Literature DB >> 8798253

Growth factors and intrauterine growth retardation. I. Serum growth hormone, insulin-like growth factor (IGF)-I, IGF-II, and IGF binding protein 3 levels in normally grown and growth-retarded human fetuses during the second half of gestation.

J Leger1, J F Oury, M Noel, S Baron, K Benali, P Blot, P Czernichow.   

Abstract

The aim of this study was to relate human fetal growth retardation to specific hormone alterations. Serum levels of GH, IGF-I, IGF-II, and IGF binding protein (BP) 3 were measured during the second half of gestation after cordocentesis in 230 fetuses who were classified into normally grown (n = 166) and growth-retarded (n = 64) groups according to ante- and neonatal measurements. The normally grown group showed a progressive decline in serum GH levels toward term (r = -0.42, p = 0.0001), whereas serum IGF-I was increased (r = 0.55, p = 0.0001), as were serum IGF-II (r = 0.21, p = 0.008) and IGFBP3 levels (r = 0.19, p = 0.02), although less markedly. For all hormone levels, wide individual differences were found at any given age of gestation. The incidental presence of fetal malformations in either the normally grown group (n = 107 cases) or the growth-retarded group (n = 50 cases) had no apparent effect on these hormone levels as compared with members of the groups showing no fetal malformations (n = 73 cases). Comparison of the normally grown group with the growth-retarded group showed that serum IGF-I levels were significantly lower in the growth-retarded group (p = 0.001). No differences were found between the groups in serum GH, IGF-II, and IGFBP3 levels, although if data for the third trimester were taken alone, serum IGF-II levels were found to be lower in the growth-retarded group (p = 0.05). In conclusion, during the second half of gestation, fetal serum IGF-I levels may be influenced by nutritional factors controlling fetal growth. However, the wide individual differences in measurements make it a very poor biologic marker of intrauterine growth retardation.

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Year:  1996        PMID: 8798253     DOI: 10.1203/00006450-199607000-00017

Source DB:  PubMed          Journal:  Pediatr Res        ISSN: 0031-3998            Impact factor:   3.756


  14 in total

1.  Repeated betamethasone treatment of pregnant sheep programs persistent reductions in circulating IGF-I and IGF-binding proteins in progeny.

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2.  Identification of newborns with Fetal Growth Restriction (FGR) in weight and/or length based on constitutional growth potential.

Authors:  Nicole Mamelle; Magali Boniol; Olivier Rivière; Marie O Joly; Georges Mellier; Bernard Maria; Bernard Rousset; Olivier Claris
Journal:  Eur J Pediatr       Date:  2006-07-12       Impact factor: 3.183

3.  Developmental pattern of fetal growth hormone, insulin-like growth factor I, growth hormone binding protein and insulin-like growth factor binding protein-3.

Authors:  P Pirazzoli; E Cacciari; R De Iasio; M C Pittalis; P Dallacasa; S Zucchini; S Gualandi; S Salardi; C David; S Boschi
Journal:  Arch Dis Child Fetal Neonatal Ed       Date:  1997-09       Impact factor: 5.747

4.  IGF2 stimulates fetal growth in a sex- and organ-dependent manner.

Authors:  Veronica White; Alicia Jawerbaum; Maria Belen Mazzucco; Martin Gauster; Gernot Desoye; Ursula Hiden
Journal:  Pediatr Res       Date:  2017-10-18       Impact factor: 3.756

5.  Esterase 1 is a novel transcriptional repressor of growth hormone receptor gene expression: a unique noncatalytic role for a carboxyesterase protein.

Authors:  Jinhong Sun; P Anil Kumar; Jamuna Thimmarayappa; Natinder Saini; Pooja Goel; Travis Maures; Chunxia Lu; Ram K Menon
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6.  The role of serum insulin-like growth factor I (IGF-I) in neonatal outcome.

Authors:  A R Hayati; F C Cheah; J F Yong; A E Tan; W M Norizah
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Review 7.  Fetal origins of adult disease: a paediatric perspective.

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Review 9.  Endocrine regulation of fetal skeletal muscle growth: impact on future metabolic health.

Authors:  Laura D Brown
Journal:  J Endocrinol       Date:  2014-04-22       Impact factor: 4.286

10.  IGFBP-1 hyperphosphorylation in response to leucine deprivation is mediated by the AAR pathway.

Authors:  Niyati Malkani; Thomas Jansson; Madhulika B Gupta
Journal:  Mol Cell Endocrinol       Date:  2015-05-05       Impact factor: 4.102

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