions of pituitary and placental GH to circulating IGF-I in pregnant women have not been well established. We measured the serum concentrations of placental growth hormone (PGH) and IGF-I in a woman with pit-1 deficiency before, during and after pregnancy, resulting in the birth of a healthy child (not pit-1 deficient). Both PGH and IGF-I concentrations were below the assay detection limit before and after pregnancy. During pregnancy, PGH and IGF-I levels increased steadily; the concentrations of PGH and IGF-I in late pregnancy were comparable with levels previously measured in normal pregnancies. PGH and IGF-I concentrations were strongly correlated throughout pregnancy (r = 0.90; P = 0.002). PGH was undetectable in cord serum, whilst the IGF-I concentration was within the normal range. The findings of this case study corroborate the notion that PGH is the prime regulator of maternal serum IGF-I during pregnancy.

Adult↗
PubMed2002

Human placental growth hormone causes severe insulin resistance in transgenic mice.

OBJECTIVE: The insulin resistance of pregnancy is considered to be mediated by human placental lactogen, but the metabolic effects of human placental growth hormone have not been well defined. Our aim was to evaluate the effect of placental growth hormone on insulin sensitivity in vivo using transgenic mice that overexpress the human placental growth hormone gene. STUDY DESIGN: Glucose and insulin tolerance tests were performed on 5 transgenic mice that overexpressed the human placental growth hormone variant gene and 6 normal littermate controls. The body composition of the mice was assessed by dual-energy radiograph absorptiometry, and free fatty acid levels were measured as a marker of lipolysis. RESULTS: The human placental growth hormone levels in the transgenic mice were comparable to those attained in the third trimester of pregnancy. These mice were nearly twice as heavy as the control mice, and their body composition differed by a significant increase in bone density and a small decrease in percentage of body fat. Fasting insulin levels in the transgenic mice that overexpressed placental growth hormone were approximately 4-fold higher than the control mice (1.57 +/- 0.22 ng/mL vs 0.38 +/- 0.07 ng/mL; P <.001) and 7 times higher 30 minutes after glucose stimulation (4.17 +/- 0.54 ng/mL vs 0.62 +/- 0.10 ng/mL; P <.0001) with no significant difference in either fasting or postchallenge glucose levels. Insulin sensitivity was markedly decreased in the transgenic mice, as demonstrated by an insignificant decline in glucose levels after insulin injection compared with the control mice, which demonstrated more than a 65% reduction in glucose levels (P <.001). CONCLUSION: Human placental growth hormone causes insulin resistance as manifested by fasting and postprandial hyperinsulinemia and minimal glucose lowering in response to insulin injection. Human placental growth hormone is a highly likely candidate to mediate the insulin resistance of pregnancy.

Animals↗
PubMed2006

Kinetics and secretion of placental growth hormone around parturition.

OBJECTIVE: During pregnancy, placental growth hormone (PGH) is secreted into the maternal circulation, replacing pituitary GH. It is controversial whether PGH levels decline during vaginal birth. After placental expulsion, PGH is eliminated from the maternal blood. GH binding protein (GHBP) and body mass index (BMI) influence GH kinetics, but their impact on PGH kinetics is unknown. The present study was undertaken to define the kinetics of PGH during vaginal delivery and Caesarian section and to relate these kinetics to GHBP and BMI. DESIGN: A short term, prospective cohort study. METHODS: Twelve women had repeated blood samples drawn during vaginal delivery. From 26 women undergoing planned Caesarian delivery (CS) repeated blood samples were withdrawn before, during and after the CS, allowing PGH half-life determination. RESULTS: During vaginal delivery, median PGH values did not change before expulsion of the placenta, although individual fluctuations were seen. Clearance of PGH from the maternal circulation was best described by a two-compartment model. The initial half-life of serum PGH was (mean +/- s.d.) 5.8 +/- 2.4 min, and the late half-life was (median) 87.0 min (range: 25.1-679.6 min). The late half-life was correlated to the pre-gestational BMI (r = 0.39, P = 0.047), but not to the serum GHBP concentration. CONCLUSIONS: Serum PGH did not decrease significantly during vaginal delivery. Elimination of PGH fitted a two-compartment model, with an estimated initial half-life of 5.8 min. The late phase serum half-life of PGH was related to BMI, suggesting a role for maternal fat mass in PGH metabolism.

Adult↗
PubMed2004

Placental growth hormone during pregnancy in a growth hormone deficient woman with type 1 diabetes compared to a matching diabetic control group.

In pregnancy, pituitary growth hormone (GH) is gradually replaced by placental growth hormone (hPGH). GH deficient pregnant women may take advantage of GH substitution during pregnancy, but this issue still remains unresolved. Also, in pregnancy diabetes may cause macrosomia. The combination of GH deficiency, GH substitution therapy and type 1 diabetes mellitus may influence pregnancy in unforeseen ways. We present a case of pregnancy in a GH deficient woman with type 1 diabetes who continued on GH replacement until week 21. In gestational week 37 a thin and mildly small-for gestational-age (length 55 cm, +3 SD, 99th centile and weight 2445 g., -1.4 SD, 10th centile) but otherwise healthy boy was born. The patient had levels of serum hPGH at the lower end of the range of values found in a matching group of diabetic women. Serum IGF-I levels were at the upper end of the range of values in the control group. A positive correlation between serum hPGH and IGF-I values was seen in the control group when using the area-under-the-curve (r=0.84; p<0.001). The patient's child had lower birth weight and ponderal index, but was otherwise healthy. Serum IGF-I, but not hPGH, correlated to the absolute birth weight (r=0.63; p=0.015) and the birth weight z-score (r=0.55; p=0.039) in the control group. Serum hPGH and IGF-I declined rapidly after delivery. In conclusion, hPGH correlated to IGF-I in type 1 diabetes mellitus (DM), and IGF-I values correlated to the birth weight. Both type 1 diabetes mellitus and GH deficiency (with GH substitution therapy) may influence fetal growth, and in combination, the net influence may be difficult to predict.

Adult↗
PubMedDate not supplied

Copulatory behavior and fertility in transgenic male mice expressing human placental growth hormone gene.

Male transgenic (TG) mice overexpressing the human placental growth hormone (GH) variant gene (hGH-V) exhibit reproductive deficits in spite of normal testosterone levels and normal sperm counts. To evaluate the relationship of copulatory behaviors to fertility, we first measured mount, intromission, and ejaculation indices in 2-5-month-old mice (10 TG and 10 normal litter mate controls) during 1 hour tests with ovariectomized, estrogen-, and progesterone-primed females. After eight tests, each male was housed with three intact females for 27 consecutive days. Females were checked daily for vaginal plugs and sacrificed 14 days after insemination to determine the numbers of corpora lutea and live and dead fetuses. Relative to their normal siblings, TG mice mounted less often and intromitted sooner after the initial mount, made marginally more intromissions (with and without ejaculation), and were slower to ejaculate. In subsequent fertility tests, TG males inseminated fewer females and sired fewer live fetuses per insemination than non-TG controls. Across TG and normal males, the length of interval between initial mount and initial intromission was inversely correlated with the number of live offspring sired. This suggests that reduced fertility in hGH-V transgenic male mice may be related to altered copulatory behavior, including a rapid progression from first mount to first intromission.

Animals↗
PubMed1989

Discordant secretion of placental protein hormones in differentiating trophoblasts in vitro.

The regulation of trophoblast secretion of the placental proteins CG (hCG), placental lactogen (hPL), and pregnancy specific-beta-1-glycoprotein (SP-1) has not been fully elucidated. We therefore studied the secretion of hCG, hCG-beta subunit, hCG-alpha subunit, hPL, and SP-1, both in the basal state and after exposure to 8-bromo-cAMP, during the in vitro differentiation of cytotrophoblasts to syncytiotrophoblasts. Term placental tissue was enzymatically digested and cytotrophoblasts purified by Percoll density gradient centrifugation. At the time of seeding of 4-6 X 10(5) cells/ml in 35-mm flasks all of the cells were mononuclear and 48% contained hCG-alpha, but none contained hCG or hCG-beta by the avidin-biotin-peroxidase immuno-histochemical method. After 3 days in culture, hCG-alpha and hCG or hCG-beta were present in multinucleated syncytiotrophoblasts and in the mononuclear cytotrophoblasts. During the 5 days in culture, the secretion of hCG, hCG-alpha, hPL and SP-1 into the media increased and reached a maximum on day 4 followed by a decrease on day 5. Basal hCG-beta secretion was very low and did not change during culture. The ratio of hCG-alpha/hCG decreased from days 1-4 of culture. Incubation with 8-bromo-cAMP for 24 h stimulated the secretion of hCG and hCG-alpha, whereas hCG-beta and hPL levels did not change. The secretion of SP-1, however, was inhibited by 8-bromo-cAMP. These results indicate that the cytotrophoblasts secrete hCG, hCG-beta and hCG-alpha during in vitro differentiation into syncytiotrophoblasts. Since the basal ratio of hCG to hCG-alpha secretion changed during 5 days in culture and a cAMP analogue differentially modulated the secretion of the different placental protein hormones, the physiological regulation of secretion of each of the proteins also may differ.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2002

Placental growth hormone is not suppressed by oral glucose loading in normal human pregnancy.

Placental growth hormone (PGH) progressively replaces pituitary growth hormone in the maternal circulation from mid-gestation onwards in human pregnancy. Our previous investigations have shown that placental growth hormone concentrations correlate well with foetal growth. Despite the apparent correlation between PGH and birthweight, the physiology of its secretion during pregnancy has not been well defined. We investigated the response of maternal serum PGH to oral glucose loading in pregnant women (n = 24) who demonstrated normal glucose tolerance at a mean gestation of 29 weeks. Mean (SEM) fasting PGH concentrations were high (36.9 [6.4] ng/ml). No suppression of PGH was noted at one, two or three hours after a 75 g oral glucose load. Similarly, no changes were noted in growth hormone binding protein or in calculated free PGH over the course of the glucose tolerance test. As expected, insulin concentrations rose sixfold and insulin like growth factor binding protein 1 concentrations fell by 20 % with glucose loading. Correlation analysis showed maternal weight, BMI, fasting serum glucose serum insulin to be significantly correlated with the babies' birthweight. Our results support the proposition that PGH concentrations in maternal serum are not suppressed by oral glucose loading in non-diabetic mothers.

Adult↗
PubMed1994

Regulation of maternal insulin-like growth factor I by placental growth hormone in pregnancy. Possible action of maternal IGF-I on fetal growth.

In normal and in pathological human pregnancies, a specific placental growth hormone variant, rather than placental lactogen, substitutes for the suppressed pituitary GH to stimulate the maternal insulin-like growth factor I (IGF-I). In pathological pregnancies with disorders of the feto-placental unit, low levels of placental GH hormone result in relatively low levels of maternal IGF-I. In normal pregnancies, the baby birth weight is positively correlated with maternal IGF-I values.

Birth Weight↗
PubMed2003

Human placental growth hormone increases expression of the p85 regulatory unit of phosphatidylinositol 3-kinase and triggers severe insulin resistance in skeletal muscle.

The insulin resistance of normal pregnancy is necessary to divert fuels to the fetus to meet fetal growth demands and is mediated by placental hormones. We recently demonstrated that human placental GH (hPGH) can trigger severe insulin resistance in transgenic (TG) mice. In this study we sought to elucidate the cellular mechanisms by which hPGH interferes with insulin signaling in muscle in TG mice. Insulin-stimulated GLUT-4 translocation to the plasma membrane (PM) was reduced in the TG compared with wild-type (WT) mice (P = 0.05). Insulin receptor (IR) levels were modestly reduced by 19% (P < 0.01) in TG mice, but there were no changes in phosphorylation of IR or IR substrate-1 (IRS-1) between WT and TG mice. A singular finding was a highly significant increase in the p85 alpha regulatory subunit of phosphatidylinositol 3-kinase (PI 3-kinase; P < 0.001), yet a reduced ability of insulin to stimulate IRS-1-associated PI 3-kinase activity (P < 0.05). Although the levels of the p110 catalytic subunit protein of PI 3-kinase and IRS-1 were unchanged in the TG mice, insulin's ability to stimulate p110 association with IRS-1 was markedly reduced (P < 0.0001). We demonstrate a unique mechanism of insulin resistance and suggest that hPGH may contribute to the insulin resistance of normal pregnancy by increasing the expression of the p85 alpha monomer, which competes in a dominant negative fashion with the p85-p110 heterodimer for binding to IRS-1 protein.

Animals↗
PubMed1993

Differential expression of human placental growth hormone variant and chorionic somatomammotropin genes in choriocarcinoma cells treated with methotrexate.

Chorionic somatomammotropin (hCS) genes (hCS-A and hCS-B) and the placental growth hormone variant (hGH-V) gene are expressed in the syncytiotrophoblast in vivo, and at low levels in cytotrophoblast-like choriocarcinoma (BeWo) cells. Treatment of choriocarcinoma cells with methotrexate (MTX) will induce a cell type intermediate between a cytotrophoblast and syncytiotrophoblast. After treatment with MTX, hCS/hGH-V mRNA levels were decreased in BeWo cells, and only hGH-V and minor hCS-A related transcripts of 1.6, 2.1 and 4.2 kilobases, termed hCS-A2, hCS-A3 and hCS-A4, respectively, were detected. By contrast, chorionic gonadotropin RNA levels were increased. This pattern of hCS/hGH-V expression resembles that observed when BeWo cells are grown in thyroid hormone (T3)-depleted serum, where hGH-V/hCS RNA increases in response to T3. This increase is blunted by MTX treatment, but is not due to a decrease in number or affinity of T3 receptors. These data indicate that the hGH-V and hCS genes can be differentially regulated by MTX, and are consistent with MTX interfering with T3 responsiveness of these genes. Also, if BeWo cells treated with MTX do represent a transitional state, these data raise the possibility that hGH-V and hCS possess a different temporal pattern of expression in the developing trophoblast.

Actins↗
PubMed2005

Elevated maternal cortisol early in pregnancy predicts third trimester levels of placental corticotropin releasing hormone (CRH): priming the placental clock.

The purposes of this study were to determine the intervals when placental corticotrophic-releasing hormone (CRH) was most responsive to maternal cortisol. A sample of 203 women each were evaluated at 15, 19, 25 and 31 weeks gestation and followed to term. Placental CRH and maternal adrenocorticotropin hormone (ACTH), B-endorphin and cortisol were determined from plasma. CRH levels increased faster and were higher in women who delivered preterm compared with women who delivered at term (F3,603 = 5.73, p < .001). Simple effects indicated that CRH levels only at 31 weeks predicted preterm birth (F1,201 = 5.53, p = .02). Levels of cortisol were higher in women who delivered preterm at 15 weeks gestation (F1,201 = 4.45, p = .03) with a similar trend at 19 weeks gestation. Hierarchical regression suggested that the influence on birth outcome of maternal cortisol early in pregnancy was mediated by its influence on placental CRH at 31 weeks. Elevated cortisol at 15 weeks predicted the surge in placental CRH at 31 weeks (R = .49, d.f. = 1,199, Fchange = 61.78, p < .0001). Every unit of change in cortisol (microg/dl) at 15 weeks was associated with a 34 unit change of CRH (pg/ml) at 31 weeks. These findings suggested that early detection of stress signals by the placenta stimulated the subsequent release of CRH and resulted in increased risk for preterm delivery.

Adrenocorticotropic Hormone↗