Ontogeny of intestinal nutrient transport.
Children born prematurely lack the ability to digest and to absorb nutrients at rates compatible with their nutritional needs. As a result, total parenteral nutrition may need to be given. While this nutritional support may be lifesaving, the baby who receives this therapy is exposed to the risks of possible sepsis, catheter dysfunction, and liver disease. The rodent model of postnatal development provides a useful framework to investigate some of the cellular features of human intestinal development. The up-regulation of intestinal gene expression and precocious development of intestinal nutrient absorption can be achieved by providing growth factor(s) or by modifying the composition of the maternal diet during pregnancy and nursing or the weaning diet of the infant. Accelerating the digestive and absorptive functions of the intestine would thereby allow for the maintenance of infant nutrition through oral food intake, and might possibly eliminate the need for, and risks of, total parenteral nutrition. Accordingly, this review was undertaken to focus on the adaptive processes available to the intestine, to identify what might be the signals for and mechanisms of the modified nutrient absorption, and to speculate on approaches that need to be studied as means to possibly accelerate the adaptive processes in ways which would be beneficial to the newborn young.
Department of Medicine, University of Alberta, Edmonton, Canada.
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Thiesen
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Wild
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Keelan
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Clandinin
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McBurney
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Van Aerde
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Thomson
D000222:Adaptation, Physiological; D000305:Adrenal Cortex Hormones / Q000494:pharmacology; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D016259:Genes, myc / Q000502:physiology; D013006:Growth Hormone / Q000494:pharmacology; D006801:Humans; D007231:Infant, Newborn; D007408:Intestinal Absorption / Q000187:drug effects; D009955:Ornithine Decarboxylase / Q000378:metabolism
D000305:Adrenal Cortex Hormones; D013006:Growth Hormone; D009955:Ornithine Decarboxylase