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Steroidogenesis in human polycystic ovary.

D K Mahajan1

  • 1Department of Obstetrics and Gynecology, Louisiana State University School of Medicine, New Orleans.

Endocrinology and Metabolism Clinics of North America
|December 1, 1988
PubMed
Summary

Polycystic ovarian disease (PCOD) involves high androgen levels due to potential enzyme blocks or hypothalamic-pituitary axis dysfunction. Treatments suggest gonadotropin response is key, with insulin

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Area of Science:

  • Endocrinology
  • Reproductive Medicine
  • Biochemistry

Background:

  • Polycystic ovarian disease (PCOD) is a complex endocrine disorder characterized by a spectrum of clinical and pathological features.
  • Elevated androgen levels, particularly delta 4-androstenedione and testosterone, are a hallmark of PCOD, often linked to steroidogenic enzyme dysfunction.
  • The polycystic ovary itself exhibits distinct follicular and stromal abnormalities contributing to abnormal steroidogenesis.

Purpose of the Study:

  • To explore the diverse etiologic factors contributing to Polycystic Ovarian Disease (PCOD).
  • To investigate the role of steroidogenic enzyme blocks and hypothalamic-pituitary axis dysfunction in PCOD pathogenesis.
  • To examine the influence of insulin and IGF-I on androgen production in PCOD.

Main Methods:

  • Analysis of circulating steroid levels, including androgens and estrogens.
  • Steroid analysis of follicular fluid from polycystic ovaries.
  • Review of therapeutic responses to treatments like gonadotropins and LHRH.

Main Results:

  • Evidence suggests various steroidogenic enzyme blocks (aromatase, beta-hydroxydehydrogenase, 17-hydroxylase) may contribute to PCOD.
  • High concentrations of delta 4-androstenedione and low estrogens are found in polycystic ovarian fluid.
  • Therapeutic success with gonadotropins and LHRH indicates potential defects in gonadotropin response and the hypothalamic-pituitary axis.

Conclusions:

  • The pathogenesis of PCOD likely involves a combination of steroidogenic enzyme abnormalities and hypothalamic-pituitary axis dysfunction.
  • Insulin and IGF-I are implicated in androgen overproduction in PCOD, though their mechanisms require further elucidation.
  • Understanding these complex interactions is crucial for developing effective PCOD management strategies.

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