The effects of hyperinsulinemia on serum testosterone, progesterone, dehydroepiandrosterone sulfate, and cortisol levels in normal women and in a woman with hyperandrogenism, insulin resistance, and acanthosis nigricans.
Insulin may mediate the hyperandrogenism that frequently occurs in patients with insulin-resistant states. To test this hypothesis, we studied five normal women and one woman with hyperandrogenism, insulin resistance, and acanthosis nigricans with the hyperinsulinemic-euglycemic clamp technique. Each woman received a 0.1 U/kg insulin bolus dose, followed by a 10 mU/kg X min insulin infusion for 12-16 h. In the normal women, an average insulin level of 1832 +/- 292 (+/- SEM) microU/ml was achieved; serum glucose was clamped at 116 +/- 5 mg/dl. At this level, insulin may bind to the insulin-like growth factor I receptor as well as to its own receptor. Contrary to our working hypothesis, a rise in serum testosterone did not occur in any women during insulin infusion, and in one women, serum testosterone levels decreased. When analyzed as a percentage of the basal value, serum progesterone levels fell 20% in the normal women within the first 2 h of insulin infusion, but did not change thereafter. Dehydroepiandrosterone sulfate (DHEA-S) levels, however, uniformly and progressively decreased by 39% after 12 h of insulin infusion in the normal women and by 31% at 14 h in the woman with hyperandrogenism, insulin resistance, and acanthosis nigricans. The fall in serum DHEA-S levels was not due to diurnal rhythmicity, as the changes in serum DHEA-S levels did not correlated with those in serum cortisol. Suppression of PRL release also was excluded as a cause of the fall in DHEA-S levels. These results indicate that acute hyperinsulinemia of 12- to 16-h duration does not increase serum testosterone or DHEA-S concentrations and, indeed, can cause a decline in serum DHEA-S levels in both normal women and the single woman studied with hyperandrogenism, insulin resistance, and acanthosis nigricans.
D000052:Acanthosis Nigricans / Q000097:blood* / Q000150:complications; D000328:Adult; D000728:Androgens / Q000097:blood*; D003687:Dehydroepiandrosterone / Q000031:analogs & derivatives* / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D006946:Hyperinsulinism / Q000097:blood* / Q000150:complications; D007332:Insulin Infusion Systems; D007333:Insulin Resistance; D007986:Luteinizing Hormone / Q000097:blood; D011374:Progesterone / Q000097:blood*; D013739:Testosterone / Q000097:blood*
D000728:Androgens; D013739:Testosterone; D003687:Dehydroepiandrosterone; D011374:Progesterone; D019314:Dehydroepiandrosterone Sulfate; D007986:Luteinizing Hormone; D006854:Hydrocortisone