The digestive and absorptive capacities of the gastrointestinal tract of a newborn mammal are ontogenically adapted to the food it may receive at birth, ie, mainly to the quality of the milk of its dam. Thus the intestinal mucosa of an infant sea lion has no lactase activity, the milk of the female sea lion being lactose-free. The intestinal mucosa of an infant rat, which can only suckle its mother, has no sucrase activity because it has no access to sucrose. In fact, in rodents, weaning is an abrupt process that is accompanied by a similar abrupt genetically programmed change in several intestinal enzyme activities; for example, as the rat turns from milk to chow, its intestinal mucosa loses lactase activity and gains sucrase activity. Indeed, weaning may be considered as the final step of the gastrointestinal tract development in many rodents.
In humans, the situation is different. Weaning, the period of introduction of complementary feeding, is more progressive and corresponds to the introduction of only a few new molecules including starch, sucrose, and later, fiber. At the same time the volume of breast milk, and, hence, the intake of growth factors and other bioactive molecules decrease. Also, the digestive and absorptive processes are mature well before birth for most of them. The main incompletely developed functions are the secretion of pancreatic amylase and of bile salts that reach adult levels at 3 years and 6 months of age, respectively; starch and fat digestion are thus the main nutrients whose utilization may be limited in the newborn infant.1
Although our knowledge concerning the molecular basis of gene transcription is rapidly expanding,1 it remains extremely scanty concerning the possible permanent alterations of some of the digestive and absorptive processes by early introduction of a given complementary food (new molecule), despite its obvious importance regarding infant feeding practices; thus, the only well-established fact concerns lactase activity levels that cannot be modulated in children or in adults by the amount of ingested lactose.2
1. Can a decrease in the amount of ingested breast milk alter intestinal trophicity?
Breast milk is well-known for containing hormones and growth factors among which some have gastrointestinal regulatory functions such as gastric inhibitory peptides, choleystokinin, and neurotensin; it also contains growth factors such as insulin-like growth factor 1 (IGF-1), transforming growth factor (TGF), and epidermal growth factor (EGF). The latter has been shown to enhance differentiation of human fetal intestine in organ culture leading to increased lactase activity but decreased sucrase activity.3 Cell renewal is linked to the presence in intestinal crypts of a few (a single one in mice) active multipotent stem cells from which the four major intestinal cell types originate. We do not know whether the ingested growth factors contained in human milk act on these stem cells.4 Could decreased amounts of such growth factors lead to slight alterations in stem cell activity and thus to subtle long-lasting modifications of the epithelial and mucosal architecture and functions?
2. Can early and prolonged ingestion of starch permanently modify pancreatic amylase activity?
Amylase activity is barely assayable in the fetal pancreas even in term infants. Intubation studies including assay of amylase activity in duodenal juice have shown that it remains extremely low during the first months of life. Interestingly enough, despite this low activity, 1-month-old infants absorb quite efficiently up to 10 g of starch per day. Signs of malabsorption appear when 20 g/d are ingested.5 A unique study suggested that infants having received starch during their first months of life had higher amylase activity than control infants.6 Given the obvious practical consequences of such an observation, it would certainly be useful to revisit the question of the early development of amylase activity in response to the early introduction of starch to the diet.
3. Can early and prolonged fructose ingestion permanently increase fructose absorption?
Fructose is mainly supplied by sucrose in the diet, but is also found in honey and fruit. It is less efficiently absorbed than glucose. It enters the intestinal epithelium through the facilitative carrier GLUT 5. Although GLUT 5 is be present in the intestinal epithelium as soon as the 12th through the 15th week of gestation, nothing is known regarding the possible transcriptional regulation of its synthesis by the concentration of its substrate.7 Because fructose malabsorption may cause diarrhea in children, the possibility of upregulating its absorption is worth exploring.
- Koldovsky O. Digestive functions and their hormonal regulation during perinatal development in man and experimental animals. In: Salle BL, Swyer PR, eds. Nutrition of the Low Birthweight Infant. (Nestlé Nutrition Workshop, Series, Vol. 32). New York, NY: Raven Press; 1993:9–19
- Gordon JI
- Werlin SL. Development of the exocrine pancreas. In: Walker WA, Durie PR, Hamilton JR, Walker-Smith JA, Watkins JB eds. Pediatric Gastrointestinal Disease. St Louis, MO: Mosby; 1996:143–161
- Copyright © 2000 American Academy of Pediatrics