Demers-Mathieu Veronique, Qu Yunyao, Underwood Mark A, Borghese Robyn, Dallas David Charles
Nutrition Program, School of Biological and Population Health Sciences, College of Public Health and Human Sciences, Oregon State University, Corvallis, OR.
Department of Pediatrics, University of California, Davis, Sacramento, CA.
J Pediatr Gastroenterol Nutr. 2018 May;66(5):816-821. doi: 10.1097/MPG.0000000000001835.
Whether premature infants have lower gastric protein digestive capacity than term infants and the extent to which human milk proteases contribute to overall gastric digestion are unknown and were investigated in this study.
Human milk and infant gastric samples were collected from 16 preterm (24-32 wk gestational age) and 6 term (38-40 wk gestational age) mother-infant pairs within a range of 5 to 42 days postnatal age. For each pair, an aliquot of human milk was adjusted to pH 4.5 and incubated for 2 hours at 37 °C to simulate the gastric conditions without pepsin (milkinc). Their gastric protein digestion capacity was measured as proteolysis (free N-terminals) and protease activities. Two-way analysis of variance followed by Tukey post hoc test was applied to compare measurements between preterm and term infants as well as among human milk, milkinc, and gastric samples.
Measurements of gastric protein digestion were significantly lower in preterm infants than term infants. Overall milk protease activity did not differ between human milk samples from term- and preterm-delivering mothers. As protease activity did not increase with simulated gastric incubation, milk proteases likely contributed minimally to gastric digestion.
Preterm infants have lower gastric protein digestion capacity than term infants, which could impair nutrient acquisition. Human milk proteases contribute minimally to overall gastric digestion. The limited activity of milk proteases suggests that these enzymes cannot compensate for the premature infant's overall lower gastric protein digestion.
本研究旨在探究早产儿的胃蛋白消化能力是否低于足月儿,以及人乳蛋白酶对整体胃消化的贡献程度,目前这些情况尚不清楚。
收集了16对早产(胎龄24 - 32周)母婴和6对足产(胎龄38 - 40周)母婴在出生后5至42天内的人乳和婴儿胃样本。对于每对母婴,将一份人乳调节至pH 4.5,并在37°C下孵育2小时以模拟无胃蛋白酶的胃环境(模拟乳)。通过蛋白水解(游离N端)和蛋白酶活性来测量他们的胃蛋白消化能力。采用双向方差分析并随后进行Tukey事后检验,以比较早产儿和足月儿之间以及人乳、模拟乳和胃样本之间的测量结果。
早产儿的胃蛋白消化测量值显著低于足月儿。足月分娩母亲和早产分娩母亲的人乳样本中,总体乳蛋白酶活性没有差异。由于蛋白酶活性在模拟胃孵育过程中没有增加,乳蛋白酶对胃消化的贡献可能最小。
早产儿的胃蛋白消化能力低于足月儿,这可能会损害营养物质的获取。人乳蛋白酶对整体胃消化的贡献最小。乳蛋白酶的有限活性表明这些酶无法弥补早产儿整体较低的胃蛋白消化能力。