Background: Maternal diabetes is a pathologic state that increases the incidence of complications in both the mother and the foetus. Patients with diabetes mellitus (DM) may exhibit reproductive abnormalities, including PCOS and hypogonadotropic hypogonadism. Diabetes during pregnancy is an endocrine disruptor and studies performed in animal models have shown abnormalities in gonadal function in the offspring, but it is unknown whether pre-gestational (PGDM) and gestational diabetes (GDM) may affect ovarian function in the offspring of women with DM in the short or long term.
Objective and hypotheses: To evaluate anthropometric profile and serum concentration of testosterone, SHBG and anti-müllerian hormone (AMH), in healthy infant girls born to women who had diabetes during pregnancy (PGDM or GDM) at the time of mini-puberty.
Method: Healthy girls born product of a normal pregnancy in non-diabetic mothers (N=21)§ and healthy daughters of mothers who had diabetes during pregnancy (DM, N=17) were estudied. Anthropometry and blood sample was obtained. Circulating concentrations of testosterone, SHBG and AMH were determined by specific assays.§ The control group is an historic group that was previously studied by Sir-Petermann T, Codner E, Maliqueo M, et al. (Increased Anti-Mullerian Hormone Serum Concentrations in Prepubertal Daughters of Women with Polycystic Ovary Syndrome. J Clin Endocrinol Metab 2006;91:31059).
Results: Daughters of DM mothers had higher AMH (32.2±32.8 vs 9.1±8.6 pM/l, P<0.05) and SHBG levels (251.1±76 nM/l vs 95.8±42.3 nM/l, P<0.05) than daughters of healthy mothers, but similar testosterone levels (0.17±0.3 vs 0.3±0.2 ng/ml).
Conclusion: AMH is produced by the granulosa cells and their serum levels are correlated with the development of preantral and small antral follicles. This preliminary report shows higher AMH levels measured in mini-puberty in a group of female infants born after a pregnancy with diabetes, suggesting that these girls may show evidence of an altered follicular development during early infancy.
Funding: This work was supported by Proyecto Fondecyt N° 11121460, 2012.
01 - 03 Oct 2015
European Society for Paediatric Endocrinology