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Overcoming in vitro gastric destabilisation of emulsion droplets using emulsion microgel particles for targeted intestinal release of fatty acids

机译:使用乳剂微凝胶颗粒克服脂肪酸在肠胃中的不稳定作用

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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 (d(32) similar to 0.13 mu m- similar to 12 mu m 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 (d(32) similar to 50 mu m- similar to 20 mu m 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).
机译:通过使用钙离子(0.1 M)的冷定型沉淀法生产出基于乳清蛋白的乳剂微凝胶颗粒(9.6 wt%乳清蛋白-20 wt%葵花籽油),并使用常规水包油型乳剂研究了它们在体外胃肠道消化中的行为(9.6重量%乳清蛋白-20重量%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尺寸分布,ζ电位,微观结构和水解以及在体外肠消化过程中游离脂肪酸的释放。通过SDS-PAGE(十二烷基硫酸钠聚丙烯酰胺)证明,由于胃内吸附蛋白层的溶解,乳剂在体外胃消化过程中发生了絮凝和凝聚(d(32)类似于0.13μm-类似于12μm,类似于12μm)凝胶电泳)。这种失稳导致随后的肠内消化过程中游离脂肪酸(44%FFA)的释放不受控制和限制,这主要是由于界面面积的减少。相比之下,乳剂微凝胶颗粒在体外胃消化过程中明显更稳定,颗粒大小仅略有减小(d(32)类似于50μm,类似于120分钟后类似于20μm)。乳状液微凝胶颗粒中乳状液小滴对胃部聚结的保护作用是由颗粒中钙离子与乳清蛋白之间的物理化学相互作用控制的,从而限制了胃蛋白酶在胃蛋白酶活性部位的扩散和裂解。在随后的体外肠消化中,由于肠蛋白酶的作用,微凝胶颗粒降解,释放出细小的乳剂液滴,然后释放出明显更高的游离脂肪酸(54%FFA)。

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