Alteration of Maternal Growth Hormone Levels during Pregnancy Influences both Fetal and Postnatal Growth in Rats

Spencer, G. S. G.; Robinson, G.; Berry, Carole; Dobbie, P. M.

doi:10.1159/000244098

Cited by 21 publications

(17 citation statements)

References 25 publications

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“…There have been a number of reports supporting a critical role for maternal IGFs and maternal GH as determinants of fetal growth (11)(12)(13)(14)22). The present report is the first in which PGH, GHBP, IGFs, and IGFBPs in late pregnancy have all been measured in the same sample set.…”

Section: Discussionmentioning

confidence: 60%

Placental Growth Hormone (GH), GH-Binding Protein, and Insulin-Like Growth Factor Axis in Normal, Growth-Retarded, and Diabetic Pregnancies: Correlations with Fetal Growth

McIntyre¹

2000

Journal of Clinical Endocrinology & Metabolism

101

151

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We previously described significant changes in GH-binding protein (GHBP) in pathological human pregnancy. There was a substantial elevation of GHBP in cases of noninsulin-dependent diabetes mellitus and a reduction in insulin-dependent diabetes mellitus. GHBP has the potential to modulate the proportion of free placental GH (PGH) and hence the impact on the maternal GH/insulin-like growth factor I (IGF-I) axis, fetal growth, and maternal glycemic status. The present study was undertaken to investigate the relationship among glycemia, GHBP, and PGH during pregnancy and to assess the impact of GHBP on the concentration of free PGH. We have extended the analysis of specimens to include measurements of GHBP, PGH, IGF-I, IGF-II, IGF-binding protein-1 (IGFBP-1), IGFBP-2, and IGFBP-3 and have related these to maternal characteristics, fetal growth, and glycemia. The simultaneous measurement of GHBP and PGH has for the first time allowed calculation of the free component of PGH and correlation of the free component to indexes of fetal growth and other endocrine markers. PGH, free PGH, IGF-I, and IGF-II were substantially decreased in IUGR at 28 -30 weeks gestation (K28) and 36 -38 weeks gestation (K36). The mean concentration (ϮSEM) of total PGH increased significantly from K28 to K36 (30.0 Ϯ 2.2 to 50.7 Ϯ 6.2 ng/mL; n ϭ 40), as did the concentration of free PGH (23.4 Ϯ 2.3 to 43.7 Ϯ 6.0 ng/mL; n ϭ 38). The mean percentage of free PGH was significantly less in IUGR than in normal subjects (67% vs. 79%; P Ͻ 0.01). Macrosomia was associated with an increase in these parameters that did not reach statistical significance. Multiple regression analysis revealed that PGH/IGF-I and IGFBP-3 account for 40% of the variance in birth weight. IGFBP-3 showed a significant correlation with IGF-I, IGF-II, and free and total PGH at K28 and K36. Noninsulin-dependent diabetes mellitus patients had a lower mean percentage of free PGH (65%; P Ͻ 0.01), and insulin-dependent diabetics had a higher mean percentage of free PGH (87%; P Ͻ 0.01) than normal subjects. Mean postprandial glucose at K28 correlated positively with PGH and free PGH (consistent with the hyperglycemic action of GH). GHBP correlated negatively with both postprandial and fasting glucose. Although GHBP correlated negatively with PGH (r ϭ Ϫ0.52; P Ͻ .001), free PGH and total PGH correlated very closely (r ϭ 0.98). The results are consistent with an inhibitory function for GHBP in vivo and support a critical role for placental GH and IGF-I in driving normal fetal growth. (J Clin Endocrinol

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Section: Discussionmentioning

confidence: 60%

Placental Growth Hormone (GH), GH-Binding Protein, and Insulin-Like Growth Factor Axis in Normal, Growth-Retarded, and Diabetic Pregnancies: Correlations with Fetal Growth

McIntyre¹

2000

Journal of Clinical Endocrinology & Metabolism

101

151

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“…Litter size and fetal size are also reduced in female GHR-knockout mice, in comparison with normal females (Bartke et al 1999). Enhanced GH secretion as a result of SRIF immunoneutralization similarly increases the mean birth weight of rat pups (Spencer et al 1994). Fetal weight in pigs is similarly increased by maternal GH administration (Sterle et al 1995).…”

Section: Roles Of Placental Ghmentioning

confidence: 95%

“…Conversely, in animals without a placental GH variant, pituitary GH is closely linked with fetal weight. For instance, GH-deficient rats are characterized by low IGF-I, maternal weight gain, and litter size (Gargosky et al 1993), and GH replacement results in heavier fetuses and faster postnatal growth of pups (Spencer et al 1994). Litter size and fetal size are also reduced in female GHR-knockout mice, in comparison with normal females (Bartke et al 1999).…”

Section: Roles Of Placental Ghmentioning

confidence: 99%

Growth hormone: roles in female reproduction

Hull¹,

Harvey²

2001

Journal of Endocrinology

197

124

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GH, as its name suggests, is obligatory for growth and development. It is, however, also involved in the processes of sexual differentiation and pubertal maturation and it participates in gonadal steroidogenesis, gametogenesis and ovulation. It also has additional roles in pregnancy and lactation. These actions may reflect direct endocrine actions of pituitary GH or be mediated by its induction of hepatic or local IGF-I production. However, as GH is also produced in gonadal, placental and mammary tissues, it may act in paracrine or autocrine ways to regulate local processes that are strategically regulated by pituitary GH. The concept that GH is an important modulator of female reproduction is the focus of this review.

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“…Maternal blood concentrations of GH, IGF-I and/or IGF-II are increased during early or throughout all of pregnancy in a number of mammalian species (Donovan et al 1991, Gargosky et al 1990, Hills et al 1996, Kelly et al 1976, Mirlesse et al 1993, Nason et al 1996, Owens 1991, Sinha et al 1990. Intrauterine growth retardation is associated with lower than normal concentrations of GH and IGF-I in maternal plasma in humans (Chowden et al 1996, Lassarre et al 1991, Mirlesse et al 1993, whilst GH-deficiency in dams impairs fetal growth in rats (Spencer et al 1994). This indicates that maternal GH and/or IGF-I are required for normal fetal growth.…”

Section: Introductionmentioning

confidence: 99%

Treatment of underfed pigs with GH throughout the second quarter of pregnancy increases fetal growth

Gatford

Owens

Campbell

et al. 2000

Journal of Endocrinology

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Circulating growth hormone (GH) concentrations increase in pregnancy and administration of GH during early-mid pregnancy increases fetal growth in well-fed pigs. To determine whether increased maternal GH could promote fetal growth when feed availability is restricted, fifteen cross-bred primiparous sows (gilts) were fed at approximately 30% of ad libitum intake, from mating onwards and were injected daily i.m. with recombinant porcine GH (pGH) at doses of 0, 13·4 0·3 and 25·6 0·5 µg/kg live weight from day 25 to day 51 of pregnancy (term 115 days). Treatment with pGH increased maternal backfat loss between day 25 and day 51 of pregnancy, and increased maternal plasma IGF-I concentrations measured at day 51 of pregnancy. Fetal body weight, length and skull width at day 51 of pregnancy were increased by maternal treatment with pGH. Fetal plasma glucose concentrations were increased and maternal/fetal plasma glucose concentration gradients were decreased by maternal pGH treatment at 13·4, but not 25·6 µg/kg.day. Fetal plasma concentrations of urea were decreased by both levels of pGH treatment. Overall, fetal weight was negatively correlated with fetal plasma concentrations of urea, positively correlated with maternal plasma -amino nitrogen concentrations and unrelated to glucose concentrations in either maternal or fetal plasma. This suggests that the availability of amino acids, not glucose, limits fetal growth in the first half of pregnancy in underfed gilts, and that maternal GH treatment may improve amino acid delivery to the fetus.

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Alteration of Maternal Growth Hormone Levels during Pregnancy Influences both Fetal and Postnatal Growth in Rats

Cited by 21 publications

References 25 publications

Placental Growth Hormone (GH), GH-Binding Protein, and Insulin-Like Growth Factor Axis in Normal, Growth-Retarded, and Diabetic Pregnancies: Correlations with Fetal Growth

Placental Growth Hormone (GH), GH-Binding Protein, and Insulin-Like Growth Factor Axis in Normal, Growth-Retarded, and Diabetic Pregnancies: Correlations with Fetal Growth

Growth hormone: roles in female reproduction

Treatment of underfed pigs with GH throughout the second quarter of pregnancy increases fetal growth

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