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17 beta-estradiol secretion in normal and hypophysectomized chick embryos.

J P Weniger1, J Chouraqui, A Zeis

  • 1Laboratoire de Zoologie et d'Embryologie Expérimentale de l'Université Louis-Pasteur, Strasbourg, France.

Reproduction, Nutrition, Developpement
|January 1, 1989
PubMed
Summary
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The pituitary gland does not control 17 beta-estradiol secretion in chick embryo ovaries near hatching. Decapitated embryos showed lower ovarian 17 beta-estradiol release, indicating hypophyseal independence.

Area of Science:

  • Endocrinology
  • Developmental Biology
  • Avian Reproduction

Background:

  • The role of the hypophysis in regulating embryonic ovarian function is not fully understood.
  • Previous studies suggest potential hormonal influences on steroidogenesis during avian development.

Purpose of the Study:

  • To investigate the influence of the hypophysis on 17 beta-estradiol secretion by chick embryo ovaries.
  • To determine if hypophyseal control over ovarian steroidogenesis exists near hatching.

Main Methods:

  • Ovaries from 18-day-old chick embryos (decapitated, sham-operated, intact) were cultured for 6 hours.
  • 17 beta-estradiol levels in culture media and serum were quantified using radioimmunoassay.

Main Results:

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  • Ovaries from decapitated embryos secreted significantly less 17 beta-estradiol compared to intact embryos.
  • No significant difference in 17 beta-estradiol secretion was observed between decapitated and sham-operated groups.
  • Ovarian weight-adjusted 17 beta-estradiol production was highest in decapitated embryos.
  • Serum 17 beta-estradiol concentrations were similar in both decapitated and intact embryos.

Conclusions:

  • The hypophysis does not appear to control 17 beta-estradiol secretion by the chick embryo ovary near hatching.
  • Ovarian steroidogenesis exhibits a degree of independence from direct hypophyseal regulation in late-stage chick embryos.