SFEBES2022 Poster Presentations Metabolism, Obesity and Diabetes (96 abstracts)
1Kings College London, London, United Kingdom; 2Kings BHF Centre of Research Excellence, London, United Kingdom
During pregnancy progressive maternal insulin resistance occurs which is normal, sparing glucose that can be transported across the placenta to be used by the fetus. In gestational diabetes mellitus (GDM) maternal glucose dysregulation is exacerbated, characterised by hyperglycaemia and associated with long-term adverse outcomes in mother and child, such as increased risk of diabetes and/or cardiovascular disease in later-life. Continuous glucose monitoring (CGM) is an emerging technology aimed at improving glucose homeostasis in pregnant and non-pregnant diabetic patients. This study sought to use CGM in a well-known mouse model of GDM to ascertain if a similar gestational glucose dysregulation could be observed, and to assess the effect of a potential therapy for GDM, the dietary isothiocyanate sulforaphane, on maternal glucose homeostasis. Glucose telemetry probes (HD-XG probes, DSI) were implanted in WT C57BL/6J dams fed a normal chow diet (lean) or high-fat high-sugar diet (Ob). A subset of obese dams received sulforaphane (ObSFN) from mating or gestational day (GD) 0. Blood glucose is continuously monitored throughout gestation and the postpartum period, with glucose and insulin tolerance testing performed. Data represent mean±SD or SEM n=4-7. In early pregnancy (GD2.5) obese mice demonstrate raised blood glucose levels (8.58±0.45 mM) vs. lean (7.94±0.44 mM) and show increased glucose excursions. Later in gestation (GD17.5) all groups demonstrate reduced blood glucose levels compared with early pregnancy although obese groups maintained elevated 24h blood glucose (Lean 6.25±0.73 mM, Ob 7.59±0.78 mM vs. ObSFN 7.48±0.70 mM). By the postpartum period, SFN improved maternal glucose tolerance (AUC 2806±117 Ob vs. 2270±249 ObSFN) and insulin (AUC 298±16 Ob vs. 242±23 ObSFN). To conclude, CGM in obese dams reveals gestational glucose dysregulation with SFN treatment in pregnancy reducing maternal hyperglycaemia, at least partially by increasing sensitivity to insulin.