Endocrine Abstracts

Intro/Aims: Maternal obesity is a major risk factor for the development of first onset of diabetes in pregnancy, also known as gestational diabetes mellitus (GDM). Recent studies also indicate that non-alcoholic fatty liver disease (NAFLD) is an independent predictor of GDM. Sulforaphane (SFN) is a well-known dietary activator of the redox-sensitive transcription factor Nrf2, with reported anti-adipogenic and NAFLD ameliorating effects in non-pregnant obese rodent models. In this study we sought to determine whether sulforaphane could exert metabolic protection in GDM murine dams.

Methods: Wildtype (WT) and Nrf2 deficient C57BL/6 dams were fed a highly palatable obesogenic diet 6 weeks prior to pregnancy, then received either vehicle (corn oil) or SFN throughout pregnancy and the postpartum period. Bodyweight was measured throughout the developmental period, with visceral and subcutaneous adiposity (parametrial and inguinal fat pads, respectively measured relative to bodyweight and tibia length) determined upon post-partum termination. H&E staining of liver tissue was used to quantify maternal steatosis.

Results: SFN significantly reduced postnatal weight retention, with a reduction in subcutaneous inguinal adipose tissue depots noted in WT not Nrf2 deficient dams. Preliminary results also indicate that hepatic lipid deposition quantified as % lipid area and mean lipid area were also attenuated by SFN intervention in WT not Nrf2 deficient dams.

Conclusion: SFN exerts maternal metabolic protection against obesogenic dietary feeding, reducing subcutaneous adipose deposition as well as liver lipid accumulation. Protection is ameliorated in Nrf2 deficient dams suggesting that SFNs protective effects are mediated via Nrf2 activation.