Gastrointestinal Physiology
AnS 536
Spring 2016
Topics
Embryology & Development
Problems during development
Transport
Absorbance/Colostrum importance
Closure
DEVELOPMENT
Quiz
What layer in the embryo do digestive
organs come from?
endoderm
What does a developing GIT look like?
A straight tube!
What also forms from the same layer as
the digestive tract?
Lungs
3 layers
3 layers
Anatomy Review
Vascular Blood Supply
Video
intestinal development
 4 wks: liver/stomach buds
 5 wks: canalization
 6 wks: Developing GIT leaves
abdominal cavity
 10 wks: GIT returns to
abdominal cavity
 11 Weeks: Villi begin forming
 34 weeks: full digestive tract
Rotation
Rotate 270 degrees counter clockwise
through the umbilicus around the SMA
Duodenojejunal loop fixes in the upper left
quadrant (in relation to SMA)
Cecum fixes in lower right quadrant
DEVELOPMENTAL
COMPLICATIONS
Malrotation
Failure of the gut to rotate 270 degrees
counter clockwise into normal position
Varying degrees of malrotation
Most rare is midgut volvulus
Malrotation
Occurs in adults as well
1/500 asymptomatic births, 1/6000 with
symptomatic rotation
Symptoms
Neonates: bilious vomit, bloody stool, failure to
thrive
Infants: recurrent abdominal pain, food
intolerance, distension, septic shock
Mostly nonspecific pain
Midgut Volvulus
Intestines twist around its mesenteric
attachment
Primarily in neonates
Intestinal obstruction at birth & bilious
vomiting
Requires surgical intervention
Malrotations
Video:
Rotation & Malrotation
Until 530
Intestinal Aganglionosis
Rare neurological condition
Lack of enteric nervous system in
gastrointestinal tract
No peristalsis in affected regions
Intestinal Enterocolitis:
Preterm infants- necrotic bacterial infection that
destroys the wall of the bowel
50% mortality
Lumen Abnormalities
Atresia: Interruption of the
lumen
Closed or absence of a part
of the passage
95% of cases
Stenosis: Narrowing of the
lumen
Caused by partial/incomplete
obstruction
5% of cases
Both cause obstruction
DIGESTION
Sugar Digestion and Transport in
Infants
Digestion of sugars is different in the
neonate vs the adult
Dependent upon sources of sugar and CHO’s
Neonates: Lactose is primary sugar
• Sucrase/Maltase increase at weaning
Adults: Starches and sucrose
Sugars must be broken down into more
absorbable form
Brush border disaccharidases are essential
Fatty Acid (FA) Transport in Infants
 Fat breakdown
 Stomach motility and lipase facilitate
breakdown of fat into smaller globules
 Globules have polar, hydrophilic
surfaces that undergo absorption in
the small intestines
 Brush border of small intestines
absorbs free fatty acid acylglycerols
into the mucosal cell
 FA bind to FA-binding protein in the
endoplasmic reticulum
 Triacylglycerols are resynthesized into
chylomicrons
 Chylomicrons are released into
circulation and metabolized by the
liver
Adult
Fatty Acid (FA) Transport in Infants
 Fatty acids are contained in:
Triacylglycerols
Phospholipids
Cholesterol esters
 Fat digestion in the neonate is limited initially
Pancreatic secretory function and bile salt metabolism need
to mature
 Milk
99% of FAs in the form of triacylglycerols
Fat is emulsified in the stomach via pre-duodenal lipase
 Weaning
Feed salts of SCFA-butyrate in starter feeds to stimulate
growth of rumen papillae in calves
Acid Production in the Stomach
Capacity to secrete gastric juices remains
low at birth but increases significantly
Newborn (15 min) stomach pH: 5.4
Newborn (1 hr) stomach pH: 3.1
Gastric juice production follows colostrum
intake and immunoglobulin absorption
Bioactive Peptides and Hormones
Secreted by Newborn Digestive Tract
 Somatostatin
Secreted by D cells within the stomach
Serve to inhibit parietal G and enterochromaffin-like cells
 Gastrin
Secreted by G cells in the stomach when protein products
are present
Function to stimulate parietal, chief, and enterochromaffinlike cells
 Cholecystokinin
Important in regulating pancreatic digestive enzyme
secretion
Pancreatic secretions minimal at time of birth but increase
with age
Amino Acid Digestion in Infants
First 24 hours post parturition
Ability to absorb intact proteins as
immunoglobulins via clostrum
Lack of placental transfer in bovine species
After 24 hrs ability to absorb intact proteins
drastically reduces
Inability to cross the plasma barrier of the
intestinal lumen
Proteins (milk) broken down into amino acids
Amino Acid Digestion in Infants
Mechanisms for protein digestion
Brush border peptidases are present in
neonatal mucosa
Amino acid transporters are functional at birth
but there may be quantitative changes as the
animal matures
Arginine limiting AA
• Necessary for ammonia detoxification
Influences on gut closure
 Insulin (IGF-1)
Hormone secreted by pancreas
Aids in glucose regulation
 Alkaline Phosphatase
intestinal maturation
Epidermal Growth Factor (EGF)
EGF promotes growth of several organs and
epithelia
Receptors present from very early in gestation
Fetal rat hepatocytes secrete IGF in response
to EGF
Glucose
 Glucose
Transported from the lumen by the sodium-dependent
hexose transporter & phosphorylated
Expression of transporter does not change with age
(Exception - ruminants)
 Ruminants
Dramatic ↓ in glucose transporter GLUT-1 during first
few weeks after birth
Very low levels after weaning
Fructose transport is also low during suckling
 Rises after weaning
Glucose
In piglets, gut closure is diet dependent
Can withhold feed/inject insulin to delay gut closure
Do not mobilize glycogen store postpartum.
Rely on feed intake to get glucose & need to absorb it
Ruminant gut closure is not diet
dependent
Mobilize glycogen stores postpartum
Can somewhat delay with insulin
Immunoglobulin Absorption
24 hr period of time for attainment of passive
immunity in livestock
Proteolytic activity of the digestive tract is low
trypsin inhibitors in colostrum
Nutrients are able to pass the stomach
without degradation to the small intestine
where absorption occurs
Colostrum Importance
Contains 3-12x the amount of AB than
maternal serum
 Neonate does not have ability to digest complex
feedstuff
 Provides first immunity (IgG> IgM, IgA) to
agammaglobulinemic calf
 A neonate that is not given colostrum does not
reach comparable blood IgG levels of a 24-hour
colostrum-fed calf until 3-4 months.
 Provides: immunity, encourages microbial
colonization of previously sterile GIT, GF that
encourage closure
Absorptive Mechanism
AB travel intercellular routes (enterocytes)
Filled vacuole pinches off at luminal end
Nucleus and vacuole change places
Vacuole merges with basolateral
membrane
Enhanced by large intercellular spaces in
neonatal intestine
Material in vacuole is “purged” into
intercellular spaces
Factors of “Closure” of Small
Intestine
Extreme cold/heat stress decreases
antibody transport
O2 availability
Hypotheses about closure as a function of
increasing digestive capability
Closure in ungulates independent of gastric and
pancreatic development
In pigs, closure is diet-induced (glucose)
Colostrum intake accelerates closure in all
ungulates to varying degrees
“Closure” of Small Intestine
 Uptake continues as long as vacuolization is present
 Gaps between enterocytes close: shifting and
hyperplasia of existing cells in the mucosal lining as well
as shedding of cells on villi.
 When enterocytes are no longer able to exocytose
vacuolar contents, a neonates gut is considered closed
 Occurs approx. 24hrs postpartum
 Vacuolated enterocytes disappear following definite
patterns
 Proximal segments of small intestine lose ability long before
distal portions