Martini M C, Bollweg G L, Levitt M D, Savaiano D A
Am J Clin Nutr. 1987 Feb;45(2):432-6. doi: 10.1093/ajcn/45.2.432.
Lactase-deficient subjects more effectively digest lactose in yogurt than lactose in other dairy products, apparently due to yogurt microbial beta-galactosidase (beta-gal) which is active in the GI tract. We evaluated the effects of buffering capacity of yogurt, gastric pH, and microbial cell disruption on beta-gal activity and lactose digestion. Three times more acid was required to acidify yogurt than to acidify milk. Yogurt beta-gal was stable at pH 4.0 but inactivated at lower pH. When yogurt was sonicated to disrupt microbial cell structure, only 20% activity remained after incubation at pH 4.0 for 60 min. In vivo gastric pH remained greater than 2.7 for 3 h after ingestion of yogurt. Acidified milk alone or with disrupted yogurt microorganisms caused twice as much lactose malabsorption as did acidified milk containing intact yogurt microorganisms. The results provide a possible explanation for the survival of beta-gal activity from yogurt in the GI tract.
乳糖酶缺乏的受试者消化酸奶中的乳糖比消化其他乳制品中的乳糖更有效,这显然是由于酸奶中的微生物β-半乳糖苷酶(β-gal)在胃肠道中具有活性。我们评估了酸奶的缓冲能力、胃内pH值和微生物细胞破裂对β-gal活性和乳糖消化的影响。酸化酸奶所需的酸量是酸化牛奶所需酸量的三倍。酸奶β-gal在pH 4.0时稳定,但在较低pH值下失活。当对酸奶进行超声处理以破坏微生物细胞结构时,在pH 4.0下孵育60分钟后,仅保留20%的活性。摄入酸奶后,体内胃内pH值在3小时内保持高于2.7。单独的酸化牛奶或与破裂的酸奶微生物一起的酸化牛奶导致的乳糖吸收不良是含有完整酸奶微生物的酸化牛奶的两倍。这些结果为酸奶中的β-gal活性在胃肠道中得以保留提供了一种可能的解释。