Background:
Global levels of obesity are rising, with 39% of people overweight or obese (WHO). Obese women experience reduced fertility and increased pregnancy risks including preeclampsia. Advanced Glycation Endproducts (AGEs), a proinflammatory modification of proteins exposed to sugars, are elevated in the uterine fluid of obese women versus lean. AGEs compromise both preimplantation embryo development and endometrial cell functions.
Aim: To investigate therapeutics to restore endometrial cell function, and characterise the effect of obesity-associated AGEs on human endometrial epithelial cell organoids (hEEO).
Methods:
Endometrial epithelial cell line (ECC-1) and hEEO were cultured in AGEs equimolar with lean (2 umol/mol lysine) and obese (8 umol/mol lysine) uterine environments. Real time cell analysis (xCelligence) of ECC-1 examined remedial effects of i) 100 uM metformin; ii) antioxidants (10 uM N-acetyl-cysteine, 10 uM N-acetyl-L-carnitine, 5 uM α-lipoic acid); iii) 25 nM RAGE antagonist (FPS-ZM1). hEEO-derived primary epithelial cells exposed to obese AGEs were examined by xCelligence. Multiplex analysis of chemokine & cytokine secretion (inflammatory determinants) in hEEO conditioned medium. CXCL16 profiled by Luminex analysis and glucose by Randox Daytona analyser in uterine fluid of women undergoing IVF.
Results:
Obese AGEs-reduced ECC-1 proliferation (P<0.001) which was successfully restored by antioxidants. hEEO were functionally impacted by obese AGEs, demonstrating a donor-dependent effect on proliferation. AGEs increased secretion of proinflammatory factors associated with poor pregnancy outcomes, including CXCL16 (P=0.04). Uterine fluid CXCL16 correlated positively to BMI (R=0.26; P=0.02) and uterine glucose (AGEs precursor; R=0.74, P<0.0001), but was not significantly different between IVF cycles resulting in pregnancy vs no pregnancy (P=0.46), nor live birth vs miscarriage (P=0.27).
Conclusion:
AGEs promote a uterine inflammatory milieu hostile to implantation. Antioxidants alleviate the effects of AGEs on ECC1 cells, providing a potential therapeutic for obese women. Clinically, reduced uterine AGEs may improve fertility for obese women wishing to conceive.