Glucocorticoid Programming

@article{Seckl2004GlucocorticoidP,
  title={Glucocorticoid Programming},
  author={Jonathan R Seckl and Michael J. Meaney},
  journal={Annals of the New York Academy of Sciences},
  year={2004},
  volume={1032}
}
  • J. Seckl, M. Meaney
  • Published 1 December 2004
  • Biology, Medicine
  • Annals of the New York Academy of Sciences
Abstract: Epidemiological evidence suggests that an adverse fetal environment permanently programs physiology, leading to increased risks of cardiovascular, metabolic, and neuroendocrine disorders in adulthood. Prenatal glucocorticoid excess or stress might link fetal maturation and adult pathophysiology. In a variety of animal models, prenatal glucocorticoid exposure or inhibition of 11β‐hydroxysteroid dehydrogenase type 2 (11β‐HSD2), the fetoplacental “barrier” to maternal glucocorticoids… 
Glucocorticoid “Programming” and PTSD Risk
  • J. Seckl, M. Meaney
  • Medicine, Psychology
    Annals of the New York Academy of Sciences
  • 2006
TLDR
The data suggest that prenatal exposure to excess glucocorticoids programs peripheral and CNS functions in adult life, predisposing to some pathologies, perhaps protecting from others, and these may be transmitted perhaps to one or two subsequent generations.
The Role of 11β-Hydroxy Steroid Dehydrogenase Type 2 in Glucocorticoid Programming of Affective and Cognitive Behaviours
TLDR
Potential mechanisms underpinning early-life programming of adult neuropsychiatric disorders and the novel therapeutic potential of statins are discussed.
A genetic approach to prenatal glucocorticoid programming
TLDR
Prenatal DEX programmes stress-potentiatiated anxiety are shown and are shown to programme low birth weight and anxiety, associated with hypothalamic pituitary adrenal (HPA) axis hyperactivity and the decreased hippocampal gene expression of corticosteroid receptors.
Prenatal dexamethasone exposure induces changes in nonhuman primate offspring cardiometabolic and hypothalamic-pituitary-adrenal axis function.
Prenatal stress or glucocorticoid administration has persisting "programming" effects on offspring in rodents and other model species. Multiple doses of glucocorticoids are in widespread use in
Hypothalamic – Pituitary – AdrenalAxis , GC Secretion , and Effects on Adipose Tissue
TLDR
In this review, insights are given into the role of maternoplacental adverse interactions under the specific context of maternal undernutrition, for later-in-life MetS development, with a special emphasis on the roles of GCs.
Effects of intrauterine exposure to synthetic glucocorticoids on fetal, newborn, and infant hypothalamic-pituitary-adrenal axis function in humans: a systematic review.
TLDR
The way in which intrauterine exposure to various regimens of synthetic glucocorticoids affects various forms of hpa function is guided in terms of which variables need to be focused on in order to further strengthen the understanding of such therapy, whilst continuing to profit from its clinical benefits.
Developmental programming of cardiovascular disorders: Focus on hypertension
TLDR
Maternal overnutrition, maternal nutrition, sex steroids and other endocrine factors could play a major role in programming, during the in utero period, of future hypertension in the offspring of obese mothers.
Mechanisms of developmental programming of the metabolic syndrome and related disorders.
TLDR
A better understanding of the programming mechanisms is a prerequisite for developing early life interventions to arrest the increasing epidemic of the metabolic syndrome, type 2 diabetes and other related disorders.
Sex-Specific Programming of Offspring Emotionality after Stress Early in Pregnancy
TLDR
The results indicate that stress experience early in pregnancy may contribute to male neurodevelopmental disorders through impacts on placental function and fetal development.
Perinatal maternal undernutrition programs the offspring hypothalamo–pituitary–adrenal (HPA) axis
TLDR
It is suggested that HPA axis alterations in adults may be implicated in the aetiology of several disorders related to the metabolic syndrome as well as to immune or inflammatory diseases.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 213 REFERENCES
Dexamethasone in the last week of pregnancy attenuates hippocampal glucocorticoid receptor gene expression and elevates blood pressure in the adult offspring in the rat.
TLDR
It is suggested that glucocorticoid excess in the last trimester of rat pregnancy is sufficient to programme offspring hypertension; also increases basal plasma CORT levels, and permanently attenuates GR and MR mRNA expression in specific hippocampal subfields.
Circadian rise in maternal glucocorticoid prevents pulmonary dysplasia in fetal mice with adrenal insufficiency.
TLDR
It is found that in the presence of fetal adrenal insufficiency, normal fetal lung development is maintained by the transfer of maternal glucocorticoid to the fetus, specifically during the circadian peak in maternal glucomagneticoid secretion.
Prenatal Stress, Glucocorticoids and the Programming of the Brain
TLDR
The data suggest that key targets for programming include glucocorticoid receptor gene expression and the corticotrophin‐releasing hormone system, and that approaches to minimize or reverse the consequences of such early life events may have therapeutic importance.
Intergenerational consequences of fetal programming by in utero exposure to glucocorticoids in rats.
  • A. Drake, B. Walker, J. Seckl
  • Biology, Medicine
    American journal of physiology. Regulatory, integrative and comparative physiology
  • 2005
TLDR
The persistence of such programming effects through several generations, transmitted by either maternal or paternal lines, indicates the potential importance of epigenetic factors in the intergenerational inheritance of the "programming phenotype" and provides a basis for the inherited association between low birth weight and cardiovascular risk factors.
Is programming of glucocorticoid receptor expression by prenatal dexamethasone in the rat secondary to metabolic derangement in adulthood?
TLDR
It is concluded that neither hypercorticosteronaemia nor hyperinsulinaemia are sufficient to cause the changes in GR expression in dex-programmed rats, implying that these changes may be primary in determining the programmed insulin resistant phenotype.
Glucocorticoid exposure in late gestation permanently programs rat hepatic phosphoenolpyruvate carboxykinase and glucocorticoid receptor expression and causes glucose intolerance in adult offspring.
TLDR
It is shown that dexamethasone (a poor substrate for 11beta-HSD2) administered to pregnant rats selectively in the last week of pregnancy reduces birth weight, and produces adult fasting hyperglycemia, which suggests that excessive glucocorticoid exposure late in pregnancy predisposes the offspring to glucose intolerance in adulthood.
Antenatal Glucocorticoids and Programming of the Developing CNS
TLDR
It is important to understand the potential long-term consequences of prenatal GC exposure on brain development as well as the underlying mechanisms involved, and the current state of knowledge in this rapidly expanding field is explored.
Programming hyperglycaemia in the rat through prenatal exposure to glucocorticoids-fetal effect or maternal influence?
TLDR
Findings show that glucocorticoids programme hyperglycaemia through mechanisms that operate on the fetus or directly on the neonate, rather than via effects that alter maternal postnatal behaviour during the suckling period.
Repeated maternal glucocorticoid administration and the developing liver in fetal sheep.
TLDR
Prenatal betamethasone exposure in the ovine fetus results in alterations in cord glucose and insulin levels as well as alterations in hepatic 11betaHSD1 mRNA and protein expression, which increase the potential to generate local cortisol from circulating cortisone.
Inhibition of 11-beta-hydroxysteroid dehydrogenase in pregnant rats and the programming of blood pressure in the offspring.
TLDR
The hypothesis that excess exposure of the fetoplacental unit to maternal glucocorticoids reduces birth weight and programs subsequent hypertension is supported and a key role for placental 11beta-HSD in controlling such exposure is indicated.
...
1
2
3
4
5
...