Regulation of Fetal Growth

Gluckman, Peter D.; Liggins, G. C.

doi:10.1016/b978-0-407-00366-8.50022-8

Cited by 98 publications

(48 citation statements)

References 154 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, the relative importance of growth hormone (GH) and the insulin-like growth factors (IGFs-I and -II) appears to differ in pre-and postnatal life (1,2). Whereas abnormalities of fetal GH secretion are not associated with major alterations in body size at birth (3,4), IGF-I deficiency has been shown to cause marked fetal growth retardation (5,6).…”

Section: Introductionmentioning

confidence: 99%

IGF-I and IGF-binding protein-1 are related to cortisol in human cord blood

Cianfarani

Germani

Rossi³

et al. 1998

European Journal of Endocrinology

View full text Add to dashboard Cite

Objective: To assess cortisol concentrations in cord blood and investigate their relationships with the IGF system. Study design: Fifteen newborns with birth weight appropriate for gestational age (AGA) and 30 children with intrauterine growth retardation (IUGR) were studied. Serum samples were collected from umbilical cord blood and cortisol, IGF-I and IGF-binding proteins (IGFBPs)-1 and -3 were measured. IUGR infants were followed up for 3 months with repeated measurements of weight, supine length and knee-heel length (by knemometry). Results: IUGR newborns showed significantly greater concentrations of IGFBP-1 (P<0·0001) and lower concentrations of IGF-I (P < 0.0001) and IGFBP-3 (P < 0.0001) than did controls. In AGA children, cortisol correlated inversely with IGF-I (r ¼ ¹0.75, P < 0.002) and directly with IGFBP-1 (r ¼ 0.52, P < 0·05), whereas no correlation between cortisol and IGF system-related variables was observed in IUGR. Finally, in IUGR children an inverse correlation was found between length gain in the first trimester of life and cortisol concentrations at birth (r ¼ ¹0.54, P < 0.005). Conclusions: Cortisol might be a physiological regulator of fetal growth, at least in the last part of pregnancy, by modulating IGF-I and IGFBP-1 release under conditions of fetal stress. In IUGR children, a rearrangement of this growth control mechanism seems to occur. The close inverse relationship of cortisol with linear growth, if confirmed by large-scale studies, suggests cord blood cortisol to be potentially predictive of early postnatal catch-up growth in IUGR infants.

show abstract

Section: Introductionmentioning

confidence: 99%

IGF-I and IGF-binding protein-1 are related to cortisol in human cord blood

Cianfarani

Germani

Rossi³

et al. 1998

European Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…Although it is accepted that the most common challenges limiting fetal growth are reduced nutrient and oxygen delivery to the fetal circulation (15), the partial contributions of each of these substrates to fetal growth impairment remain to be determined. Several studies have shown that poor maternal nutrition is associated with reduced birth weight in humans (16 -19), rats (20 -22), and sheep (23,24) and that the extent of the reduction depends on the severity, duration, and timing of the challenge (23,24).…”

mentioning

confidence: 99%

Effects of Altitude versus Economic Status on Birth Weight and Body Shape at Birth

et al. 2001

View full text Add to dashboard Cite

“…Earlier reports suggested that GH cannot affect growth in the immediate postnatal period of several mammals (21) despite its very high concentrations in the circulation at this age period (22)(23)(24). However, in a previous study (1) we showed that in the rat passive immunization against GHRH during the early postnatal period has profound and long-term effects on subsequent somatic growth and somatotropic function.…”

Section: Discussionmentioning

confidence: 81%

Somatotropic Dysfunction in Growth Hormone-Releasing Hormone-Deprived Neonatal Rats: Effect of Growth Hormone Replacement Therapy

Colonna

Locatelli

et al. 1994

Pediatr Res

View full text Add to dashboard Cite

In a previous work, we reported that passive immunization with anti-growth hormone-releasing hormone (GHRH) antibodies (GHRH-Ab) in neonatal rats caused disruption of somatotropic function that was still present 60 d posttreatment. We studied the reversibility of this condition by growth hormone (GH) replacement therapy. Neonatal rats received GHRH-Ab (50 ~U r d t , s.c.) or normal rabbit serum every second day from birth up to postnatal d 10 and received hGH (0.4 &g body weight, s.c., b i d . ) or vehicle in a 2 x 2 factorial design. Animals were studied on d 11 of age. In GHRH-Abtreated rats, GH therapy 1 ) counteracted the reduced body weight and low plasma IGF-I levels; 2) failed to modify the reduced pituitary weight and GH content; 3) further reduced the low plasma GH levels; 4) partially restored the defective GH responsiveness to GHRH; 5) failed to modify the reduced hypothalamic somatostatin and increased GHRH gene expression in the hypothalamus; and 6) reverted the decreased pituitary somatostatin binding. Morphologic and morphometric evaluation of the pituitary gland from GHRH-Ab+GH pups showed that the number of GH-labeled structures was lower than in normal rat serum-GH-treated pups, whereas the total GH immunoreact~ty per unit surface, an index of intracellular hormone concentration, was slightly higher than in vehicle-GH or GHRH-Ab pups. As determined by electron microscopy, somatotropes from GHRH-Ab+GH pups had morphologic features of high cellular activity. It appears that in GHRH-deprived pups GH replacement therapy can normalize most but not all altered indices of the somatotropic function. The effects of GH are mainly directed at the pituitaly, whereas the sensitivity of the hypothalamus to GH replacement is lower. (Pediatr Res 36: 315-322, 1994) Abbreviations GH, growth hormone GHRH, growth hormone-releasing hormone GHRH-Ab, anti-GHRH-antibodies NRS, normal rabbit serum dCTP, deoxycytidine triphosphate PRL, prolactin SS, somatostatin Recent studies by us (1,2) and by other groups (3,4) have shown that rat pups treated with GHRH-Ab may represent a suitable animal model for the study of the human growth disorders caused b y a primary hypothalamic dysfunction. Neonatal administration of GHRH-Ab permanently inhibits the growth rate and alters several indices of the hypophyseal somatotropic function (I). Received November 11, 1993: accepted March 21, 1994. Correspondence and reprint requests: Eugenio E. Muller, MD. Department of Pharmacology. Chemotherapy and Toxicology. University of Milan, via VanviIt is presently unknown whether these changes are due t o the G H R H deficiency itself o r to the consequent reduction of G H secretion. Therefore, we studied the effects of concomitant G H and GHRH-Ab treatment. W e have administered G H daily to GHRH-deprived and control pups from postnatal d 1 to 10 and subsequently evaluated in vivo and in vitro several hypothalamic and pituitary indices of somatotropic activity. METHODStelli 32.

show abstract

Regulation of Fetal Growth

Cited by 98 publications

References 154 publications

IGF-I and IGF-binding protein-1 are related to cortisol in human cord blood

IGF-I and IGF-binding protein-1 are related to cortisol in human cord blood

Effects of Altitude versus Economic Status on Birth Weight and Body Shape at Birth

Somatotropic Dysfunction in Growth Hormone-Releasing Hormone-Deprived Neonatal Rats: Effect of Growth Hormone Replacement Therapy

Contact Info

Product

Resources

About