Short-term hyperinsulinemia does not acutely increase androgen production in pubertal girls with obesity

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 498-523-Female Reproductive Endocrinology & Case Reports
Clinical
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-504
Amy Denise Anderson*1, Jessicah S. P. Collins1, Ruchi Bhabhra2, Christine Michele Burt Solorzano2, John C Marshall1 and Christopher Rolland McCartney1
1University of Virginia, Charlottesville, VA, 2Division of Endocrinology, University of Virginia, Charlottesville, VA
Short-term hyperinsulinemia does not acutely increase androgen production in pubertal girls with obesity

A. D. Anderson, J. S. P. Collins, R. Bhabhra, C. Burt Solorzano, J. C. Marshall, C. R. McCartney

University of Virginia, Charlottesville, VA

Background: Polycystic ovary syndrome (PCOS) is associated with obesity, insulin resistance, and compensatory hyperinsulinemia. The latter can augment ovarian/adrenal androgen production, but whether short-term hyperinsulinemia can acutely augment HA remains unclear, as studies in adults are contradictory. Many peripubertal girls with obesity (BMI-for-age-percentile [BMI%] >95) demonstrate HA. Fasting insulin predicts free testosterone (T) in obese girls; and weight loss is associated with reduced HA in obese girls. We hypothesized that short-term hyperinsulinemia acutely increases androgens in obese girls. Methods: We studied 11 obese girls: age 12.3 ± 2.4 y; Tanner stage 3.7 ± 1.5; BMI% 98.6 ± 1.0 (reported as mean ± SD). Insulin was measured at least every 30 min for 2 h after a standardized mixed meal (at 1900 h), while fasting (0700-0900 h), and during a 2-h hyperinsulinemic euglycemic clamp (“insulin clamp”). For the clamp, regular human insulin was infused intravenously at 80 mU/m2/min (0900-1100 h), and plasma glucose was maintained via variable infusion of 20% dextrose. The following were measured at the start (0900 h) and end (1100 h) of the clamp: progesterone, 17-hydroxyprogesterone (17-OHP), dehydroepiandrosterone (DHEA), androstenedione, T, and estradiol (E2). Wilcoxon signed rank tests were used to compare values at 0900 h to those at 1100 h. Results are reported as mean ± SEM. Results: Mean insulin concentrations (uIU/ml) were 161.9 ± 25.8 after the meal, 25.2 ± 3.2 while fasting, and 162.1 ± 17.2 during the insulin clamp. No significant changes (0900 to 1100 h) were observed for progesterone (0.49 ± 0.06 to 0.53 ± 0.05 ng/ml), 17-OHP (0.90 ± 0.14 to 1.02 ± 0.12 ng/ml), DHEA (8.9 ± 2.9 to 9.5 ± 2.4 ng/ml), or androstenedione (2.1 ± 0.5 to 2.1 ± 0.4 ng/ml). However, both T (39.7 ± 9.4 to 34.7 ± 7.9 ng/dl) and E2 (24.5 ± 3.1 to 19.3 ± 2.0 pg/ml) decreased slightly (p = 0.014 and 0.027, respectively). Conclusions: These data do not support the hypothesis that short-term hyperinsulinemia acutely increases androgens or their precursors in obese girls. Since insulin concentrations during the insulin clamp were similar to those following a standardized meal, it is probable that the insulin clamp did not produce unusual hyperinsulinemia in these subjects. Testosterone and E2 decreased slightly during the clamp; given that both hormones normally demonstrate early morning peaks, the observed changes may reflect normal diurnal variations.

Nothing to Disclose: ADA, JSPC, RB, CMB, JCM, CRM

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