Glucagon-like peptide-1 (7-36) amide or GLP-1 is an incretin hormone released postprandially from intestinal endocrine L-cells1. GLP-1 has multiple metabolic regulatory functions including glucose-dependent potentiation of insulin secretion, inhibition of gastrointestinal secretions, reduced motility and delayed gastric emptying thereby reducing caloric intake, enhancing satiety and aiding weight loss2. Oestrogen is also an important hormone regulating metabolic homeostasis in both males and females, and while most of its actions are attributed to nuclear receptors ERα and ERβ, rapid non-genomic signalling may also be mediated via the G protein-coupled oestrogen receptor (GPER)3. It has been reported that GLP-1 levels increase during the third trimester of pregnancy but also that fasting GLP-1 is reduced post-menopause suggesting potential regulation of circulating GLP-1 levels by oestrogen and other female sex hormones. It is known that oestrogen receptors are expressed in intestinal epithelial cells, but their expression and potential role in intestinal endocrine cells has not been established. Aims: This study aims to identify the expression and role of oestrogen receptors and their agonists on L-cell function and secretion of GLP-1 using the established GLUTag cell line. Methods: The expression of oestrogen receptors in GLUtag cells was assessed using PCR and immunocytochemistry. The effects of nuclear and membrane oestrogen receptor agonists on changes in intracellular calcium was examined in Fura-2 loaded GLUTag cells. GLP-1 release was assessed over 2h using GLUTag cells seeded on matrigel coated 24-well plates, with measurement of GLP-1 in supernatant using the Total GLP-1 ELISA kit, Millipore. Results: ER alpha and beta and GPER are expressed in GLUTag L-cells, suggesting a potential role for oestrogen in function of GLP-1 secreting cells. In the presence of glucose, oestrogen did not appear to have any significant effect on intracellular calcium, however glucose-dependent (10 mM) GLP-1 was enhanced 1.6 – 1.8- fold (P<0.05-0.01) by oestrogen. GPER agonist G1 had little effect on GLP-1 secretion. Interestingly, ERα agonist PPT and ERβ agonist WAY200070 had inverse concentration-dependent inhibitory effects on GLP-1 release indicating a potential inhibitory role at ER alpha activating concentrations. Conclusion: Oestrogen receptors may play a role in regulating GLP-1 secretion, with native oestrogen having a stimulatory effect on GLP-1 secretion, suggesting that oestrogen receptor activation may increase endogenous GLP-1 as a means to regulating satiety. However, the role of specific oestrogen receptors in L-cell function and GLP-1 secretion require further investigation.