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Consumption of bioactive molecules protecting from necrotising enterocolitis in premature newborns receiving natural or pasteurised human milk

Published online by Cambridge University Press:  30 June 2021

C. Garcia
Affiliation:
UMR INSERM U476/INRA 1260, Faculty of Medicine Timone, Mediterranean University, Marseille, France
R. D. Duan
Affiliation:
Departments of Clinical Sciences, Medicine (Gastroenterology and Nutrition), Lund University, Lund, Sweden
S. Confort Gouny
Affiliation:
UMR CNRS 6612 CRMBM, Faculty of Medicine Timone, Mediterranean University, Marseille, France
V. Millet
Affiliation:
Neonatology Department, Conception Hospital, Marseille, France
C. Gire
Affiliation:
Neonatology Department, Nord Hospital, Marseille, France
C. Palix
Affiliation:
Neonatology Department, Nord Hospital, Marseille, France
N. W. Lutz
Affiliation:
UMR CNRS 6612 CRMBM, Faculty of Medicine Timone, Mediterranean University, Marseille, France
P. Deprez
Affiliation:
UMR INSERM U476/INRA 1260, Faculty of Medicine Timone, Mediterranean University, Marseille, France
M. Bernard
Affiliation:
UMR CNRS 6612 CRMBM, Faculty of Medicine Timone, Mediterranean University, Marseille, France
M. Armand
Affiliation:
UMR INSERM U476/INRA 1260, Faculty of Medicine Timone, Mediterranean University, Marseille, France
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Abstract

Type
Abstract
Copyright
Copyright © The Authors 2008

The aim of the present study was to investigate, in very-low-birth-weight (VLBW) premature newborns susceptible to developing a necrotising enterocolitis (NEC), the consumption of bioactive molecules (DHA, sphingomyelin (SM), acid sphingomyelinase (Smase), and CD14) over 1 month, and to compare their levels in natural mother's milk (NM) v. pasteurised mother's milk from a milk bank (PM).

Nine VLBW premature newborn babies (<1 kg body weight, <32 weeks of gestational age) were followed up for 4 weeks after the commencement of digestive stimulation using NM or PM( Footnote 1 ) (feeding rate 10–140 ml/kg body weight per d). A representative sample of the feeds was collected for a complete day in each week of the study. Milk lipids were extracted for lipid quantification( Footnote 2 ), determination of the fatty acid profile (by GC) and identification and quantification of classes of phospholipid (PL; by 31P NMR). Acid Smase activity was measured using radiolabelled SM( Footnote 3 ) and CD14 was quantified using ELISA.

DHA levels were not different in NM and PM but were low compared with the nutritional recommendations (% total fatty acids; NM, 0.39 (se 0.23; range 0.17–0.85); PM, 0.33 (se 0.09; range 0.22–0.55)). The proportion of SM was similar between groups (28–30% total PL) but levels varied among all milk samples from 0.07 mm to 0.17 mm. Consumption of SM varied from 3 to 27 mg/d; SM has been shown to have a beneficial effect on gut maturity at levels of 60–150 mg/d( Footnote 4 ). Acid Smase activity was significantly lower (30%) in PM than in NM (pmol/h per ml; 215 v. 308 respectively; P<0.01), and soluble CD14 was not detected in PM while in NM the level ranged from 9 to 21 μg/ml, leading to a consumption of 0.4–3.3 mg/d.

The present preliminary study raises several questions: (1) what are the minimal amounts of each bioactive molecule that can protect against NEC; (2) is PM quality sufficient to protect against NEC; (3) what are the main reasons for the low level of DHA in the milk of these Mediterranean mothers (nutritional and/or genetic).

The authors thank the Benjamin Delessert Institute for financial support.

References

1. Berseth, CL, Bisquera, JA & Paje, VU (2003) Pediatrics 111, 529534.CrossRefGoogle Scholar

2. Hernell, O, Staggers, JE & Carey, MC (1990) Biochemistry 29, 20412056.CrossRefGoogle Scholar

3. Wu, J, Cheng, Y, Jonsson, BA, Nilsson, A & Duan, RD (2005) J Lipid Res 46, 19441952.CrossRefGoogle Scholar

4. Motouri, M, Matsuyama, H, Yamamura, J, Tanaka, M, Aoe, S, Iwanaga, T & Kawakami, H (2003) J Pediatr Gastroenterol Nutr 36, 241247.CrossRefGoogle Scholar