title: Intrauterine growth retardation predisposes to insulin resistance but not to hyperandrogenism in young women.
abstract: It was recently suggested that precocious pubarche associated with subsequent functional ovarian hyperandrogenism and hyperinsulinemia could have a common origin in reduced fetal growth. We previously reported that young women born with intrauterine growth retardation (IUGR: birth weight less than the third percentile) were hyperinsulinemic and less insulin sensitive than women born with normal birth weight. The aim of the present study was to investigate whether these IUGR-born women demonstrated hyperandrogenism compared 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). Hormonal contraception in terms of frequency and medication, including antiandrogenic therapy, was identical in the 2 groups. After adjustment for hormonal contraception, being born with IUGR had no independent effect on serum androgen concentrations. In women who were not receiving hormonal contraception, no statistical differences were found between IUGR-born women (n = 67) and controls (n = 64) for delta4-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 +/- 0.26 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 groups, sex hormone-binding protein correlated negatively with fasting insulin (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 young women born with IUGR is not associated with hyperandrogenism. Consequently, our results do not support the hypothesis of a common in utero programming of hyperandrogenism and hyperinsulinemia.
authors.affiliation: INSERM U-457, Hôpital R. Debré, Paris, France. djacquet@infobiogen.fr
authors.forename: D
authors.initials: D
authors.lastname: Jaquet
authors.forename: J
authors.initials: J
authors.lastname: Leger
authors.forename: D
authors.initials: D
authors.lastname: Chevenne
authors.forename: P
authors.initials: P
authors.lastname: Czernichow
authors.forename: C
authors.initials: C
authors.lastname: Levy-Marchal
mesh_terms: D000293:Adolescent; D000328:Adult; D000735:Androstenedione / Q000097:blood; D001724:Birth Weight; D001786:Blood Glucose / Q000378:metabolism; D015331:Cohort Studies; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D005260:Female; D005317:Fetal Growth Retardation / Q000150:complications*; D005951:Glucose Tolerance Test; D006801:Humans; D017588:Hyperandrogenism; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood; D012738:Sex Hormone-Binding Globulin / Q000378:metabolism; D013739:Testosterone / Q000097:blood
chemical_list: D001786:Blood Glucose; D007328:Insulin; D008055:Lipids; D012738:Sex Hormone-Binding Globulin; D013739:Testosterone; D000735:Androstenedione; D019314:Dehydroepiandrosterone Sulfate