Malabsorption is a large topic that covers a variety of states in which the small
intestine absorbs any nutrient incompletely. This can range from congenital malabsorptive
states (e.g., Hartnup disease) in which basic amino acids are poorly absorbed,
to immunologically induced problems (e.g., gluten sensitive enteropathy),
to iatrogenic problems (e.g., gastric resection or radiation-induced injury), or to the
' 'programmed'' malabsorptive state of lactose in older children.
The function of the esophagus, the first organ of the digestive tube, appears very
simple: it is an anteroposteriorly flattened hollow tube organ that transports material
from the mouth into the stomach.
Celiac disease is caused by ingested gluten. In genetically susceptible individuals,
it leads to malabsorption of food and nutrients. Characteristically, it has manifested
The surface area covered by mucosal epithelia probably amounts to more than
200 times that of the skin, thus comprising almost 400 m2 in an adult individual.
This extensive and generally vulnerable monolayered epithelial barrier is protected
by numerous innate chemical and physical mechanisms that cooperate intimately
with adaptive, specific mucosal immunity.
The mucosa lining the small and large intestine needs fuel to maintain energy
metabolism, to express genes, to allow growth during the process of rapid cell
turnover, and for nutrient transport and absorption.
The gastric epithelium not only has a protective barrier function (against hydrochloric
acid, peptidases, Helicobacter pylori, and so on) and a primary role in epithelial
restitution (ulcer healing), but it also has specific digestive functions.
The control of human pancreatic enzyme secretion is still a matter of open debate,
as indicated by a recent statement by Adler:
"Human pancreatic secretion is regulated through a complicated coordination of neural,
hormonal and possibly paracrine effects. Cholinergic input is essential for full action of
any other agonist like cholecystokinin (CCK) and secretin" (1).
The epithelium of the small intestine is fashioned to produce crypts (tubular structures
containing the proliferating cells of the system) and villi (finger-shaped projections
covered with cells that perform the absorptive functions of the gut).
Digestive processes involve several organs composed of highly specialized epithelial
cells. Despite a great diversity of function, all epithelial cells along the digestive
tract have certain common structural and functional features.
The gastrointestinal tract is responsible for acquisition of energy and nutrients to
sustain life. The small intestine, an important tissue of this organ, is responsible for
the terminal stages of digestion and absorption (1-3).
Over the past decade, advances in molecular biology have revolutionized studies
on intestinal nutrient absorption in humans. Before the advent of molecular biology,
the study of nutrient absorption was largely limited to in vivo and in vitro animal
The intestinal epithelium is a very dynamic tissue, which depends on a variety
of factors for the regulation of its growth as well as for the expression of digestive
functions during development and in the adult (1,2).
The structure and function of the gut results from a complex interplay between
various cell types and components that is regulated by growth factors and hormones
together with immune and neural inputs (1).
Carbohydrates are essential constituents of the mammalian diet. They occur as
oligosaccharides, such as starch and cellulose (plant origin), as glycogen (animal
origin), and as free disaccharides such as sucrose (plant) and lactose (animal).
The 13co2 breath test is a reliable, noninvasive method of studying the principal
gastrointestinal functions, including the assimilation of food ingredients. Stable isotopes
offer the possibility of monitoring various metabolic events as well.
The definition, presentation, and outcome of the syndrome of intractable diarrhea
of infancy (IDI) have changed considerably during the last three decades because
of a better understanding of the pathology of the small bowel mucosa and major
improvements in nutritional management.
In the clinical setting, inflammatory bowel disease usually presents as either
Crohn's disease or ulcerative colitis (1), and emerging consensus indicates that the
underlying disorder, which is characterized by chronic inflammation of the gastrointestinal
tract, is the endpoint of several, possibly many, distinct pathophysiologic
Recent advance in the molecular genetics of Hirschsprung's disease have confirmed
the complex genetic basis of this congenital disorder. In particular, after the
demonstration of mutations of the RET proto-oncogene in a significant proportion
of both familial and sporadic cases, additional genes have been identified as responsible
for colonic aganglionosis in humans and rodents.
We have the difficult and demanding task of summarizing what has been covered
for the past 3 days. We will highlight some of the points that have been made, and
pose a few questions about future developments.