Placental growth hormone as a potential regulator of maternal IGF-I during human pregnancy

Caufriez, Anne; Frankenne, Françis; Englert, Y.; Golstein, J.; Cantraine, Francis; Hennen, Georges; Copinschi, Georges

doi:10.1152/ajpendo.1990.258.6.e1014

Cited by 76 publications

(94 citation statements)

References 15 publications

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“…We did not confirm recently reported data that PGH levels were different according to the sex of the fetus (41). PGH was the major determinant of IGF-I concentrations, confirming the strong correlation between both variables in normal and IUGR pregnancies (3,4,10). We have reported that PGH and IGF-I concentrations were within the normal range and were highly correlated in a pregnant woman with absent GH secretion owing to pit-1-deficiency (35).…”

Section: Discussionsupporting

confidence: 68%

Placental GH, IGF-I, IGF-Binding Protein-1, and Leptin during a Glucose Challenge Test in Pregnant Women: Relation with Maternal Body Weight, Glucose Tolerance, and Birth Weight

Verhaeghe

Pintiaux

Herck

et al. 2002

The Journal of Clinical Endocrinology & Metabolism

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The prediction of birth weight may be improved by the measurement of hormones or growth factors in the mother. We measured body weight (BW) and plasma levels of placental GH (PGH), IGF-I, IGF-binding protein-1 (IGFBP-1), and leptin at the time of the glucose challenge test (GCT) in 289 women, who were pregnant with a single fetus, between 24 and 29 wk gestational age (GA). Delivery occurred 12 ؎ 2 (mean ؎ SD) wk later.First, we examined which variables regulate these hormonal factors. Multiple regression showed that PGH concentrations were determined by GA at sampling and were negatively related to BW. IGF-I levels were mainly determined by PGH, and also by insulin, BW, and (negatively) age. IGFBP-1 concentrations were negatively determined by BW, insulin, and IGF-I. BW was also a powerful determinant of leptin levels, with insulin as a less robust determinant.Second, we examined the relation to glucose levels. PGH, IGF-I, and IGFBP-1 concentrations were not correlated with post-GCT glucose levels and were comparable in women with a normal or disturbed GCT (glucose >7.8 mmol/liter; n ‫؍‬ 72).Finally, we examined the relation with birth weight and placental weight. Birth weight, corrected for GA and stratified into percentile groups, and the ponderal index at birth were strongly related to maternal BW, but not to maternal PGH, IGF-I, or IGFBP-1 levels. Neither was maternal leptin related to birth weight, but leptin concentrations were slightly higher in women who delivered obese babies. Placental weight was not related to any of the hormonal factors.This prospective study indicates that the variation in circulating PGH, IGF-I, IGFBP-1, and leptin between 24 and 29 wk of pregnancy is strongly dependent on maternal BW, but is unrelated to glucose tolerance. In addition, the measurement of PGH, IGF-I, IGFBP-1, or leptin at the time of the GCT is not useful clinically to predict birth weight. (J Clin Endocrinol Metab 87: 2875-2882, 2002)

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Section: Discussionsupporting

confidence: 68%

Placental GH, IGF-I, IGF-Binding Protein-1, and Leptin during a Glucose Challenge Test in Pregnant Women: Relation with Maternal Body Weight, Glucose Tolerance, and Birth Weight

Verhaeghe

Pintiaux

Herck

et al. 2002

The Journal of Clinical Endocrinology & Metabolism

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“…In the patient with a TSH-secreting macroadenoma given octreotide during the third trimester of gestation, serum hPGH and IGF-I levels were higher in late pregnancy than in first and second trimesters of gestation and decreased rapidly after elective cesarean section. Therefore, changes in hPGH and IGF-I levels were comparable to those reported during normal pregnancy (2,3). The normal neonate at birth suggests physiological IGF-I secretion during pregnancy and implies that IGF-I levels were biologically sufficient for normal fetal development.…”

Section: Discussionsupporting

confidence: 70%

“…It appears likely that hPGH is biologically active as a growth-promoting hormone; in the second half of pregnancy, serum insulin-like growth factor I (IGF-I) increases when hPGH concentrations are high, whereas pituitary GH secretion is suppressed (2,3). In nonpregnant women, pituitary GH secretion is pulsatile as a result of the actions of neurotransmitters and neuropeptides, with both stimulatory (GHRH) and inhibitory (somatostatin) effects.…”

mentioning

confidence: 99%

Expression of Somatostatin Receptor SST4 in Human Placenta and Absence of Octreotide Effect on Human Placental Growth Hormone Concentration during Pregnancy1

Caron

Buscail

Beckers³

et al. 1997

The Journal of Clinical Endocrinology &Amp; Metabolism

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In pregnancy, the human placenta GH acts as a growth-promoting hormone and appears to be the main stimulator of insulin-like growth factor I (IGF-I) secretion. In a woman with a TSH-secreting macroadenoma, successful treatment with the somatostatin analog octreotide was conducted during the first month and the second half of pregnancy without side-effects on placental and fetal development. As observed in normal pregnancy, both serum placental GH and IGF-I levels increased throughout pregnancy and dropped sharply after delivery. In placental membranes from both treated and healthy untreated patients, we demonstrated the presence of high affinity binding sites for somatostatin-14 (Kd, 4.6 and 5.3 nmol/L; binding capacity, 1.53 and 1.35 pmol/mg protein, respectively). These receptors displayed low affinity for octreotide (IC50, 1.2–2 μmol/L), suggesting the presence of SST1 and/or SST4 receptors. We found that messenger ribonucleic acids of these two subtypes were expressed in both human placental tissue and purified human cytotrophoblast cells. Finally, the SST1-selective analog, des-AA1,2,5[d-Trp8,IAmp9]S-14 had low affinity for placental somatostatin receptors. These results argue in favor of the presence of the SST4 subtype in human placenta. At the doses administered, octreotide did not bind to placental somatostatin receptors. Our results may explain the absence of changes in both human placental GH and IGF-I concentrations that we observed during octreotide treatment.

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“…It is found in high concentrations during the last half of pregnancy, and at the same time pituitary GH is virtually absent in plasma (4,5). The regulation and physiology of PGH is far from being understood, but the secretion of PGH is described as non-pulsatile (7).…”

Section: Discussionmentioning

confidence: 99%

“…Secretion is evident early in the first trimester (3), and PGH gradually replaces pituitary growth hormone (GH), which is stabilised at very low, but still detectable levels, in the last half of pregnancy (2,4,5). Maximum levels of PGH approach acromegalic levels of GH around gestational weeks 35 -37 (3 -6).…”

Section: Introductionmentioning

confidence: 99%

Kinetics and secretion of placental growth hormone around parturition

Fuglsang¹,

Sandager²,

Møller³

et al. 2006

eur j endocrinol

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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 halflife was correlated to the pre-gestational BMI (r ¼ 0.39, P ¼ 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.European Journal of Endocrinology 154 449-457

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Placental growth hormone as a potential regulator of maternal IGF-I during human pregnancy

Cited by 76 publications

References 15 publications

Placental GH, IGF-I, IGF-Binding Protein-1, and Leptin during a Glucose Challenge Test in Pregnant Women: Relation with Maternal Body Weight, Glucose Tolerance, and Birth Weight

Placental GH, IGF-I, IGF-Binding Protein-1, and Leptin during a Glucose Challenge Test in Pregnant Women: Relation with Maternal Body Weight, Glucose Tolerance, and Birth Weight

Expression of Somatostatin Receptor SST4 in Human Placenta and Absence of Octreotide Effect on Human Placental Growth Hormone Concentration during Pregnancy1

Kinetics and secretion of placental growth hormone around parturition

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