Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Polycystic ovary syndrome

V T Goudas1, D A Dumesic

  • 1Department of Obstetrics and Gynecology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota, USA.

Endocrinology and Metabolism Clinics of North America
|January 16, 1998
PubMed
Summary

Polycystic ovary syndrome (PCOS) involves hyperandrogenism and irregular ovulation, often linked to obesity and insulin resistance. Biochemical issues like LH hypersecretion and hyperinsulinemia drive androgen excess, impacting reproductive and metabolic health.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Clustering of PCOS-like traits in naturally hyperandrogenic female rhesus monkeys.

Human reproduction (Oxford, England)·2017
Same author

Early prenatal androgenization results in diminished ovarian reserve in adult female rhesus monkeys.

Human reproduction (Oxford, England)·2009
Same author

Insights into the development of polycystic ovary syndrome (PCOS) from studies of prenatally androgenized female rhesus monkeys.

Trends in endocrinology and metabolism: TEM·2008
Same author

Prenatal androgen excess negatively impacts body fat distribution in a nonhuman primate model of polycystic ovary syndrome.

International journal of obesity (2005)·2007
Same author

Androgen excess fetal programming of female reproduction: a developmental aetiology for polycystic ovary syndrome?

Human reproduction update·2005
Same author

Treatment of atypical endometrial hyperplasia with an insulin-sensitizing agent.

Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology·2004

Area of Science:

  • Reproductive Endocrinology
  • Metabolic Syndrome
  • Neuroendocrinology

Background:

  • Polycystic Ovary Syndrome (PCOS) is characterized by clinical signs of hyperandrogenism (hirsutism) and anovulation, frequently co-occurring with obesity and insulin resistance.
  • Biochemical abnormalities in PCOS include luteinizing hormone (LH) hypersecretion, elevated androgens, acyclic estrogen production, reduced sex hormone-binding globulin (SHBG) capacity, and hyperinsulinemia, all contributing to increased ovarian androgen production.

Purpose of the Study:

  • To elucidate the complex interplay of neuroendocrine and metabolic factors contributing to ovarian hyperandrogenism in PCOS.
  • To explore the potential role of early-life events in altering neuroendocrine function and predisposing individuals to PCOS.
  • To understand the regulatory mechanisms of hyperinsulinemia on ovarian steroidogenesis and its contribution to PCOS pathophysiology.

Main Methods:

  • Review of clinical features, biochemical abnormalities, and hormonal profiles in women with hyperandrogenic anovulation.
  • Analysis of the impact of insulin resistance and hyperinsulinemia on LH secretion and ovarian androgen production.
  • Consideration of neuroendocrine factors, including pulsatile LH secretion and responses to GnRH analogue (GnRHa) testing.

Main Results:

  • LH hypersecretion is a fundamental mechanism driving ovarian hyperandrogenism in PCOS, potentially influenced by early neuroendocrine alterations.
  • Hyperinsulinemia significantly potentiates ovarian hyperandrogenism by enhancing LH secretion, steroidogenic enzyme activity (17-hydroxylase, 17,20-lyase), and suppressing SHBG.
  • Upper-body obesity, linked to hyperinsulinemia, is an independent risk factor for cardiovascular disease and diabetes, highlighting the metabolic comorbidities of PCOS.

Conclusions:

  • PCOS pathophysiology involves a complex interaction between neuroendocrine dysfunction (LH hypersecretion) and metabolic disturbances (hyperinsulinemia, insulin resistance).
  • Hyperinsulinemia plays a critical role in exacerbating ovarian androgen excess and is closely associated with central obesity and increased risk of cardiovascular disease and diabetes.
  • Therapeutic strategies for PCOS should address endometrial normalization, androgen antagonism, insulin resistance reduction, and correction of anovulation.

Related Experiment Videos