Endocrine mechanisms of intrauterine programming.

@article{Fowden2004EndocrineMO,
  title={Endocrine mechanisms of intrauterine programming.},
  author={Abigail L. Fowden and Alison J. Forhead},
  journal={Reproduction},
  year={2004},
  volume={127 5},
  pages={
          515-26
        }
}
Epidemiological findings and experimental studies in animals have shown that individual tissues and whole organ systems can be programmed in utero during critical periods of development with adverse consequences for their function in later life. Detailed morphometric analyses of the data have shown that certain patterns of intrauterine growth, particularly growth retardation, can be related to specific postnatal outcomes. Since hormones regulate fetal growth and the development of individual… 

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References

SHOWING 1-10 OF 140 REFERENCES
Effects of nutrition and environmental factors on the fetal programming of the reproductive axis.
TLDR
Although reproductive performance is clearly influenced by prenatal factors, much further work is required to identify the relationships between developmental abnormalities and adult reproductive function and to elucidate further the critical windows in development and the mechanisms by which environmental factors affect the reproductive organs of developing offspring.
Prenatal programming of postnatal endocrine responses by glucocorticoids.
TLDR
Current data indicate that key targets for programming may include not only the HPA axis but also glucocorticoid receptor gene and 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) gene expression in a range of tissues.
Glucocorticoid programming of the fetus; adult phenotypes and molecular mechanisms
  • J. Seckl
  • Medicine, Biology
    Molecular and Cellular Endocrinology
  • 2001
Endocrine regulation of fetal growth.
  • A. Fowden
  • Medicine, Biology
    Reproduction, fertility, and development
  • 1995
TLDR
Fetal hormones promote growth and development in utero by altering both the metabolism and gene expression of the fetal tissues to ensure that fetal growth rate is commensurate with the nutrient supply and that prepartum maturation occurs in preparation for extrauterine life.
GLUCOCORTICOIDS, HYPOTHALAMO-PITUITARY-ADRENAL (HPA) DEVELOPMENT, AND LIFE AFTER BIRTH
TLDR
It is shown that exposure of fetuses to sGC in late gestation permanently alters HPA function in pre-pubertal, post-pupertal, and aging offspring, in a sex-dependent manner, and these effects are linked to changes in central glucocorticoid feedback.
Intra-uterine programming of the endocrine pancreas.
TLDR
Although the human epidemiological observations suggest that the fetal origin of adult glucose intolerance is due primarily to changes in insulin sensitivity rather than to defective insulin secretion, subtle changes in islet morphology and function sustained in utero may well contribute to the increased susceptibility to type 2 diabetes observed in adults who were growth-retarded in uterno.
Effects of repeated maternal betamethasone administration on growth and hypothalamic-pituitary-adrenal function of the ovine fetus at term.
TLDR
Ant antenatal betamethasone given to pregnant sheep in a manner similar to that used in human obstetric practice results in reduced weight at birth at 125 and 146 days, and altered basal cord levels of plasma ACTH and corticosteroid binding capacity, but these changes are not reflective of changes in steady state concentrations of POMC and CRH mRNA in the fetal pituitary or hypothalamus.
A model of intrauterine growth retardation caused by chronic maternal undernutrition in the rat: effects on the somatotrophic axis and postnatal growth.
TLDR
It is demonstrated that nutritional deprivation in the pregnant rat leads to IUGR and postnatal growth failure and to changes in allometric growth patterns and endocrine parameters of the somatotrophic axis postnatally.
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.
Intrauterine growth retardation leads to the development of type 2 diabetes in the rat.
TLDR
The hypothesis that an abnormal intrauterine milieu can induce permanent changes in glucose homeostasis after birth and lead to type 2 diabetes in adulthood is supported.
...
...