Pharmacological modulation of insulin resistance and hyperinsulinemia in polycystic ovary syndrome: The emerging role

Subodh Verma, Kieren Mather, Aaron S. Dumont, Todd J. Anderson

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder affecting premenopausal women. Traditional views have emphasized the underlying role of hyperandrogenism and anovulation in this clinical disorder. A growing body of evidence, however, recently has emerged to suggest that insulin resistance and hyperinsulinemia assume an early and integral role in the development and natural history of PCOS. Furthermore, pharmacological interventions targeted at reducing insulin resistance have proven to produce beneficial effects in patients with PCOS. In addition, by enhancing insulin sensitivity through pharmacological modulation, other metabolic derangements commonly associated with insulin resistance and hyperinsulinemia, such as diabetes, hypertension, dyslipidemia, and coronary artery disease, may be improved or prevented. An understanding of the emerging role of insulin resistance and hyperinsulinemia in PCOS will enable appropriate pharmacological strategies to be employed to complement current treatment regimens, thereby facilitating the optimal management of patients with this common and important endocrinopathy.

Original languageEnglish (US)
Pages (from-to)418-424
Number of pages7
JournalEndocrinologist
Volume8
Issue number6
StatePublished - Dec 1998
Externally publishedYes

Fingerprint

Polycystic Ovary Syndrome
Hyperinsulinism
Insulin Resistance
Pharmacology
Anovulation
Hyperandrogenism
Dyslipidemias
Coronary Artery Disease
Hypertension

ASJC Scopus subject areas

  • Endocrinology

Cite this

Pharmacological modulation of insulin resistance and hyperinsulinemia in polycystic ovary syndrome : The emerging role. / Verma, Subodh; Mather, Kieren; Dumont, Aaron S.; Anderson, Todd J.

In: Endocrinologist, Vol. 8, No. 6, 12.1998, p. 418-424.

Research output: Contribution to journalArticle

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