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:
MD, MS*
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.

Introduction
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-
quences.
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.

NeoReviews Vol.4 No.1 January 2003 e7

Downloaded from http://neoreviews.aappublications.org/ by guest on May 17, 2018
gastroenterology anatomy & physiology
absorptive epithelium, Paneth cells (involved in secretion
of defensins and other peptides involved in innate immu-
nity), goblet cells (involved in the secretion of the mucus
overlying the intestine), and other cell types associated
with the intestinal neuroendocrine system and immune
system.
Physiologic Development
Amniotic Fluid Swallowing
Many physiologic processes develop during fetal life.
One that is considered particularly important is fetal
swallowing. The fetus swallows about 450 mL/d of
amniotic fluid in the third trimester. This fluid contains
nutrients and growth factors, but its availability is inter-
rupted suddenly at the time of preterm birth. There is
speculation that this sudden interruption of large fluid
fluxes from fetal life to extrauterine life might have
detrimental consequences (Fig. 3).
Gastroesophageal Sphincter Tone
Gastroesophageal (GE) sphincter tone also undergoes
remarkable changes during development. The lower
esophageal pressure is approximately 4 cm H2O and
28 cm H2O in preterm and term infants, respectively
(Fig. 4). This is related to the high incidence of GE reflux
(GER) in preterm infants. Of note, GER has been impli-
cated as one of the causes of apnea and bradycardia in
very low-birthweight (VLBW) infants. This has led to the
frequent use of prokinetic agents, although well-
designed, controlled studies supporting their safety and
efficacy are lacking. More recent data suggest that most
cases of apnea and bradycardia in VLBW infants are not
causally related to GER.
Intestinal Motility
Delayed gastric emptying also is related to GER because
gastric emptying is slower in preterm than in term in-
fants. In the adult, the rate of gastric emptying is con-
trolled by feedback from the small intestine. Stimulation
of duodenal receptors by acid, fat, carbohydrate, trypto-
phan, or increasing osmolality decreases the rate of gas-
tric emptying. Studies of the effects of various formula
components on gastric emptying have yielded conflicting
results. Incremental increases of caloric density from
0.2 to 0.66 kcal/mL decreased the rate of gastric emp-
tying among infants of 32 to 39 weeks’ gestation, but
there were no differences with increments of 0.6 to
0.8 kcal/mL formula. Despite the reduced emptying rate
at higher caloric density, the quantity of calories deliv-
ered into the duodenum from the stomach increased
with concentrated formula. Changes in osmolality from
e8 NeoReviews Vol.4 No.1 January 2003
Downloaded from http://neoreviews.aappublications.org/ by guest on May 17, 2018
279 to 448 mOsm/kg do not alter significantly the rates
of gastric emptying of isocaloric formulas. No informa-
tion on the ability of duodenal feedback to control the
rate of gastric emptying in the VLBW infant between
25 and 32 weeks’ gestation is available. Inadequate con-
trol of emptying could overwhelm the intestinal tract,
leading to malabsorption and feeding intolerance.
Therapeutic agents that increase gastric emptying
rates in children and adults also appear to be effective in
preterm infants. Metoclopramide and cisapride increase
the gastric emptying rate in preterm and term infants.
Nasojejunal feeding may provide only limited improve-
ment in feeding tolerance because intestinal motility
beyond the gastric outlet is also immature.
The small bowel motility patterns are poorly devel-
oped before 28 weeks’ gestation. The small intestine
shows disorganized motility patterns between 27 and
30 weeks’ gestation, which progress to a more mature
pattern in which migrating myoelectric complexes are
present at 33 to 34 weeks’ gestation. Gastroanal transit
ranges from 8 to 96 hours in preterm infants compared
with 4 to 12 hours in adults. In preterm infants, the
motilin receptor is not present until 32 weeks’ gestation,
and the cyclic release of motilin is not present. This
suggests that the use of erythromicin would not be
effective prior to 32 weeks’ gestation, although more
recent studies suggest improved feeding tolerance with
erythromicin.
Protein Digestion
Knowledge of digestive-absorptive processes has in-
creased significantly in the past 2 decades. Gastric acid
secretion is limited in VLBW infants. In the first 24 to
48 hours after birth, intragastric pH remains at about
5.5 to 7.0 and is relatively resistant to pentagastrin.
However, both basal and pentagastrin-stimulated acid
secretion doubles from the first to fourth week of post-
natal life in preterm infants.
This process should be kept in mind when considering
the use of histmine2 (H2) blockers, which are widely
prescribed in many neonatal intensive care units. Gastric
acid can serve as a barrier to microorganisms. When
gastric acid secretion is decreased by the use of inhibitors,
this can lead to a higher load of bacteria in the more distal
regions of the intestine. Several studies suggest that
critically ill patients treated with H2 blockers have a
higher incidence of nosocomial sepsis.
Some of the enzymes involved in intraluminal diges-
tion of proteins are also relatively limited in preterms.
Pepsin secretion usually is fully developed by 3 to 8
months of postnatal age, and levels are much lower in

preterm than in term newborns (639 U/Kg versus
3,352 U/Kg in adults). This could be a limiting factor
for the digestion of certain types of protein in preterm
infants.
The protease cascade in the small intestine is catalyzed
by food-stimulated secretion of enterokinase from the
upper small intestinal epithelium (Fig. 5). This enzyme
catalyzes the activation of trypsinogen to trypsin that, in
turn, activates several other inactive zymogens into pro-
teases, which are active in the intestinal lumen. However,
even though enterokinase is detectable at 24 weeks’
gestation, its concentration is relatively low and reaches
only 25% of adult activity at term. This can be limiting to
protein digestion and may be responsible for an increased
capability of larger antigens or microorganisms to pass
into the intestine without breakdown by luminal en-
zymes.
Lipid Digestion and Absorption
Lipid requirements are limited to the 18-carbon essential
fatty acids (linoleic or linolenic acid). Lipid makes up
about 50% of the nonprotein energy content of human
milk and formulas, both of which contain these fatty
acids. However, both term and preterm infants have
pancreatic insufficiency compared with older children
and adults.
The digestion of lipid can be split into several phases.
The luminal phase involves de-esterification of triglycer-
ides to 3-monoglyerides and free fatty acids and bile
acid-mediated micellar solubilization.
In the process of fat digestion, several lipases hydro-
lyze fatty acids from glycerol. Figure 6 shows some of
these, which include the lipase found in human milk (bile
salt-stimulated lipase) and lingual, gastric, pancreatic,
and epithelial lipases. Bile acid-stimulated lipase is
present in milk and becomes active in the small intestine
lumen in the presence of bile acids. Lingual lipase is
secreted by glands at the base of the tongue and is
involved in gastric lipid hydrolysis. Lipases produced in
the stomach, secreted from the pancreas, and present in
the mucosa also are involved in lipid hydrolysis.
Bile acids are critical to efficient fat digestion and
absorption. These processes are limited in VLBW infants
because the duodenal concentration of bile acids is low
due to lower synthesis and ileal reabsorption (Fig. 7).
Lower micellar solubilization leads to inefficient cell-
mucosal interaction and subsequently lower absorption
of the molecules of the mucosal-cell surface interface
(Fig. 8). Long-chain fatty acids but not medium-chain
fatty acids depend on bile acids for solubilization and,
thus, are the most susceptible to inefficient absorption.
Downloaded from http://neoreviews.aappublications.org/ by guest on May 17, 2018
gastroenterology anatomy & physiology
The permeation of fatty acids and 2-monoglycerides
from the lumen into the cell, intracellular re-
esterification, chylomicron formation, and transport to
the chylomicrons from the cell into the circulation are
the primary absorptive events. After lumenal digestion,
fatty acids and monoglycerides approximate the absorp-
tive surface and enter the intracellular milieu by processes
that are not yet well understood. After entry into the cell,
medium-chain triglycerides undergo a relatively simple
process of assimilation in which they do not undergo
re-esterification and chylomicron formation, as the long-
chain lipids do. Medium-chain triglycerides are taken
directly into the portal venous system; chylomicrons
formed from long-chain fats enter the lymphatics. In
conditions that involve obstruction of the lymphatics,
feeding formulas containing primarily medium-chain
triglycerides rather than long-chain triglycerides are rec-
ommended.
There is considerable interest in the capability of
neonates to convert the essential fatty acids into longer-
chain fatty acids with 20 or more carbons. These long-
chain polyunsaturated fatty acids (LCPUCAs) are critical
in the formation of eicosanoids and structural compo-
nents of the central nervous system. They are found in
relatively high concentrations in human milk but are not
found in total parenteral nutrition or most neonatal
formulas. Whether the addition of LCPUCAs to formu-
las results in improved neurodevelopment is the subject
of current intense investigation.
Most essential fatty acids provided to neonates are
derived from the omega-6 family (linoleic acid). This is
because much of the lipid derived from formulas or
intravenous lipid solutions is from vegetable oil, which is
rich in the omega-6 but not the omega 3 fraction. The
implications of this will be discussed in the article on
immunonutrients in this issue of NeoReviews.
Carbohydrate Digestion and Absorption
Carbohydrates ingested by neonates are either natural
lactose (the primary carbohydrate in most human and
mammalian milks) or glucose polymers, sucrose, or hy-
drolyzed starches. Mechanisms for carbohydrate absorp-
tion mature in a defined sequence during human fetal
development. The intestinal enzymes lactase, sucrase,
maltase, isomaltase, and glucoamylase are at mature lev-
els in the term fetus. Pancreatic amylase activity is low in
both term and preterm neonates and appears to require
several months to reach mature levels. In the preterm
infant, sucrase, maltase, and isomaltase are usually fully
active, but lactase activity, which increases markedly from
24 to 40 weeks’ gestation, may be low, depending on
NeoReviews Vol.4 No.1 January 2003 e9
gastroenterology anatomy & physiology
fetal age. Despite these developmental patterns, clinical
lactose intolerance is uncommon. Postnatal adaptive re-
sponses to ingested carbohydrates lead to competent
carbohydrate absorption. Inadequately absorbed carbo-
hydrates are salvaged by colonic flora through fermenta-
tion to hydrogen gas and short-chain fatty acids, the
latter of which the colon readily absorbs.
One study was designed to ascertain whether the
timing of feeding initiation affected the development of
intestinal lactase activity and whether there are clinical
ramifications of lower lactase activity. Early feeding in-
creased intestinal lactase activity in preterm infants. Lac-
tase activity is a marker of intestinal maturity and may
influence clinical outcomes. Whether the effects of milk
on lactase activity were due to the greater concentration
of lactose in human milk compared with that in formula
has not yet been determined.
The presence of a high lactose concentration in hu-
man milk should not be a contraindication for its use in
the VLBW infant. Feedings for VLBW infants rarely are
initiated at levels intended to meet the infants’ entire
nutritional requirements and usually are advanced
slowly. The rationale for using a lactose-free formula
instead of human milk or even a commercial lactose-
containing formula is weak and theoretically may be
harmful. Slow initiation of enteral feedings is unlikely to
exceed the lactose hydrolytic and salvage capability of the
small and large intestines. This is especially unlikely when
the quantity fed is less than 50% of the caloric require-
ment provided via the GI tract (unless the infant has a
bowel that has been radically shortened by surgery).
Human milk also contains several lactose-derived oligo-
saccharides and other glycoconjugates that may play
important roles in the infant’s host defense.
Studies examining the crypt-to-villus gradient of in-
testinal carbohydrase activities demonstrate that most
lactase activity is found at the mid- to upper villus;
sucrase, maltase, and glucoamylase are concentrated at
the mid-villus region (Fig. 9). This is likely to be perti-
nent to intestinal injury and villus damage. Lactase usu-
ally is the first enzyme to be lost and the last to be
regenerated fully.
Pancreatic amylase, which cleaves internal alpha-1 to
-4 glucose bonds to maltose, maltoriose, limit dextrin,
and glucose, is a major enzyme that hydrolyzes starches
(Fig. 10). Because pancreatic secretion is poorly devel-
oped in the first several months following birth, this
mode of starch hydrolysis could serve as a limiting factor
that leaves substantial undigested starch in the intestine.
Some data suggest that glucose polymers (18 to 29
glucose units) can be hydrolyzed by salivary amylases,
e10 NeoReviews Vol.4 No.1 January 2003
Downloaded from http://neoreviews.aappublications.org/ by guest on May 17, 2018
but this digestion still falls substantially short of that
accomplished by the usual concentrations of pancreatic
amylase. Many infant formulas, including those formu-
lated for preterm infants, contain corn syrup solids or
tapioca, which are partially hydrolyzed starches. The
more extensively the starch is hydrolyzed, the less reli-
ance is placed on an immature digestive capability, but
the greater the osmolality. Whether there is any advan-
tage of these hydrolyzed starch formulas over those
containing disaccharides or lactose has not been estab-
lished.
Minimal Enteral Nutrition
Considerable emphasis has been placed on nutrition of
the low-birthweight infant after the period of critical
illness. Until recently, few systematic studies evaluated
the best method of nourishing the infant during the
period of critical illness, when he or she is receiving
mechanical ventilation and is likely to be the most cata-
bolic in the first 2 to 3 weeks after birth. This is a period
of extremely high vulnerability and high nutrient re-
quirement. A lack of essential nutrients during this time
may result in life-long consequences.
Because of individual patient characteristics, one feed-
ing protocol or guideline cannot be used for all infants.
Data from the available studies suggest that minimal
enteral feedings should be instituted within the first days
after birth. Because of the fear of necrotizing enteroco-
litis, feeding intolerance, and metabolic problems result-
ing from inappropriate intakes of parenteral nutrients,
neonatologists commonly withhold both enteral and
intravenous amino acids and lipids. Commonly used
excuses to withhold enteral feedings include low Apgar
scores, umbilical catheter use, apnea and bradycardia,
mechanical ventilation, continuous positive airway pres-
sure, and administration of vasoactive drugs and indo-
methacin. None of these has been demonstrated to pre-
clude enteral feedings in the low-birthweight infant. At
least 10 studies of minimal enteral nutrition have been
published, all of which document safety and efficacy (Fig.
11). Minimal enteral nutrition is defined as an enteral
intake that is less than the full nutrient requirements of
the neonate, but that has been found to prime the GI
tract for subsequent feedings (usually ⬍20 mL/kg of
human milk or formula).
Infants given early minimal enteral nutrition have
faster maturation of motor patterns and release of GI
hormones than infants given no enteral feedings. These
infants also have less feeding intolerance, establish oral
feedings sooner, and do not differ from nonfed infants in
their incidence of necrotizing enterocolitis. Motor re-

sponses appear to be less intense with the more diluted
formulas. The amount of volume does not appear to
benefit maturing motor function. Motor responses are
equally intense whether feedings are instilled intragastri-
cally or transpylorically. They are similar whether feed-
ings are provided chilled, at room temperature, or
warmed to body temperature. When infants are fed a
slow infusion over 120 minutes, they display an intense
fed response that is accompanied by brisk gastric empty-
ing. However, when the same volume is fed over 15 min-
utes, duodenal motor responses are far less intense and
are accompanied by delayed gastric emptying. Because
two thirds of preterm infants display an immature duo-
denal fed pattern that is accompanied by delayed gastric
emptying, many preterm infants may not be as physio-
logically prepared to process bolus feedings as well as
slow infusion feedings from the viewpoint of motor
activity.
Parenteral Nutrition
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
in utero intake are reached by 7 to 10 days. This can lead
to a significant decrement in protein and lipid nutrition.
Studies now suggest that it is safe to initiate amino acids
at 3.0 g/kg per day as early as day 1 after birth. Lipids
also can be started within the first days after birth. There
is no evidence of harm at lipid infusion rates of less than
0.2 g/kg per hour.
The Future
Current developments, such as the Human Genome
Project, proteomics, and other technologies, will in-
crease the understanding of neonatal nutrition and GI
development, thereby allowing diagnosis and prevention
of some illnesses.
A few of the biggest challenges for the future include
understanding:
● Mucosa-microbial interactions (cross-talk between mi-
crobes, epithelium, submucosa)
● Barrier function (intercellular junctions)
● Activation and deactivation of genes and interaction
between genomic and extragenomic metabolic path-
ways
Figure 12 describes terms that will aid in understanding
these future directions.
One example of an area that will receive intense scru-
tiny involves early metabolic “programming” and subse-
quent disease. Several studies suggest that nutrient re-
Downloaded from http://neoreviews.aappublications.org/ by guest on May 17, 2018
gastroenterology anatomy & physiology
striction in utero may have major implications for
postnatal development long-term. Very little is known
about the effects of nutrient restriction in the neonatal
intensive care unit during very vulnerable periods of
growth and development that might result in program-
ming that can have long-term effects. An improved un-
derstanding of GI development and neonatal biochemi-
cal nutrition from future studies should provide
important information that can be used to improve the
status of critically ill infants well beyond the neonatal
period.
Conclusion
A better understanding of GI development nutrition and
metabolism and application of this understanding to
clinical practice are likely to have a major impact on not
only short-term morbidity, but also on the quality of
survival into adulthood and succeeding generations. This
constitutes one of our most current challenging areas in
neonatology.
Suggested Reading
Antonowicz I, Lebenthal E. Developmental pattern of small intes-
tinal enterokinase and disaccharidase activities in the human
fetus. Gastroenterology. 1977;72:1299 –1303
Armand M, Hamosh M, Mehta NR, et al. Effect of human milk or
formula on gastric function and fat digestion in the premature
infant. Pediatr Res. 1996;40:429 – 437
Berseth CL. Gastrointestinal motility in the neonate. Clin Perina-
tol. 1996;23:179 –190
Brans YW, Ritter DA, Kenny JD, Andrew DS, Dutton EB, Carrillo
DW. Influence of intravenous fat emulsion on serum bilirubin in
very low birthweight neontates. Arch Dis Child. 1987;62:
156 –160
Foote KD, MacKinnon MJ, Innis SM. Effect of early introduction
of formula vs fat-free parenteral nutrition on essential fatty acid
status of preterm infants. Am J Clin Nutr. 1991;54:93–97
Hamosh M. Digestion in the newborn. Clin Perinatol. 1996;23:
191–209
Hyman PE, Abrams C, Dubors A. Effect of metaclopramide and
bethanacol on gastric emptying in infants. Pediatr Res. 1985;
19:1029
Hyman PE, Clarke DD, Everett SL, et al. Gastric acid secretory
function in preterm infants. J Pediatr. 1985;106:467– 471
Janssens G, Melis K, Vaerenberg M. Long-term use of cisapride
(Propulsid) in premature neonates of ⬍34 weeks gestational
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:
215–220
Kien CL. Digestion, absorption, and fermentation of carbohydrates
in the newborn. Clin Perinatol. 1996;23:211–228
Koldovsky O. Small and large intestine. In: Polin RA, Fox WW, eds.
Fetal and Neonatal Physiology. Vol 2. Philadelphia, Pa: WB
Saunders; 1992:1059
NeoReviews Vol.4 No.1 January 2003 e11
gastroenterology anatomy & physiology
Kunz C, Rudloff S. Biological functions of oligosaccharides in
human milk. Acta Pediatr. 1993;82:903–912
La Gamma EF, Browne LE. Feeding practices for infants weighing
less than 1500 grams at birth and the pathogenesis of necrotiz-
ing enterocolitis. Clin Pernatol. 2000;21:271–306
Leung AK, Liay PC. Use of metoclopramide in the treatment of
gastroesophageal reflux in infants and children. Curr Ther Res.
1984;36:911
Murray RD, Kerzner B, Sloan HR, McClung HJ, Gilbert M,
Ailabouni A. The contribution of salivary amylase to glucose
polymer hydrolysis in premature infants. Pediatr Res. 1986;20:
186 –191
Neu J. Feeding strategies of the premature/sick infant. In: Lifshitz
C, ed. Pediatric Gastroenterology and Nutrition in Clinical
Practice. New York, NY: Marcel Dekker, Inc; 2002:203–222
Newell SJ, Sarkar PK, Durbin G. Maturation of the lower oesoph-
ageal sphincter function in the preterm baby. Gut. 1988;29:
1677
e12 NeoReviews Vol.4 No.1 January 2003
Downloaded from http://neoreviews.aappublications.org/ by guest on May 17, 2018
Novak DA. Gastroesophageal reflux in the preterm infant. Clin
Perinatol. 1996;23:305–320
Rubin M, Naor N, Sirota L, et al. Are bilirubin and plasma lipid
profiles of premature infants dependent on the lipid emulsion
infused? J Pediatr Gastroenterol Nutr. 1995;21:25–30
Siegel M. Gastric emptying time in premature and compromised
infants. J Pediatr Gastroenterol Nutr. 1983;2(suppl 1):S136
Thureen PJ, Hay WW Jr. Early aggressive nutrition in preterm
infants. Semin Perinatol. 2001;6:403– 415
Widdowson EM. Changes in body proportions and composition
during growth. In: Davis JA, Dobbing J, eds. Scientific Founda-
tions of Pediatrics. Philadelphia, Pa: WB Saunders; 1974:
153–163
Young VR. 2001 W. O. Atwater Memorial Lecture and the 2001
ASNS President’s Lecture: human nutrient requirements: the
challenge of the post-genome era. J Nutr. 2002;132:621– 629
Ziegler EE. Protein in premature feeding. Nutrition. 1994;10:
69 –71
 gastroenterology anatomy & physiology

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
triglycerides.
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

Downloaded from http://neoreviews.aappublications.org/ by guest on May 17, 2018
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:
Services http://neoreviews.aappublications.org/content/4/1/e7
References This article cites 20 articles, 3 of which you can access for free at:
http://neoreviews.aappublications.org/content/4/1/e7#BIBL
Subspecialty Collections This article, along with others on similar topics, appears in the
following collection(s):
Gastroenterology
http://classic.neoreviews.aappublications.org/cgi/collection/gastroent
erology_sub
Permissions & Licensing Information about reproducing this article in parts (figures, tables) or
in its entirety can be found online at:
http://classic.neoreviews.aappublications.org/site/misc/Permissions.x
html
Reprints Information about ordering reprints can be found online:
http://classic.neoreviews.aappublications.org/site/misc/reprints.xhtml

Downloaded from http://neoreviews.aappublications.org/ by guest on May 17, 2018

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:
http://neoreviews.aappublications.org/content/4/1/e7

Data Supplement at:

http://neoreviews.aappublications.org/content/suppl/2002/12/23/4.1.e7.DC1

Neoreviews is the official journal of the American Academy of Pediatrics. A monthly publication,
it has been published continuously since . Neoreviews is owned, published, and trademarked by
the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois,
60007. Copyright © 2003 by the American Academy of Pediatrics. All rights reserved. Online
ISSN: 1526-9906.

Downloaded from http://neoreviews.aappublications.org/ by guest on May 17, 2018