3-Monochloropropane-1,2-diol reduced bioaccessibility of sn-2 palmitate via bounding with pancreatic lipase in infant formula during gastrointestinal digestion

Description

Infant formula contains 3-monochloropropane-1,2-diol esters which are formed during the deodorization step of vegetable oils refining. European Food Safety Authority stated that 3-monochloropropane-1,2-diol esters can be hydrolyzed in the gastrointestinal tract to free-form 3-monochloropropane-1,2-diol, which has potential toxicity and can be rapidly absorbed. Evaluating the effect of 3-monochloropropane-1,2-diol on nutrition absorption is a prerequisite for establishing effective management strategies. A total of 66 crucial lipid molecules associated with 3-monochloropropane-1,2-diol were identified based on Debiased Sparse Partial Correlation analysis. 3-Monochloropropane-1,2-diol affected triglyceride hydrolyzation and increased the concentration of undigested sn-2 palmitate (9.57 to 17.06 mg kg-1). 3-Monochloropropane-1,2-diol reduced the bioaccessibility of fatty acids and more short- (31.42 to 58.02 mg kg-1) and medium-chain fatty acids (17.03 to 26.43 mg kg-1) remained unabsorbed. Lipidomics profiles of infant formula models spiked with different 3-MCPDE levels were investigated and the results were consistent with the experiments with the commercial formula indicating lipid alteration was mainly affected by the digestive 3-MCPD. The formation of 3-monochloropropane-1,2-diol ester-pancreatic lipase with the binding energy of -4.9 kcal mol-1 was more stable than triglyceride-pancreatic lipase (-4.0 kcal mol-1), affecting triglyceride hydrolyzation. 3-Monochloropropane-1,2-diol was bound to Glu13 and Asp331 residues of the pancreatic lipase via hydrogen bonds, which resulted in a conformational change of pancreatic lipase and spatial shielding effect. The existence of the spatial shielding effect reduced the accessibility of pancreatic lipase and further affected triglyceride hydrolyzation. These findings indicated that 3-monochloropropane-1,2-diol obstructed nutrient acquisition and laid the foundation for the subsequent nutrition enhancement design.

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