Oral Presentation ESA-SRB-ANZOS 2025 in conjunction with ENSA

Food for thought: the impact of diet on endometrial decidualisation and embryo implantation (128710)

Laura M Rogers 1 , Gendie E Lash 2 , Greg M Anderson 1 , Jane E Girling 1
  1. Department of Anatomy, School of Biomedical Sciences, University of Otago | Ōtākou Whakaihu Waka, Dunedin, Aotearoa New Zealand
  2. Division of Uterine Vascular Biology, Guangdong Provincial Clinical Research Center for Child Health, Guangzhou Institute of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou

We postulate that maternal diet induced obesity is a complex, but modifiable, contributing factor to the burden of spontaneous early pregnancy loss which reportedly occurs in up to 15% of clinical pregnancies1. High levels of adipose tissue are linked to dysregulation of decidualisation2,3; a crucial cell transformation in the uterus that facilitates embryo implantation and provides the maternal component of the placenta. We are using mouse models to investigate how a high fat diet impacts decidualisation and embryo implantation.

 

C57BL/6 mice were fed a high fat (HFD), high sucrose (HSD) or control diet for 8 weeks and mated before being culled on gestational day (GD) 5.5 or 7.5. Body composition was measured using minispec NMR. The number of implantation sites were recorded, and uteri were taken for histology and immunohistochemistry for markers of vasculature, proliferation, apoptosis, senescence and immune cells. Serum was collected to determine progesterone, prolactin, leptin and adiponectin levels.

 

After 6 weeks, the high fat group had significantly higher fat composition (HFD=27.8±1.23; HSD=19.2±0.82; control=17.0±1.04) and less lean mass than other diet groups (p<0.0001). There was no significant effect of diet (p=0.86) or GD (p=0.79) on the number of implantation sites, and no significant interaction effect (p=0.13). Histological and serum analyses of the tissue are currently underway.

 

Although no embryo loss was observed at the time points examined, we predict there will be impacts on decidualisation that may negatively impact embryos should pregnancy have progressed. Our ongoing studies will elucidate the subtle effects of high fat and/or high sucrose diets on endometrial processes. Such studies are fundamental if we are to further understand the mechanisms responsible for early pregnancy loss.

  1. (1) Regan, L. et al., (2011). The investigation and treatment of couples with recurrent first-trimester and second-trimester miscarriage. RCOG Green Top Guideline, 17, 1-17.
  2. (2) Chen, Z. et al., (2023). Dysregulated glycolysis underpins high-fat-associated endometrial decidualization impairment during early pregnancy in mice. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1869(4), 166659.
  3. (3) Rhee, J. S. et al., (2016). Diet-induced obesity impairs endometrial stromal cell decidualization: a potential role for impaired autophagy. Human reproduction, 31(6), 1315-1326.