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Overcoming in vitro gastric destabilisation of emulsion droplets using emulsion microgel particles for targeted intestinal release of fatty acids
Food Hydrocolloids ( IF 10.7 ) Pub Date : 2019-04-01 , DOI: 10.1016/j.foodhyd.2018.11.010
Ophelie Torres , Brent S. Murray , Anwesha Sarkar

Abstract Whey protein based emulsion microgel particles (9.6 wt% whey protein – 20 wt% sunflower oil) were produced via cold set precipitation using calcium ions (0.1 M) and their behaviour under in vitro gastrointestinal digestion was investigated with conventional oil-in-water emulsions (9.6 wt% whey protein – 20 wt% sunflower oil) as a control. The droplet size distribution, zeta-potential, microstructure and hydrolysis of interfacial whey protein during in vitro gastric digestion and free fatty acid release during in vitro intestinal digestion were compared for both samples. During in vitro gastric digestion, emulsions flocculated and coalesced (d32 ∼ 0.13 μm–∼12 μm after 120 min) due to pepsinolysis of the adsorbed protein layer, as evidenced by SDS-PAGE (sodium dodecyl sulphate polyacrylamide gel electrophoresis). This destabilisation led to uncontrolled and limited release of free fatty acids (44% FFA) during subsequent intestinal digestion, largely due to the reduction in interfacial area. In comparison, emulsion microgel particles were noticeably more stable during in vitro gastric digestion, with only a slight decrease in particle size (d32 ∼ 50 μm–∼20 μm after 120 min). The protection of emulsion droplets against gastric coalescence in emulsion microgel particles was controlled by physicochemical interactions between calcium ions and whey protein in the particles, limiting both pepsin-diffusion and cleavage at the pepsin active site. Under subsequent in vitro intestinal digestion, the microgel particles degraded due to the action of intestinal proteases, releasing fine emulsion droplets, which then gave significantly higher release of free fatty acids (54% FFA).

中文翻译:

使用乳液微凝胶颗粒靶向肠道释放脂肪酸克服乳液液滴的体外胃失稳

摘要 乳清蛋白基乳液微凝胶颗粒(9.6 wt% 乳清蛋白 - 20 wt% 葵花籽油)通过使用钙离子(0.1 M)的冷凝固沉淀制备,并用常规水包油研究了它们在体外胃肠消化下的行为。乳液(9.6 wt% 乳清蛋白 – 20 wt% 葵花籽油)作为对照。比较了两种样品在体外胃消化过程中界面乳清蛋白的液滴大小分布、zeta 电位、微观结构和水解以及体外肠道消化过程中的游离脂肪酸释放。在体外胃消化过程中,如 SDS-PAGE(十二烷基硫酸钠聚丙烯酰胺凝胶电泳)所证明的,由于吸附的蛋白质层的胃蛋白酶溶解,乳液絮凝和聚结(120 分钟后 d32 ∼ 0.13 μm–∼12 μm)。这种不稳定导致在随后的肠道消化过程中游离脂肪酸 (44% FFA) 不受控制和有限的释放,这主要是由于界面面积的减少。相比之下,乳液微凝胶颗粒在体外胃消化过程中明显更稳定,粒径仅略有减小(120 分钟后 d32~50 μm-~20 μm)。乳剂液滴在乳剂微凝胶颗粒中防止胃聚结的保护作用是通过颗粒中钙离子和乳清蛋白之间的物理化学相互作用来控制的,从而限制了胃蛋白酶活性部位的胃蛋白酶扩散和裂解。在随后的体外肠道消化下,微凝胶颗粒在肠道蛋白酶的作用下降解,释放出细小的乳液液滴,
更新日期:2019-04-01
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