Talk:Normal Development - Milk: Difference between revisions
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PMID: 20105661 | PMID: 20105661 | ||
http://www.ncbi.nlm.nih.gov/pubmed/20105661 | http://www.ncbi.nlm.nih.gov/pubmed/20105661 | ||
==2009== | |||
===Reevaluation of the DHA requirement for the premature infant=== | |||
Prostaglandins Leukot Essent Fatty Acids. 2009 Aug-Sep;81(2-3):143-50. Epub 2009 Jul 5. | |||
Lapillonne A, Jensen CL. | |||
Source | |||
APHP, Paris Descartes University, Paris, France. alexandre.lapillonne@svp.aphp.fr | |||
Abstract | |||
The long-chain polyunsaturated fatty acid (LC-PUFA) intake in preterm infants is crucial for normal central nervous system development and has the potential for long-lasting effects that extend beyond the period of dietary insufficiency. While much attention has focused on improving their nutritional intake, many premature infants do not receive an adequate DHA supply. We demonstrate that enterally fed premature infants exhibit daily DHA deficit of 20mg/kg.d, representing 44% of the DHA that should have been accumulated. Furthermore, the DHA content of human milk and current preterm formulas cannot compensate for an early DHA deficit which may occur during the first month of life. We recommend breast-feeding, which supplies preformed LC-PUFA, as the preferred method of feeding for preterm infants. However, to fulfill the specific DHA requirement of these infants, we recommend increasing the DHA content of human milk either by providing the mothers with a DHA supplement or by adding DHA directly to the milk. Increasing the DHA content above 1% total fatty acids appears to be safe and may enhance neurological development particularly that of infants with a birth weight below 1250 g. We estimate that human milk and preterm formula should contain approximately 1.5% of fatty acid as DHA to prevent the appearance of a DHA deficit and to compensate for the early DHA deficit. | |||
PMID: 19577914 | |||
http://www.ncbi.nlm.nih.gov/pubmed/19577914 | |||
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Cite this page: Hill, M.A. (2026, September 17) Embryology Normal Development - Milk. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Normal_Development_-_Milk |
2011
COMPANION ANIMALS SYMPOSIUM: Development of the mammalian gastrointestinal tract, the resident microbiota, and the role of diet in early life
J Anim Sci. 2011 May;89(5):1506-19. Epub 2011 Jan 14.
Buddington RK, Sangild PT. Source Department of Health and Sport Science, University of Memphis, Memphis, TN 38152.
Abstract
Mammalian gastrointestinal (GI) development is guided by genetic determinants established during the evolution of mammals and matched to the natural diet and environment. Coevolution of the host GI tract (GIT) and the resident bacteria has resulted in commensal relationships that are species and even individual specific. The interactions between the host and the GI bacteria are 2-way and of particular importance during the neonatal period, when the GIT needs to adapt rapidly to the external environment, begin processing of oral foods, and acquire the ability to differentiate between and react appropriately to colonizing commensal and potentially pathogenic bacteria. During this crucial period of life, the patterns of gene expression that determine GI structural and functional development are modulated by the bacteria colonizing the previously sterile GIT of fetuses. The types and amounts of dietary inputs after birth influence GI development, species composition, and metabolic characteristics of the resident bacteria, and the interactions that occur between the bacteria and the host. This review provides overviews of the age-related changes in GIT functions, the resident bacteria, and diet, and describes how interactions among these 3 factors influence the health and nutrition of neonates and can have lifelong consequences. Necrotizing enterocolitis is a common GI inflammatory disorder in preterm infants and is provided as an example of interactions that go awry. Other enteric diseases are common in all newborn mammals, and an understanding of the above interactions will enhance efforts to support neonatal health for infants and for farm and companion animals.
PMID: 21239667 http://www.ncbi.nlm.nih.gov/pubmed/21239667
2010
Bioactive proteins in human milk: mechanisms of action
J Pediatr. 2010 Feb;156(2 Suppl):S26-30.
Lönnerdal B. Source Department of Nutrition, University of California, Davis, CA, USA. bllonnerdal@ucdavis.edu
Abstract
Human milk contains a multitude of bioactive proteins, with very diverse functions. Some of these proteins are involved in the synthesis and expression of milk, but the majority appears to have evolved to provide physiological activities in the breast-fed infant. These activities are exerted by a wide variety of mechanisms and have largely been unraveled by in vitro studies. To be active in the gastrointestinal tract, these proteins must be able to resist proteolytic degradation, at least for some time. We have evaluated the human milk proteins lactoferrin, haptocorrin, alpha(1)-antitrypsin, and transforming growth factor -beta in an in vitro digestion model, mimicking the conditions of the infant gastrointestinal milieu. These bioactive proteins are resistant against proteolysis and can remain intact or as larger fragments through passage of the gastrointestinal tract. In vitro digestibility assays can be helpful to assess which human milk proteins can resist proteolysis and to what extent.
Copyright 2010 Mosby, Inc. All rights reserved.
PMID: 20105661 http://www.ncbi.nlm.nih.gov/pubmed/20105661
2009
Reevaluation of the DHA requirement for the premature infant
Prostaglandins Leukot Essent Fatty Acids. 2009 Aug-Sep;81(2-3):143-50. Epub 2009 Jul 5.
Lapillonne A, Jensen CL. Source APHP, Paris Descartes University, Paris, France. alexandre.lapillonne@svp.aphp.fr
Abstract
The long-chain polyunsaturated fatty acid (LC-PUFA) intake in preterm infants is crucial for normal central nervous system development and has the potential for long-lasting effects that extend beyond the period of dietary insufficiency. While much attention has focused on improving their nutritional intake, many premature infants do not receive an adequate DHA supply. We demonstrate that enterally fed premature infants exhibit daily DHA deficit of 20mg/kg.d, representing 44% of the DHA that should have been accumulated. Furthermore, the DHA content of human milk and current preterm formulas cannot compensate for an early DHA deficit which may occur during the first month of life. We recommend breast-feeding, which supplies preformed LC-PUFA, as the preferred method of feeding for preterm infants. However, to fulfill the specific DHA requirement of these infants, we recommend increasing the DHA content of human milk either by providing the mothers with a DHA supplement or by adding DHA directly to the milk. Increasing the DHA content above 1% total fatty acids appears to be safe and may enhance neurological development particularly that of infants with a birth weight below 1250 g. We estimate that human milk and preterm formula should contain approximately 1.5% of fatty acid as DHA to prevent the appearance of a DHA deficit and to compensate for the early DHA deficit.
PMID: 19577914 http://www.ncbi.nlm.nih.gov/pubmed/19577914