Chronic hyperinsulinemia and the adrenal androgen response to acute corticotropin-(1–24) stimulation in hyperandrogenic women

Ricardo Azziz, Edwin L. Bradley, H. Downing Potter, C. Richard Parker, Larry R. Boots

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

OBJECTIVE: Many women with androgen excess demonstrate elevated circulating insulin levels independent of obesity. In addition, in these women some investigators have demonstrated a negative correlation between the circulating levels of the adrenal androgens,dehydroepiandrosterone or dehydroepiandrosterone sulfate and insulin. The mechanism by which insulin decreases adrenal androgens is unclear. The objective of this study was to determine whether chronic hyperinsulinemia in hyperandrogenic women results in an alteration in the adrenocortical response to corticotropin, resulting in decreased androgen secretion. STUDY DESIGN: We studied seven hyperandrogneic women with severe chronic hyperinsulinemia and eight hyperandrogenic normoinsulinemic patients. Nine healthy women served as controls for the basal hormonal levels and the response to a 3-hour, 100 gm oral glucose tolerance test. In all subjects insulin and glucose were measured hourly during the oral glucose tolerance test and the baseline sample was assayed for total testosterone, dehydroepiandrosterone sulfate, dehydroepiandrosterone, androstenedione, sex hormone-binding globulin, and free testosterone. In hypernadrogenic women cortisol, dehydroepiandrosterone, and androstenedione were also measured, before and 60 minutes, after acute intravenous administration of 0.25 mg corticotropin (1–24). RESULTS: There was no difference in the response of cortisol, dehydroepiandrosterone, or androstenedione to corticotropin-(1–24) stimulation between normoinsulinemic and hyperinsulinemic hyperandrogenic patients. As defined, the hyperinsulinemic patients had higher basal and peak insulin levels and areas under the insulin response curve compared with the normoinsulinemic patients or controls. Total testosterone and dehydroepiandrosterone did not differ among study groups. As expected, hyperandrogenic patients demonstrated lower sex hormone-binding globulin activity and higher free testosterone, androstenedione, and dehydroepiandrosterone sulfate basal levels compared with controls. CONCLUSIONS: The results of this study do not support the hypothesis that chronic hyperinsulinemia in hyperandrogenic patients significantly inhibits the andrenocortical secretion of dehydroepiandrosterone or androstenedione in response ot corticotropin stimulation or the basal circulating adrenal androgen levels. Additional studies, including a greater number of patients, may be needed to fully establish these conclusions.

Original languageEnglish (US)
Pages (from-to)1251-1256
Number of pages6
JournalAmerican Journal of Obstetrics and Gynecology
Volume172
Issue number4
DOIs
StatePublished - Jan 1 1995

Fingerprint

Hyperinsulinism
Dehydroepiandrosterone
Adrenocorticotropic Hormone
Androgens
Androstenedione
Insulin
Dehydroepiandrosterone Sulfate
Testosterone
Sex Hormone-Binding Globulin
Glucose Tolerance Test
Hydrocortisone
Intravenous Administration
Obesity
Research Personnel
Glucose

Keywords

  • Insulin
  • adrenal
  • androgens
  • polycystic ovary syndrome

ASJC Scopus subject areas

  • Obstetrics and Gynecology

Cite this

Chronic hyperinsulinemia and the adrenal androgen response to acute corticotropin-(1–24) stimulation in hyperandrogenic women. / Azziz, Ricardo; Bradley, Edwin L.; Potter, H. Downing; Parker, C. Richard; Boots, Larry R.

In: American Journal of Obstetrics and Gynecology, Vol. 172, No. 4, 01.01.1995, p. 1251-1256.

Research output: Contribution to journalArticle

Azziz, Ricardo ; Bradley, Edwin L. ; Potter, H. Downing ; Parker, C. Richard ; Boots, Larry R. / Chronic hyperinsulinemia and the adrenal androgen response to acute corticotropin-(1–24) stimulation in hyperandrogenic women. In: American Journal of Obstetrics and Gynecology. 1995 ; Vol. 172, No. 4. pp. 1251-1256.
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AU - Boots, Larry R.

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N2 - OBJECTIVE: Many women with androgen excess demonstrate elevated circulating insulin levels independent of obesity. In addition, in these women some investigators have demonstrated a negative correlation between the circulating levels of the adrenal androgens,dehydroepiandrosterone or dehydroepiandrosterone sulfate and insulin. The mechanism by which insulin decreases adrenal androgens is unclear. The objective of this study was to determine whether chronic hyperinsulinemia in hyperandrogenic women results in an alteration in the adrenocortical response to corticotropin, resulting in decreased androgen secretion. STUDY DESIGN: We studied seven hyperandrogneic women with severe chronic hyperinsulinemia and eight hyperandrogenic normoinsulinemic patients. Nine healthy women served as controls for the basal hormonal levels and the response to a 3-hour, 100 gm oral glucose tolerance test. In all subjects insulin and glucose were measured hourly during the oral glucose tolerance test and the baseline sample was assayed for total testosterone, dehydroepiandrosterone sulfate, dehydroepiandrosterone, androstenedione, sex hormone-binding globulin, and free testosterone. In hypernadrogenic women cortisol, dehydroepiandrosterone, and androstenedione were also measured, before and 60 minutes, after acute intravenous administration of 0.25 mg corticotropin (1–24). RESULTS: There was no difference in the response of cortisol, dehydroepiandrosterone, or androstenedione to corticotropin-(1–24) stimulation between normoinsulinemic and hyperinsulinemic hyperandrogenic patients. As defined, the hyperinsulinemic patients had higher basal and peak insulin levels and areas under the insulin response curve compared with the normoinsulinemic patients or controls. Total testosterone and dehydroepiandrosterone did not differ among study groups. As expected, hyperandrogenic patients demonstrated lower sex hormone-binding globulin activity and higher free testosterone, androstenedione, and dehydroepiandrosterone sulfate basal levels compared with controls. CONCLUSIONS: The results of this study do not support the hypothesis that chronic hyperinsulinemia in hyperandrogenic patients significantly inhibits the andrenocortical secretion of dehydroepiandrosterone or androstenedione in response ot corticotropin stimulation or the basal circulating adrenal androgen levels. Additional studies, including a greater number of patients, may be needed to fully establish these conclusions.

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