Prenatal Exposure to Prednisone in Humans and Animals Retards Intrauterine Growth

Reinisch, June Machover; Simon, Neal G.; Karow, William G.; Gandelman, Ronad

doi:10.1097/00006254-197905000-00004

Cited by 138 publications

(163 citation statements)

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“…The second possibility is that under stressful conditions, the fetus must compete with its host (the mother) for resources required for coping and survival (Stearns, 2005). This possibility is consistent with findings indicating that fetal exposure to stress hormones and synthetic corticosteroid administration are associated with fetal growth restriction (Bloom et al, 2001;French et al, 1999;Reinisch et al, 1978;Wadhwa et al, 2004). The purposes of the present study were to (1) test these competing hypotheses by evaluating the consequences of exposure to stress hormones during pregnancy for physical and neuromuscular development in infants and (2) determine the specific periods during pregnancy during which stress hormones influence newborn physical and neuromuscular maturation.…”

Section: Introductionsupporting

confidence: 73%

“…Specifically, during the last trimester of pregnancy, exposure to cortisol is critical for the maturation of fetal physiological systems and organs, such as the cardiovascular system, the pulmonary system, renal systems, and overall fetal growth (Murphy, Smith, Giles, & Clifton, 2006;Trainer, 2002;Welberg, Seckl, & Holmes, 2001). Despite the necessity of cortisol for fetal maturation, it has been repeatedly demonstrated that women receiving synthetic corticosteroids (administration commencing typically around the 24th week gestation) were more likely to deliver infants with fetal growth restriction and low birth weight, even when controlling for length of gestation, suggesting that high levels of glucocorticoids may be detrimental to fetal growth (Bloom, Sheffield, McIntire, & Leveno, 2001;French, Hagan, Evans, Godfrey, & Newnham, 1999;Reinisch, Simon, Karow, & Gandelman, 1978). Similarly, exposure to CRH at 33 weeks' gestation has been associated with fetal growth restriction (Wadhwa et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Timing of fetal exposure to stress hormones: Effects on newborn physical and neuromuscular maturation

Ellman

Schetter

Hobel

et al. 2008

Developmental Psychobiology

153

147

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The purpose of the study was to determine the specific periods during pregnancy in which human fetal exposure to stress hormones affects newborn physical and neuromuscular maturation. Blood was collected from 158 women at 15, 19, 25, and 31 weeks' gestation. Levels of placental corticotropin-releasing hormone (CRH) and maternal cortisol were determined from plasma. Newborns were evaluated with the New Ballard Maturation Score. Results indicated that increases in maternal cortisol at 15, 19, and 25 weeks and increases in placental CRH at 31 weeks were significantly associated with decreases in infant maturation among males (even after controlling for length of gestation). Results also suggested that increases in maternal cortisol at 31 weeks were associated with increases in infant maturation among females, although these results were not significant after controlling for length of gestation. Findings suggest that stress hormones have effects on human fetal neurodevelopment that are independent of birth outcome.

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Section: Introductionsupporting

confidence: 73%

Section: Introductionmentioning

confidence: 99%

Timing of fetal exposure to stress hormones: Effects on newborn physical and neuromuscular maturation

Ellman

Schetter

Hobel

et al. 2008

Developmental Psychobiology

153

147

View full text Add to dashboard Cite

show abstract

“…Chez l'homme, il est clair que l'exposition prénatale à des taux élevés d'hormones glucocorticoïdes, par exemple lors de traitements de la mère aux corticostéroïdes comme la prednisone, ou dans le cas d'un syndrome de Cushing 1 , est associée à un retard de croissance intra-utérin [33], mais les conséquences méta-boliques plus tardives ne sont pas connues. Nous avons vu qu'un stress élevé libère des hormones glucocorticoïdes [35] qui exercent sur le pancréas foetal des rongeurs une empreinte qui a des conséquences à long terme.…”

Section: Modèles De Restriction Alimentaireunclassified

Le concept des origines développementales de la santé

Munier¹,

Delpierre²,

Bréant³

2016

Med Sci (Paris)

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“…A dysfunction of stress response including increased circulating glucocorticoid levels is suspected in the aetiology of several metabolic disorders such as type 2 diabetes. In humans it is known that prenatal exposure to prednisone or maternal Cushing's syndrome is associated with intrauterine growth retardation (IUGR) [11,12]. In rodents, fetal exposure to glucocorticoids induces IUGR at birth, and impaired glucose tolerance [13][14][15] and hypertension [16,17] at adult age.…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoid signalling affects pancreatic development through both direct and indirect effects

et al. 2006

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Aims/hypothesis Beta cell development is sensitive to glucocorticoid levels. Although direct effects of glucocorticoids on pancreatic precursors have been shown to control beta cell mass expansion, indirect effects of these hormones on pancreatic development remain unexplored. This issue was addressed in mice lacking the glucocorticoid receptor (GR) in the whole organism. Materials and Methods The pancreatic phenotype of GR null/null mice was studied at fetal ages (embryonic day [E]) E15.5 and E18 by immunohistochemistry and beta cell fraction measurements. To distinguish between direct and indirect effects, mutant E15.5 fetal pancreata were grafted under the kidney capsule of immunodeficient mice and analysed after 1 week. Results E18 GR null/null fetuses had smaller digestive tracts and tiny pancreata. Massive pancreatic disorganisation and apoptosis were observed despite the presence of all cell types. E15.5 GR null/null mutants were indistinguishable from wild-type regarding pancreatic size, tissue structure and organisation, beta cell fraction and production of exocrine transcription factor Ptf1a, neurogenin 3 and Pdx-1. Grafting E15.5 GR null/null pancreata into a GR-expressing environment rescued the increased apoptosis and mature islets were observed, suggesting that GR null/null pancreatic cell death can be attributed to indirect effects of glucocorticoids on this tissue. Heterozygous GR +/null mutants with reduced GR numbers showed no apoptosis but increased beta cell fraction at E18 and the adult age, strengthening the importance of an accurate GR dosage on beta cell mass expansion. Conclusions/interpretation Our results provide evidence for GR involvement in pancreatic tissue organisation and survival through indirect effects. GR does not appear necessary for early phases, but its accurate dosage is critical to modulate beta cell mass expansion at later fetal stages, presumably through direct effects.

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Prenatal Exposure to Prednisone in Humans and Animals Retards Intrauterine Growth

Cited by 138 publications

References 0 publications

Timing of fetal exposure to stress hormones: Effects on newborn physical and neuromuscular maturation

Timing of fetal exposure to stress hormones: Effects on newborn physical and neuromuscular maturation

Le concept des origines développementales de la santé

Glucocorticoid signalling affects pancreatic development through both direct and indirect effects

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