Early feeding, feeding tolerance, and lactase activity in preterm infants☆,☆☆,★,★★
Section snippets
Study Design
Infants in the study were part of a prospective feeding trial.12 They were enrolled within 96 hours of birth, stratified by gestational age (26 to 27 vs 28 to 30 weeks) and by diet (mothers’ own milk vs preterm formula), and assigned randomly among 4 treatment combinations in a balanced 2-way design where the 2 factors were the time of initiation of feeding (early, 4 days of age vs standard, 15 days of age) and the method of tube feeding (continuous infusion vs bolus). The 4 treatment
Results
Although the data at 28 days (Table I) taken in isolation suggest a difference between the early continuous and the early bolus groups, it should be borne in mind that the actual analysis took into account the repeated measures nature of the study (ie, the change over time; see Data Analyses).
Age (d) Group Early continuous Early bolus Standard continuous Standard bolus 10 2.8 ± 3.5* 3.4 ± 3.8 1.4 ± 1.1 1.3 ± 0.8 28 8.0 ± 5.4 12.1 ± 7.7 6.5 ± 4.3 7.3 ±
Discussion
Early enteral feeding had a marked effect on the development of lactase activity. Lactase activity rose at a faster rate in the early group than in the standard group. At 10 days of age lactase activity was >100% greater than that measured in the standard group and at 28 days of age was still 60% greater. These results cannot be explained by differences in clinical characteristics of the infants or the infants’ nutritional history, because these were comparable between groups. Our data also
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Cited by (124)
Uncovering the gastrointestinal passage, intestinal epithelial cellular uptake, and AGO2 loading of milk miRNAs in neonates using xenomiRs as tracers
2023, American Journal of Clinical NutritionS-layer protein 2 of vaginal Lactobacillus crispatus 2029 enhances growth, differentiation, VEGF production and barrier functions in intestinal epithelial cell line Caco-2
2021, International Journal of Biological MacromoleculesSimultaneous assessment of intestinal permeability and lactase activity in human-milk-fed preterm infants by sugar absorption test: Clinical implementation and analytical method
2021, Clinical NutritionCitation Excerpt :Therefore, the urinary lactulose/mannitol ratio is a reliable test for measuring intestinal permeability [4,12,13]. The sugar absorption test has additionally been used to assess lactase activity—the second important marker of intestinal maturation—by the enteral administration of lactulose and lactose [6,14–16]. In one study, intestinal permeability and lactase activity were assessed simultaneously in formula-fed preterm infants [16].
Modelling intestinal glucose absorption in premature infants using continuous glucose monitoring data
2019, Computer Methods and Programs in BiomedicineCitation Excerpt :As mentioned previously, another study measured mean lactose ‘digestion and absorption’ to be ∼0.7 mg/min/cm, here was calculated to a corresponding d2 = 0.009/min. Other studies have used enzyme activity to measure gut function with varying morbidities and degrees of maturity [47,48,49,50]. One study estimated intestinal lactose hydrolysation to glucose and galactose to be approximately 80% [47].
Gastrointestinal Development: Implications for Management of Preterm and Term Infants
2018, Gastroenterology Clinics of North AmericaCitation Excerpt :Preterm infants who received enteral feeds at 4 days of life had 100% and 60% more lactase activity at days 10 and 28 of life, respectively, compared with preterm infants who had feeds initiated after day of life 15. Lactase activity was higher in human milk–fed infants than those receiving formula at 10 days of life.21 The location of lactase on the villus structure makes this enzyme vulnerable to intestinal damage.
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From USDA/ARS Children’s Nutrition Research Center, Department of Pediatrics, Department of Pathology, Baylor College of Medicine; Texas Children’s Hospital, Houston, Texas, and Department of Biobehavioral Nursing, University of Washington, Seattle, Washington.
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Supported by the National Institute of Child Health and Human Development, grant No. RO-1-HD-28140, the American Gastroenterological Association, Smith-Kline Beecham Clinical Research Award, the General Clinical Research Center MO1 RR-00188, and the USDA/ARS under Cooperative Agreement No. 58-6250-1-003. This work is a publication of the USDA/ARS Children’s Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine and Texas Children’s Hospital, Houston, Texas. The contents of this publication do not necessarily reflect the views or policies of the USDA, nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government.
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Reprint requests: Robert J Shulman, MD, 1100 Bates St, Houston, TX 77030.
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