15The aim of this study was to gain knowledge about the role of triacylglycerol (TAG) 16 composition in fatty acids (FA) of o/w emulsions on both the pancreatic lipolysis kinetics and 17 the bioaccessibility of released products (i.e. contained within the bile salt micellar phase). A 18 mathematical model was developed and its predictions were compared to a set of 19 experimental data obtained during an in vitro digestion of a whey protein stabilized emulsion. 20Modeling results show that FA residues of TAG were hydrolyzed at specific rates, inducing 21 different bioaccessibility kinetics. The estimated lipolysis rate constants of the studied FA 22(C8:0, C10:0 >> C18:1 n-9 >> C12:0 > C14:0 > C16:0 ≈ C16:1 n-7 > C22:6 n-3) were in 23 close agreement with the available literature on the substrate specificity of pancreatic lipase. 24Results also suggest that lipolysis products are very rapidly solubilized in the bile salt mixed 25 micelles with no fractionation according to the FA carbon chain.

Whey protein stabilized submicron oil-in-water emulsions have been reported to remain relatively stable in size during the gastric phase and to coalesce during the intestinal phase of in vitro digestion experiments. The aim of this study was to understand the impact of oil droplet coalescence on the intestinal lipolysis kinetics during an in vitro digestion of such emulsion, and to develop a mathematical model able to predict the experimental observations. A submicron whey protein stabilized emulsion made of a mixture of medium-chain (MCT) and long-chain triacylglycerols (LCT) was prepared and submitted to gastro-intestinal in vitro digestion. Triacylglycerol concentrations and droplet size distributions were measured before and after the gastric phase and during the intestinal phase using HPLC and laser granulometry, respectively. MCT were fully digested within 15 min of intestinal digestion, whereas LCT were still detected after 5 hours. Moreover, the intestinal lipolysis of LCT showed a two-stage behavior with an initial fast rate that markedly slowed down after about 30 min, a time at which a sudden rise in the droplet sizes, attributed to coalescence, was also observed. A mathematical model based on the experimentally measured droplet sizes and assuming a rate of lipolysis proportional to the interfacial area was developed and successfully used to reproduce the observed kinetics. Our results support the idea that droplet coalescence during the intestinal phase was the main reason for the marked slowdown of the kinetics of lipid digestion, hence suggesting that inhibition of the lipolysis reaction could be a secondary factor only.