Intrauterine growth retardation predisposes to insulin resistance but not to hyperandrogenism in young women

It was recently suggested that precocious pubarche associated with subseque nt functional ovarian hyperandrogenism and hyperinsulinemia could have a co mmon origin in reduced fetal growth. We previously reported that young wome n born with intrauterine growth retardation (IUGR: birth weight less than t he third percentile) were hyperinsulinemic and less insulin sensitive than women born with normal birth weight. The aim of the present study was to in vestigate whether these IUGR-born women demonstrated hyperandrogenism compa red with controls. Our study population was composed of 130 IUGR-born women and 150 controls, of similar age (20.6 +/- 3.2 vs. 20.4 +/- 2.0 yr). Hormo nal contraception in terms of frequency and medication, including antiandro genic therapy, was identical in the 2 groups. After adjustment for hormonal contraception, being born with IUGR had no independent effect on serum and rogen concentrations. In women who were not receiving hormonal contraceptio n, no statistical differences were found between IUGR-born women (n = 67) a nd controls (n = 64) for Delta(4)-androstenedione (2.26 +/- 0.68 vs. 2.24 /- 0.55 ng/mL; P = 0.76), dehydroepiandrosterone sulfate (2294 +/- 1117 vs. 2489 +/- 1235 ng/mL; P = 0.24), testosterone (0.82 +/- 0.85 vs. 0.70 + 0.2 6 ng/mL; P = 0.80), or serum sex hormone-binding protein concentrations (45 .5 +/- 28.2 vs. 53.1 +/- 30.3 nmol/L; P = 0.27). In both IUGR and control g roups, sex hormone-binding protein correlated negatively with fasting insul in (r = -0.23; P = 0.03 and r = -0.26; P = 0.05), but serum androgen levels did not correlate with insulin. In summary, hyperinsulinemia observed in y oung women born with IUGR is not associated with hyperandrogenism. Conseque ntly, our results do not support the hypothesis of a common in utero progra mming of hyperandrogenism and hyperinsulinemia.