Poult Sci. 2017 May 1;96(5):1348-1363. doi: 10.3382/ps/pew337.
The small intestinal mucosa acts to recover nutrients from the lumen while providing a barrier against potential hazards. Its unstirred water layer (USWL) at the lumen interface involves membrane associated mucin linearly protruding from underlying microvilli that entangles secretory mucin released from local goblet cells. Both mucin sources are dominated by repetitive O-glycosylated areas dependant on threonine, serine, glycine, and proline. Secretory mucin differs from membrane attached mucin by further employing multiple cystines that interconnect these areas into a net-like molecular sieve. All of the glycosylated areas have ionizable acidic groups credited with reducing pH from that in the lumen to create a micro environment favoring enzymes finalizing digestion while optimizing nutrient terms for absorption. Erosion of the USWL and/or abuse of the membrane due to lumen threats require continuous repair. The aforementioned amino acids are necessary in substantial amounts while vitamin B6 collaborates with vitamin A as meaningful cofactors for mucin synthesis. Marginal inadequacies of these nutrients during inordinate demand are expected to impair mucin replacement. In turn, marginal increases in feed conversion likely occur while fostering the probability of necrotic enteritis together with gizzard erosions. Abuse of the absorptive membrane is of particular concern from fatty acid hydroperoxides because of their continual presence in feed and inability of the USWL to provide protection. These hydroperoxides threaten membrane integrity by their inclusion in micelles during digestive events with fat thereby permitting transit through the USWL. Once coalesced with membrane phospholipids, structural aberrations are visualized as interfering with nutrient recovery while enabling leakage of cell contents to potentiate wet excreta. Inclusion of dietary vitamin E along with vitamin A into micelles with fatty acid hydroperoxides provides relief by quenching further peroxidation. Assuring cystine, threonine, glycine, and serine that are directly available as such together with vitamins A, E, and B6 represents one approach toward optimizing maintenance of the intestinal mucosa.
小肠黏膜的作用是从腔中回收营养物质，同时提供防止潜在危害的屏障。其在腔界面的未搅动水层（USWL）涉及与膜相关的粘蛋白从下面的微绒毛线性突出，缠绕从局部杯状细胞释放的分泌粘蛋白。这两种粘蛋白来源都以依赖于苏氨酸、丝氨酸、甘氨酸和脯氨酸的重复 O-糖基化区域为主。分泌粘蛋白与膜附着粘蛋白的不同之处在于进一步使用多个半胱氨酸，将这些区域相互连接成一个网状分子筛。所有糖基化区域都具有可电离的酸性基团，可将 pH 值从腔中降低，从而创造有利于酶完成消化的微环境，同时优化吸收的营养条件。USWL 的侵蚀和/或腔威胁导致的膜滥用需要持续修复。上述氨基酸在大量情况下是必需的，而维生素 B6 与维生素 A 协作，作为粘蛋白合成的有意义的辅因子。在过度需求时，这些营养素的边缘不足预计会损害粘蛋白的替代。反过来，饲料转化率的边际增加可能会发生，同时增加坏死性肠炎和肌胃侵蚀的可能性。由于脂肪酸氢过氧化物在饲料中持续存在且 USWL 无法提供保护，因此吸收膜的滥用尤其令人关注。这些氢过氧化物在消化过程中与脂肪一起包含在胶束中，从而允许通过 USWL 转运，从而威胁到膜的完整性。一旦与膜磷脂融合，结构异常就会被视为干扰营养物质的回收，同时使细胞内容物漏出，从而加剧湿排泄物。将膳食维生素 E 与维生素 A 一起纳入含有脂肪酸氢过氧化物的胶束中，通过猝灭进一步的过氧化反应提供缓解。确保半胱氨酸、苏氨酸、甘氨酸和丝氨酸可直接作为此类物质以及维生素 A、E 和 B6 一起使用，是优化维持肠黏膜的一种方法。
