Glycidyl esters (GEs) are known to be formed during vegetable oil processing. Because of their structure, it has been hypothesised that GEs, like fatty acid esters of chloropropanols (MCPD esters), may be accepted as substrates by gut lipases to release the epoxide glycidol. If confirmed such a hypothesis would be important for risk assessment since glycidol is considered as a genotoxic carcinogen. In the present study, biotransformation was investigated using static and dynamic gastrointestinal models. During the experiments, aliquots were analysed for non-digested GEs using liquid chromatography-time-of-flight-mass spectrometry (LC-ToF-MS). In the static model, a fast hydrolysis of GEs was observed as a result of lipase action. Lipase was very efficient at pH 4.8, and totally inhibited at very low pH (1.7). In the absence of lipase, GEs were found to be relatively stable. The potential impact of food matrix was studied using milk in a dynamic model simulating human physiological conditions. The fast, pH-dependent hydrolysis of GEs was further confirmed. The possible transformation of the digestion products was then investigated using gas chromatography coupled to mass spectrometry (GC-MS), mainly the epoxide ring-opening to glycerol followed by additional reactions. In any conditions applied, neither 2- nor 3-mono-chloropropanediol (2- nor 3-MCPD) were formed, indicating that a ring-opening of the epoxide group of GEs or glycidol followed by a reaction with chloride was unlikely. A small transformation of glycidol into glycerol was observed after longer incubation time correlated with a low pH. This suggested that ring-opening and reaction with water is possible in strongly acidic conditions. Overall, it is concluded that GEs are rapidly digested by gut lipases to form glycidol. Consequently, GEs should be considered as sources of glycidol exposure. In addition, risk assessment of GEs can likely rely on hazard identification and characterisation data specific for glycidol.