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Article gastroenterology

The Neonatal Gastrointestinal

Tract: Developmental Anatomy, Physiology,
and Clinical Implications
Josef Neu, MD,* Nan Li,
Objectives After completing this article, readers should be able to:
1. Describe key elements of the developmental anatomy of the gastrointestinal tract and
how it relates to nutrition in low-birthweight infants.
2. Characterize key elements of the developmental physiology of the gastrointestinal
tract, including gastroesophageal sphincter function, gastric emptying, and intestinal
motility, along with clinical implications.
3. Describe key elements of the development of digestive absorptive functions and how
these relate to nutrition of the preterm and term neonate.
4. Explain minimal enteral and parenteral nutrition for very low-birthweight infants.
5. Describe potential areas for future investigation.

The past 20 years has witnessed a surge of interest in gastrointestinal (GI) development and
neonatal nutrition. Application of basic knowledge of intestinal development and appro-
priate nutrition for critically ill and preterm infants can be used to ameliorate short-term
morbidity in infants who would not have survived prior to 20 years ago. Long-term
morbidity also may be affected by improved nutrition because these infants are undergoing
critical periods of development during which poor nutrition may have life-long conse-
The focus of previous research has been various aspects of morphology, basic biochem-
istry and physiology of the developing GI tract, and how this knowledge can be applied to
nutrition of the neonate. More recently, the advent of molecular biology and other
technological advances has initiated a new era of research into these areas, which are being
termed “omics” and include genomics, proteomics, methylomics, and metabolomics (see
Young et al in Suggested Reading). These emerging fields offer exciting opportunities to
understand better the various aspects of development that will be subsequently applied to
diagnosis, prevention, and treatment of diseases.

Anatomic Development
The intestine undergoes tremendous growth during fetal life. It elongates 1,000-fold from
5 to 40 weeks’ gestation, with the length doubling in the last 15 weeks of gestation to a
mean of 275 cm at birth. In the small intestine, villi already are formed at 16 weeks’
gestation. Villi also are present in the large intestine, but these partially regress at
approximately 29 weeks’ gestation. Microvilli begin to cover the apical surface of the small
intestinal epithelium so that by adulthood, the intestinal surface provides the largest
interface between the outside environment and the internal milieu (approximately
2,000,000 cm2, which is nearly the size of a tennis court).
After intestinal epithelial cells undergo mitotic cell division in the crypt, they migrate up
the villus, where they undergo differentiation and become actively absorbing cells, which
are sloughed from the villus tip into the intestinal lumen. Although not adequately studied
in humans, there is reason to believe that the migration time is similar to that found in
rodents, where the turnover time in the adult is approximately 48 hours and in the infant
is about 96 hours (Fig. 1).
Numerous cell types exist in the small intestine (Fig. 2). These include the intestinal

*Department of Pediatrics, University of Florida, College of Medicine, Gainesville, FL.

This work was supported in part by NIH grant R01HD3894.

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absorptive epithelium, Paneth cells (involved in secretion 279 to 448 mOsm/kg do not alter significantly the rates
of defensins and other peptides involved in innate immu- of gastric emptying of isocaloric formulas. No informa-
nity), goblet cells (involved in the secretion of the mucus tion on the ability of duodenal feedback to control the
overlying the intestine), and other cell types associated rate of gastric emptying in the VLBW infant between
with the intestinal neuroendocrine system and immune 25 and 32 weeks’ gestation is available. Inadequate con-
system. trol of emptying could overwhelm the intestinal tract,
leading to malabsorption and feeding intolerance.
Physiologic Development Therapeutic agents that increase gastric emptying
Amniotic Fluid Swallowing rates in children and adults also appear to be effective in
Many physiologic processes develop during fetal life. preterm infants. Metoclopramide and cisapride increase
One that is considered particularly important is fetal the gastric emptying rate in preterm and term infants.
swallowing. The fetus swallows about 450 mL/d of Nasojejunal feeding may provide only limited improve-
amniotic fluid in the third trimester. This fluid contains ment in feeding tolerance because intestinal motility
nutrients and growth factors, but its availability is inter- beyond the gastric outlet is also immature.
rupted suddenly at the time of preterm birth. There is The small bowel motility patterns are poorly devel-
speculation that this sudden interruption of large fluid oped before 28 weeks’ gestation. The small intestine
fluxes from fetal life to extrauterine life might have shows disorganized motility patterns between 27 and
detrimental consequences (Fig. 3). 30 weeks’ gestation, which progress to a more mature
pattern in which migrating myoelectric complexes are
Gastroesophageal Sphincter Tone present at 33 to 34 weeks’ gestation. Gastroanal transit
Gastroesophageal (GE) sphincter tone also undergoes ranges from 8 to 96 hours in preterm infants compared
remarkable changes during development. The lower with 4 to 12 hours in adults. In preterm infants, the
esophageal pressure is approximately 4 cm H2O and motilin receptor is not present until 32 weeks’ gestation,
28 cm H2O in preterm and term infants, respectively and the cyclic release of motilin is not present. This
(Fig. 4). This is related to the high incidence of GE reflux suggests that the use of erythromicin would not be
(GER) in preterm infants. Of note, GER has been impli- effective prior to 32 weeks’ gestation, although more
cated as one of the causes of apnea and bradycardia in recent studies suggest improved feeding tolerance with
very low-birthweight (VLBW) infants. This has led to the erythromicin.
frequent use of prokinetic agents, although well-
designed, controlled studies supporting their safety and Protein Digestion
efficacy are lacking. More recent data suggest that most Knowledge of digestive-absorptive processes has in-
cases of apnea and bradycardia in VLBW infants are not creased significantly in the past 2 decades. Gastric acid
causally related to GER. secretion is limited in VLBW infants. In the first 24 to
48 hours after birth, intragastric pH remains at about
Intestinal Motility 5.5 to 7.0 and is relatively resistant to pentagastrin.
Delayed gastric emptying also is related to GER because However, both basal and pentagastrin-stimulated acid
gastric emptying is slower in preterm than in term in- secretion doubles from the first to fourth week of post-
fants. In the adult, the rate of gastric emptying is con- natal life in preterm infants.
trolled by feedback from the small intestine. Stimulation This process should be kept in mind when considering
of duodenal receptors by acid, fat, carbohydrate, trypto- the use of histmine2 (H2) blockers, which are widely
phan, or increasing osmolality decreases the rate of gas- prescribed in many neonatal intensive care units. Gastric
tric emptying. Studies of the effects of various formula acid can serve as a barrier to microorganisms. When
components on gastric emptying have yielded conflicting gastric acid secretion is decreased by the use of inhibitors,
results. Incremental increases of caloric density from this can lead to a higher load of bacteria in the more distal
0.2 to 0.66 kcal/mL decreased the rate of gastric emp- regions of the intestine. Several studies suggest that
tying among infants of 32 to 39 weeks’ gestation, but critically ill patients treated with H2 blockers have a
there were no differences with increments of 0.6 to higher incidence of nosocomial sepsis.
0.8 kcal/mL formula. Despite the reduced emptying rate Some of the enzymes involved in intraluminal diges-
at higher caloric density, the quantity of calories deliv- tion of proteins are also relatively limited in preterms.
ered into the duodenum from the stomach increased Pepsin secretion usually is fully developed by 3 to 8
with concentrated formula. Changes in osmolality from months of postnatal age, and levels are much lower in

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preterm than in term newborns (639 U/Kg versus The permeation of fatty acids and 2-monoglycerides
3,352 U/Kg in adults). This could be a limiting factor from the lumen into the cell, intracellular re-
for the digestion of certain types of protein in preterm esterification, chylomicron formation, and transport to
infants. the chylomicrons from the cell into the circulation are
The protease cascade in the small intestine is catalyzed the primary absorptive events. After lumenal digestion,
by food-stimulated secretion of enterokinase from the fatty acids and monoglycerides approximate the absorp-
upper small intestinal epithelium (Fig. 5). This enzyme tive surface and enter the intracellular milieu by processes
catalyzes the activation of trypsinogen to trypsin that, in that are not yet well understood. After entry into the cell,
turn, activates several other inactive zymogens into pro- medium-chain triglycerides undergo a relatively simple
teases, which are active in the intestinal lumen. However, process of assimilation in which they do not undergo
even though enterokinase is detectable at 24 weeks’ re-esterification and chylomicron formation, as the long-
gestation, its concentration is relatively low and reaches chain lipids do. Medium-chain triglycerides are taken
only 25% of adult activity at term. This can be limiting to directly into the portal venous system; chylomicrons
protein digestion and may be responsible for an increased formed from long-chain fats enter the lymphatics. In
capability of larger antigens or microorganisms to pass conditions that involve obstruction of the lymphatics,
into the intestine without breakdown by luminal en- feeding formulas containing primarily medium-chain
zymes. triglycerides rather than long-chain triglycerides are rec-
Lipid Digestion and Absorption There is considerable interest in the capability of
Lipid requirements are limited to the 18-carbon essential neonates to convert the essential fatty acids into longer-
fatty acids (linoleic or linolenic acid). Lipid makes up chain fatty acids with 20 or more carbons. These long-
about 50% of the nonprotein energy content of human chain polyunsaturated fatty acids (LCPUCAs) are critical
milk and formulas, both of which contain these fatty in the formation of eicosanoids and structural compo-
acids. However, both term and preterm infants have nents of the central nervous system. They are found in
pancreatic insufficiency compared with older children relatively high concentrations in human milk but are not
and adults. found in total parenteral nutrition or most neonatal
The digestion of lipid can be split into several phases. formulas. Whether the addition of LCPUCAs to formu-
The luminal phase involves de-esterification of triglycer- las results in improved neurodevelopment is the subject
ides to 3-monoglyerides and free fatty acids and bile of current intense investigation.
acid-mediated micellar solubilization. Most essential fatty acids provided to neonates are
In the process of fat digestion, several lipases hydro- derived from the omega-6 family (linoleic acid). This is
lyze fatty acids from glycerol. Figure 6 shows some of because much of the lipid derived from formulas or
these, which include the lipase found in human milk (bile intravenous lipid solutions is from vegetable oil, which is
salt-stimulated lipase) and lingual, gastric, pancreatic, rich in the omega-6 but not the omega 3 fraction. The
and epithelial lipases. Bile acid-stimulated lipase is implications of this will be discussed in the article on
present in milk and becomes active in the small intestine immunonutrients in this issue of NeoReviews.
lumen in the presence of bile acids. Lingual lipase is
secreted by glands at the base of the tongue and is Carbohydrate Digestion and Absorption
involved in gastric lipid hydrolysis. Lipases produced in Carbohydrates ingested by neonates are either natural
the stomach, secreted from the pancreas, and present in lactose (the primary carbohydrate in most human and
the mucosa also are involved in lipid hydrolysis. mammalian milks) or glucose polymers, sucrose, or hy-
Bile acids are critical to efficient fat digestion and drolyzed starches. Mechanisms for carbohydrate absorp-
absorption. These processes are limited in VLBW infants tion mature in a defined sequence during human fetal
because the duodenal concentration of bile acids is low development. The intestinal enzymes lactase, sucrase,
due to lower synthesis and ileal reabsorption (Fig. 7). maltase, isomaltase, and glucoamylase are at mature lev-
Lower micellar solubilization leads to inefficient cell- els in the term fetus. Pancreatic amylase activity is low in
mucosal interaction and subsequently lower absorption both term and preterm neonates and appears to require
of the molecules of the mucosal-cell surface interface several months to reach mature levels. In the preterm
(Fig. 8). Long-chain fatty acids but not medium-chain infant, sucrase, maltase, and isomaltase are usually fully
fatty acids depend on bile acids for solubilization and, active, but lactase activity, which increases markedly from
thus, are the most susceptible to inefficient absorption. 24 to 40 weeks’ gestation, may be low, depending on

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fetal age. Despite these developmental patterns, clinical but this digestion still falls substantially short of that
lactose intolerance is uncommon. Postnatal adaptive re- accomplished by the usual concentrations of pancreatic
sponses to ingested carbohydrates lead to competent amylase. Many infant formulas, including those formu-
carbohydrate absorption. Inadequately absorbed carbo- lated for preterm infants, contain corn syrup solids or
hydrates are salvaged by colonic flora through fermenta- tapioca, which are partially hydrolyzed starches. The
tion to hydrogen gas and short-chain fatty acids, the more extensively the starch is hydrolyzed, the less reli-
latter of which the colon readily absorbs. ance is placed on an immature digestive capability, but
One study was designed to ascertain whether the the greater the osmolality. Whether there is any advan-
timing of feeding initiation affected the development of tage of these hydrolyzed starch formulas over those
intestinal lactase activity and whether there are clinical containing disaccharides or lactose has not been estab-
ramifications of lower lactase activity. Early feeding in- lished.
creased intestinal lactase activity in preterm infants. Lac-
tase activity is a marker of intestinal maturity and may Minimal Enteral Nutrition
influence clinical outcomes. Whether the effects of milk Considerable emphasis has been placed on nutrition of
on lactase activity were due to the greater concentration the low-birthweight infant after the period of critical
of lactose in human milk compared with that in formula illness. Until recently, few systematic studies evaluated
has not yet been determined. the best method of nourishing the infant during the
The presence of a high lactose concentration in hu- period of critical illness, when he or she is receiving
man milk should not be a contraindication for its use in mechanical ventilation and is likely to be the most cata-
the VLBW infant. Feedings for VLBW infants rarely are bolic in the first 2 to 3 weeks after birth. This is a period
initiated at levels intended to meet the infants’ entire of extremely high vulnerability and high nutrient re-
nutritional requirements and usually are advanced quirement. A lack of essential nutrients during this time
slowly. The rationale for using a lactose-free formula may result in life-long consequences.
instead of human milk or even a commercial lactose- Because of individual patient characteristics, one feed-
containing formula is weak and theoretically may be ing protocol or guideline cannot be used for all infants.
harmful. Slow initiation of enteral feedings is unlikely to Data from the available studies suggest that minimal
exceed the lactose hydrolytic and salvage capability of the enteral feedings should be instituted within the first days
small and large intestines. This is especially unlikely when after birth. Because of the fear of necrotizing enteroco-
the quantity fed is less than 50% of the caloric require- litis, feeding intolerance, and metabolic problems result-
ment provided via the GI tract (unless the infant has a ing from inappropriate intakes of parenteral nutrients,
bowel that has been radically shortened by surgery). neonatologists commonly withhold both enteral and
Human milk also contains several lactose-derived oligo- intravenous amino acids and lipids. Commonly used
saccharides and other glycoconjugates that may play excuses to withhold enteral feedings include low Apgar
important roles in the infant’s host defense. scores, umbilical catheter use, apnea and bradycardia,
Studies examining the crypt-to-villus gradient of in- mechanical ventilation, continuous positive airway pres-
testinal carbohydrase activities demonstrate that most sure, and administration of vasoactive drugs and indo-
lactase activity is found at the mid- to upper villus; methacin. None of these has been demonstrated to pre-
sucrase, maltase, and glucoamylase are concentrated at clude enteral feedings in the low-birthweight infant. At
the mid-villus region (Fig. 9). This is likely to be perti- least 10 studies of minimal enteral nutrition have been
nent to intestinal injury and villus damage. Lactase usu- published, all of which document safety and efficacy (Fig.
ally is the first enzyme to be lost and the last to be 11). Minimal enteral nutrition is defined as an enteral
regenerated fully. intake that is less than the full nutrient requirements of
Pancreatic amylase, which cleaves internal alpha-1 to the neonate, but that has been found to prime the GI
-4 glucose bonds to maltose, maltoriose, limit dextrin, tract for subsequent feedings (usually ⬍20 mL/kg of
and glucose, is a major enzyme that hydrolyzes starches human milk or formula).
(Fig. 10). Because pancreatic secretion is poorly devel- Infants given early minimal enteral nutrition have
oped in the first several months following birth, this faster maturation of motor patterns and release of GI
mode of starch hydrolysis could serve as a limiting factor hormones than infants given no enteral feedings. These
that leaves substantial undigested starch in the intestine. infants also have less feeding intolerance, establish oral
Some data suggest that glucose polymers (18 to 29 feedings sooner, and do not differ from nonfed infants in
glucose units) can be hydrolyzed by salivary amylases, their incidence of necrotizing enterocolitis. Motor re-

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sponses appear to be less intense with the more diluted striction in utero may have major implications for
formulas. The amount of volume does not appear to postnatal development long-term. Very little is known
benefit maturing motor function. Motor responses are about the effects of nutrient restriction in the neonatal
equally intense whether feedings are instilled intragastri- intensive care unit during very vulnerable periods of
cally or transpylorically. They are similar whether feed- growth and development that might result in program-
ings are provided chilled, at room temperature, or ming that can have long-term effects. An improved un-
warmed to body temperature. When infants are fed a derstanding of GI development and neonatal biochemi-
slow infusion over 120 minutes, they display an intense cal nutrition from future studies should provide
fed response that is accompanied by brisk gastric empty- important information that can be used to improve the
ing. However, when the same volume is fed over 15 min- status of critically ill infants well beyond the neonatal
utes, duodenal motor responses are far less intense and period.
are accompanied by delayed gastric emptying. Because
two thirds of preterm infants display an immature duo- Conclusion
denal fed pattern that is accompanied by delayed gastric A better understanding of GI development nutrition and
emptying, many preterm infants may not be as physio- metabolism and application of this understanding to
logically prepared to process bolus feedings as well as clinical practice are likely to have a major impact on not
slow infusion feedings from the viewpoint of motor only short-term morbidity, but also on the quality of
activity. survival into adulthood and succeeding generations. This
constitutes one of our most current challenging areas in
Parenteral Nutrition neonatology.
It has been common practice to withhold both lipids and
amino acids from parenteral nutrition for several days,
then increase them slowly so that intakes approximating
Suggested Reading
in utero intake are reached by 7 to 10 days. This can lead Antonowicz I, Lebenthal E. Developmental pattern of small intes-
to a significant decrement in protein and lipid nutrition. tinal enterokinase and disaccharidase activities in the human
Studies now suggest that it is safe to initiate amino acids fetus. Gastroenterology. 1977;72:1299 –1303
at 3.0 g/kg per day as early as day 1 after birth. Lipids Armand M, Hamosh M, Mehta NR, et al. Effect of human milk or
formula on gastric function and fat digestion in the premature
also can be started within the first days after birth. There
infant. Pediatr Res. 1996;40:429 – 437
is no evidence of harm at lipid infusion rates of less than Berseth CL. Gastrointestinal motility in the neonate. Clin Perina-
0.2 g/kg per hour. tol. 1996;23:179 –190
Brans YW, Ritter DA, Kenny JD, Andrew DS, Dutton EB, Carrillo
The Future DW. Influence of intravenous fat emulsion on serum bilirubin in
very low birthweight neontates. Arch Dis Child. 1987;62:
Current developments, such as the Human Genome
156 –160
Project, proteomics, and other technologies, will in- Foote KD, MacKinnon MJ, Innis SM. Effect of early introduction
crease the understanding of neonatal nutrition and GI of formula vs fat-free parenteral nutrition on essential fatty acid
development, thereby allowing diagnosis and prevention status of preterm infants. Am J Clin Nutr. 1991;54:93–97
of some illnesses. Hamosh M. Digestion in the newborn. Clin Perinatol. 1996;23:
A few of the biggest challenges for the future include
Hyman PE, Abrams C, Dubors A. Effect of metaclopramide and
understanding: bethanacol on gastric emptying in infants. Pediatr Res. 1985;
● Mucosa-microbial interactions (cross-talk between mi-
Hyman PE, Clarke DD, Everett SL, et al. Gastric acid secretory
crobes, epithelium, submucosa) function in preterm infants. J Pediatr. 1985;106:467– 471
● Barrier function (intercellular junctions) Janssens G, Melis K, Vaerenberg M. Long-term use of cisapride
● Activation and deactivation of genes and interaction (Propulsid) in premature neonates of ⬍34 weeks gestational
between genomic and extragenomic metabolic path- age. J Pediatr Gastroentrol Nutr. 1990;11:420
Kelly EJ, Newell SJ, Brownlee KG, Promrose JN, Dear PR. Gastric
acid secretion in preterm infants. Early Human Dev. 1993;35:
Figure 12 describes terms that will aid in understanding 215–220
Kien CL. Digestion, absorption, and fermentation of carbohydrates
these future directions.
in the newborn. Clin Perinatol. 1996;23:211–228
One example of an area that will receive intense scru- Koldovsky O. Small and large intestine. In: Polin RA, Fox WW, eds.
tiny involves early metabolic “programming” and subse- Fetal and Neonatal Physiology. Vol 2. Philadelphia, Pa: WB
quent disease. Several studies suggest that nutrient re- Saunders; 1992:1059

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Kunz C, Rudloff S. Biological functions of oligosaccharides in Novak DA. Gastroesophageal reflux in the preterm infant. Clin
human milk. Acta Pediatr. 1993;82:903–912 Perinatol. 1996;23:305–320
La Gamma EF, Browne LE. Feeding practices for infants weighing Rubin M, Naor N, Sirota L, et al. Are bilirubin and plasma lipid
less than 1500 grams at birth and the pathogenesis of necrotiz- profiles of premature infants dependent on the lipid emulsion
ing enterocolitis. Clin Pernatol. 2000;21:271–306 infused? J Pediatr Gastroenterol Nutr. 1995;21:25–30
Leung AK, Liay PC. Use of metoclopramide in the treatment of Siegel M. Gastric emptying time in premature and compromised
gastroesophageal reflux in infants and children. Curr Ther Res. infants. J Pediatr Gastroenterol Nutr. 1983;2(suppl 1):S136
1984;36:911 Thureen PJ, Hay WW Jr. Early aggressive nutrition in preterm
Murray RD, Kerzner B, Sloan HR, McClung HJ, Gilbert M, infants. Semin Perinatol. 2001;6:403– 415
Ailabouni A. The contribution of salivary amylase to glucose Widdowson EM. Changes in body proportions and composition
polymer hydrolysis in premature infants. Pediatr Res. 1986;20: during growth. In: Davis JA, Dobbing J, eds. Scientific Founda-
186 –191 tions of Pediatrics. Philadelphia, Pa: WB Saunders; 1974:
Neu J. Feeding strategies of the premature/sick infant. In: Lifshitz 153–163
C, ed. Pediatric Gastroenterology and Nutrition in Clinical Young VR. 2001 W. O. Atwater Memorial Lecture and the 2001
Practice. New York, NY: Marcel Dekker, Inc; 2002:203–222 ASNS President’s Lecture: human nutrient requirements: the
Newell SJ, Sarkar PK, Durbin G. Maturation of the lower oesoph- challenge of the post-genome era. J Nutr. 2002;132:621– 629
ageal sphincter function in the preterm baby. Gut. 1988;29: Ziegler EE. Protein in premature feeding. Nutrition. 1994;10:
1677 69 –71

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NeoReviews Quiz
1. An infant is delivered at 26 weeks’ gestation following spontaneous preterm labor and rapid progression.
An understanding of the anatomic and physiologic development of the gastrointestinal tract would be
helpful in determining the nutrition management of this infant. Of the following, the most accurate
statement regarding the gastrointestinal structure and function of this infant is that:
A. Crypt-to-villus epithelial migration time is 48 hours.
B. Gastroanal transit time is 8 hours.
C. Intestinal length is 275 cm.
D. Intragastric pH is 6.0.
E. Lower esophageal sphincter pressure is 28 cm H2O.

2. Numerous types of cells that have differing functions are present in the small intestine. Of the following,
the cell most involved in the secretion of defensins as a part of innate immunity is the:
A. Dendritic cell.
B. Enteroendocrine cell.
C. Goblet cell.
D. M cell.
E. Paneth cell.

3. The digestion and absorption of protein, lipid, and carbohydrate varies in infants, depending on the
maturation of the fetus as gestation advances. Of the following, the most accurate statement regarding
digestive/absorptive function in the neonate is that:
A. Decreased bile acid synthesis in the preterm neonate causes inefficient absorption of medium-chain
B. Enterokinase enzyme activity is detectable at 24 weeks of gestational age.
C. Gastric acid secretion is responsive to pentagastrin in the first 48 hours after birth.
D. Pancreatic amylase activity reaches its mature level at birth in a term neonate.
E. Pepsin enzyme activity is fully developed at birth in a term neonate.

4. Minimal enteral nutrition is a feeding strategy for preterm neonates that is intended to enhance
maturation of the gastrointestinal motor patterns with release of related hormones. Of the following, the
gastrointestinal motor responses are most likely to be increased by:
A. Dilution of milk.
B. Route of feeding.
C. Slow rate of infusion.
D. Temperature of feedings.
E. Volume of milk.

NeoReviews Vol.4 No.1 January 2003 e13

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The Neonatal Gastrointestinal Tract: Developmental Anatomy, Physiology, and
Clinical Implications
Josef Neu and Nan Li
NeoReviews 2003;4;e7
DOI: 10.1542/neo.4-1-e7

Updated Information & including high resolution figures, can be found at:
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The Neonatal Gastrointestinal Tract: Developmental Anatomy, Physiology, and
Clinical Implications
Josef Neu and Nan Li
NeoReviews 2003;4;e7
DOI: 10.1542/neo.4-1-e7

The online version of this article, along with updated information and services, is
located on the World Wide Web at:

Data Supplement at:

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