The role of hyperinsulinemia in the pathogenesis of ovarian hyperandrogenism

R. L. Barbieri, Samuel Smith, K. J. Ryan

Research output: Contribution to journalReview article

Abstract

The evidence that supports the hypothesis that insulin and Lh both regulate ovarian androgen production was presented. The most dramatic clinical example of the association between hyperinsulinemia and hyperandrogenism is the HAIR-AN syndrome. Our hypothesis is that, in the HAIR-AN syndrome, the severe insulin resistance causes a compensatory hyperinsulinemia, which stimulates ovarian androgen production if adequate LH is present. The acanthosis nigricans is an epiphenomenon of the syndrome. Acanthosis nigricans is a dermatologic manifestation of severe insulin resistance. In vitro evidence suggests that insulin and IGF-I stimulate androgen production in incubations of human stroma and theca. The stromatropic effects of insulin may sensitize the stroma to the stimulatory effects of LH. In some hyperandrogenic-insulin-resistant women, a glucose load appears to produce an acute rise in circulating androgens. The magnitude of the rise in circulating androgens is proportional to the magnitude of the insulin response to the glucose load. These data suggest that hyperinsulinemia may play a central role in the development of ovarian hyperandrogenism.

Original languageEnglish (US)
Pages (from-to)197-212
Number of pages16
JournalFertility and sterility
Volume50
Issue number2
StatePublished - Jan 1 1988
Externally publishedYes

Fingerprint

Hyperandrogenism
Hyperinsulinism
Androgens
Insulin
Acanthosis Nigricans
Insulin Resistance
Glucose
Insulin-Like Growth Factor I

ASJC Scopus subject areas

  • Reproductive Medicine
  • Obstetrics and Gynecology

Cite this

The role of hyperinsulinemia in the pathogenesis of ovarian hyperandrogenism. / Barbieri, R. L.; Smith, Samuel; Ryan, K. J.

In: Fertility and sterility, Vol. 50, No. 2, 01.01.1988, p. 197-212.

Research output: Contribution to journalReview article

@article{736a71eba7cd41e288140d8a6b27f12d,
title = "The role of hyperinsulinemia in the pathogenesis of ovarian hyperandrogenism",
abstract = "The evidence that supports the hypothesis that insulin and Lh both regulate ovarian androgen production was presented. The most dramatic clinical example of the association between hyperinsulinemia and hyperandrogenism is the HAIR-AN syndrome. Our hypothesis is that, in the HAIR-AN syndrome, the severe insulin resistance causes a compensatory hyperinsulinemia, which stimulates ovarian androgen production if adequate LH is present. The acanthosis nigricans is an epiphenomenon of the syndrome. Acanthosis nigricans is a dermatologic manifestation of severe insulin resistance. In vitro evidence suggests that insulin and IGF-I stimulate androgen production in incubations of human stroma and theca. The stromatropic effects of insulin may sensitize the stroma to the stimulatory effects of LH. In some hyperandrogenic-insulin-resistant women, a glucose load appears to produce an acute rise in circulating androgens. The magnitude of the rise in circulating androgens is proportional to the magnitude of the insulin response to the glucose load. These data suggest that hyperinsulinemia may play a central role in the development of ovarian hyperandrogenism.",
author = "Barbieri, {R. L.} and Samuel Smith and Ryan, {K. J.}",
year = "1988",
month = "1",
day = "1",
language = "English (US)",
volume = "50",
pages = "197--212",
journal = "Fertility and Sterility",
issn = "0015-0282",
publisher = "Elsevier Inc.",
number = "2",

}

TY - JOUR

T1 - The role of hyperinsulinemia in the pathogenesis of ovarian hyperandrogenism

AU - Barbieri, R. L.

AU - Smith, Samuel

AU - Ryan, K. J.

PY - 1988/1/1

Y1 - 1988/1/1

N2 - The evidence that supports the hypothesis that insulin and Lh both regulate ovarian androgen production was presented. The most dramatic clinical example of the association between hyperinsulinemia and hyperandrogenism is the HAIR-AN syndrome. Our hypothesis is that, in the HAIR-AN syndrome, the severe insulin resistance causes a compensatory hyperinsulinemia, which stimulates ovarian androgen production if adequate LH is present. The acanthosis nigricans is an epiphenomenon of the syndrome. Acanthosis nigricans is a dermatologic manifestation of severe insulin resistance. In vitro evidence suggests that insulin and IGF-I stimulate androgen production in incubations of human stroma and theca. The stromatropic effects of insulin may sensitize the stroma to the stimulatory effects of LH. In some hyperandrogenic-insulin-resistant women, a glucose load appears to produce an acute rise in circulating androgens. The magnitude of the rise in circulating androgens is proportional to the magnitude of the insulin response to the glucose load. These data suggest that hyperinsulinemia may play a central role in the development of ovarian hyperandrogenism.

AB - The evidence that supports the hypothesis that insulin and Lh both regulate ovarian androgen production was presented. The most dramatic clinical example of the association between hyperinsulinemia and hyperandrogenism is the HAIR-AN syndrome. Our hypothesis is that, in the HAIR-AN syndrome, the severe insulin resistance causes a compensatory hyperinsulinemia, which stimulates ovarian androgen production if adequate LH is present. The acanthosis nigricans is an epiphenomenon of the syndrome. Acanthosis nigricans is a dermatologic manifestation of severe insulin resistance. In vitro evidence suggests that insulin and IGF-I stimulate androgen production in incubations of human stroma and theca. The stromatropic effects of insulin may sensitize the stroma to the stimulatory effects of LH. In some hyperandrogenic-insulin-resistant women, a glucose load appears to produce an acute rise in circulating androgens. The magnitude of the rise in circulating androgens is proportional to the magnitude of the insulin response to the glucose load. These data suggest that hyperinsulinemia may play a central role in the development of ovarian hyperandrogenism.

UR - http://www.scopus.com/inward/record.url?scp=0023713274&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023713274&partnerID=8YFLogxK

M3 - Review article

C2 - 3294042

AN - SCOPUS:0023713274

VL - 50

SP - 197

EP - 212

JO - Fertility and Sterility

JF - Fertility and Sterility

SN - 0015-0282

IS - 2

ER -