DISEASES OF THE PANCREAS, SERIES #9
Rad M. Agrawal, M.D., Series Editor
The Physiology of the Pancreas
Satyanisth Agrawal Elie Aoun
INTRODUCTION
W
hen originally studied, the pancreas was one of
the last organs in the abdomen to catch critical
attention of anatomists and physiologists.1 New
imaging techniques such as computed tomography (CT)
and magnetic resonance imaging (MRI) have enhanced
the understanding of pancreas anatomy and made
possible the surgical, endoscopic and percutaneous
manipulation of pancreas.2
Anatomy
The pancreas is a flat, long, and soft gland that is
roughly 6 inches in length and weighs between 70 and
110 g. It lies obliquely in the retroperitoneal space of
the upper abdomen and is covered by the stomach,
transverse colon, and transverse mesocolon. The head
of the pancreas lies next to the duodenal sweep at the
level of the body of L2.3,4 The neck, body, and tail span
leftward, with the tail extending close to the spleen.5
Functional Anatomy
The pancreas consists of ≥80% of acini that are
arranged in clusters that form lobules separated by
loose connective tissue. A circular shaped acinus and
Satyanisth Agrawal, DO, Elie Aoun, MD
West Penn Allegheny Health System,
Division of Gastroenterology, Pittsburgh, PA
48
its tubular draining ductule form the functional unit
of exocrine pancreas.6 Many acini arranged like a
bouquet secrete digestive enzymes into the ductule
which drains into interlobular ducts and finally into the
main pancreatic ductal system.
Pancreatic acinar cells are specialized exocrine
secretory cells that synthesize, store, and secrete the
digestive enzyme component of the pancreatic juice.
An acinar cell is shaped like a triangle, with the basal
membrane pointed outward for neurohormonal receptors
and the apical membrane located inward forming the
lumen of an acinus. The nucleus and rough endoplasmic
reticulum (RER) are located near the basal membrane
for protein synthesis.7 Zymogen granules that store
digestive enzymes are located near the apical membrane
and hence close to the lumen. Tight junctions between
acinar cells form a barrier between the lumen and apical
membrane to prevent inappropriate passage of enzymes
but allow water and ions to go through.8,9 Secretagogues
stimulate acinar cells causing the granules to fuse with
each other and the apical membrane. Microvilli covering
the apical surface of acinar cells facilitate exocytosis
of enzymes into the lumen. Gap junctions between
adjacent acinar cells allow coordinated chemical and
electrical communication between cells for passage
of small molecules such as calcium and other ions
important for digestive enzyme secretion.
PRACTICAL GASTROENTEROLOGY  •  DECEMBER 2014

The ducts collect pancreatic enzymes, and the
activity of the ductular cells dilutes and alkalinizes
pancreatic juice before it is washed out into the small
intestine. The duct epithelium is made of cuboidal
columnar cells held together by intercellular tight
junctions. These ductular cells are packed with
mitochondria to supply energy for ion transport. Once
stimulated, these cells transport bicarbonate ions into the
pancreatic juice as it passes along the duct, with water
following in response to the resulting transepithelial
osmotic gradient.10
Exocrine Secretions
Pancreatic exocrine secretions, nearly 2.5L/day in
volume, can be classified in two groups: organic and
inorganic. Organic secretions are proteins such as
digestive enzymes and inorganic secretions consist
mostly of water and electrolytes. Acinar cells secrete
digestive enzymes and ductal cells secrete bicarbonate
rich electrolyte solution.11 Depending on the organic
secretion, the enzyme component of pancreatic juice
is mixed in various proportions with the aqueous
component. Greater than 75% of proteins in organic
secretions are enzymes and proenzymes; the rest are
plasma proteins, trypsin inhibitors, and mucoproteins
(Table 1).
Organic Secretions
One of the major purposes of the pancreas is to
synthesize digestive enzymes and deliver them to the
intestine where they play a critical role in digestion.
The four major enzyme groups are proteolytic (eg,
chymotrypsin), amylolytic (eg, amylase), lipolytic
(eg, lipase), and nuclease digestive enzymes. Some
of the enzymes are present in more than one form
(e.g., cationic trypsinogen, anionic trypsinogen, and
mesotrypsinogen).12 To prevent auto digestion of the
pancreas, and hence pancreatitis, enzymes are stored
and secreted as inactive precursor forms. Enterokinase,
secreted by duodenal mucosa, converts trypsinogen
to its active form trypsin, which then catalyzes the
activation of the other inactive proenzymes. The acinar
cells also secrete a trypsin inhibitor, which inactivates
trypsin by disabling this catalytic action.13
Inorganic Secretions
Pancreatic electrolytes (sodium, potassium, chloride,
and bicarbonate) mixed with water form an alkaline
fluid that is isosmotic with extracellular fluid and
PRACTICAL GASTROENTEROLOGY  •  DECEMBER 2014
The Physiology of the Pancreas
DISEASES OF THE PANCREAS, SERIES #9
Table 1. Pancreatic Acinar Cells Secretory Products
Proenzymes Enzymes
Cationic trypsinogen (PRSS1) Amylase
Anionic trypsinogen (PRSS2) Carboxylesterase
Mesotrypsinogen (PRSS3) Sterol esterase
Chymotrypsinogen B1, B2 Lipase
Kallireinogen DNase
Procarboxypepsidase A (1,2) RNase
Procarboxypepsidase B (1,2)
Proelastase
helps neutralize gastric acid entering the duodenum.14
Postprandial stimulation mediated mainly by secretin
increases secretory flow rate from an average of 0.3
mL/minute in the resting (interdigestive) state to 4.0
mL/minute in the digestive state. The concentrations
of bicarbonate and chloride in pancreatic juice change
reciprocally as secretory flow rate increases making
the osmolality of pancreatic juice independent of flow
rate.15
Digestive Enzyme Functions
Amylase
The salivary glands and pancreas make amylases.
Pancreatic amylase hydrolyzes the 1,4-glycoside
linkages of complex carbohydrates and starches. This
produces short dextrins, which can then be digested
by brush border enzymes like maltose and maltotriose
into glucose.
Lipases
The majority of dietary lipids in western diets are
triglycerides, which cannot be digested by brush
border enzymes. Pancreatic triglyceride lipase binds
to the oil-water interface of the triglyceride oil droplet
where it cleaves the majority of fatty acids from dietary
triglycerides.
Bile acids and colipase are important for the full
activity of lipases. Bile acids emulsify triglyceride
molecules to expand surface area for lipase to act on.16
Colipase forms a complex with lipase and bile salts and
anchors lipase to allow it to act in a more hydrophilic
49
The Physiology of the Pancreas
DISEASES OF THE PANCREAS, SERIES #9
environment on the hydrophobic surface of the oil
droplet. Carboxyl ester lipase can act on a variety of
substrates and is important in digestion of cholesterol
esters, lipid-soluble vitamins such as Vitamin A, and
triglycerides.
Proteases
Pancreatic proteases and gastric pepsin digest all of
the complex dietary proteins into short peptides and
amino acids for further digestion and absorption in
the intestine. The most abundant enzyme is trypsin,
which is present in three forms. Cationic trypsinogen,
coded by PRSS1 gene, is present in a large proportion,
and anionic trypsinogen and mesotrypsinogen, which
are coded by PRSS2 and PRSS3 genes, respectively,
are present in smaller proportions. All trypsinogens
act similarly by attacking the exposed arginine and
lysine residues within a peptide chain. Chymotrypsin
and elastase are endopeptidases, just like trypsin, that
cleave specific peptide bonds adjacent to specific amino
acids. These amino acids eventually have greater effects
on stimulating pancreatic secretion, inhibiting gastric
emptying, regulating small bowel motility, and causing
satiety.
Synthesis and Transport of Digestive Enzymes
Protein synthesis occurs in the ribosomes close to the
rough endoplasmic reticulum (RER) of acinar cells.17
The cell’s messenger RNA (mRNA) then translates
these newly synthesized proteins into exportable
proteins. A terminal peptide extension on pancreatic
enzymes, known as signal protein, allows attachment
and entry of the enzyme into the RER.18 The enzyme
and signal protein interact with a membrane protein
called a docking protein. This process permits the
completion of the translocation, dissociation of the
signal protein and mRNA from enzyme, and allows
the enzyme to enter RER. Newly synthesized proteins
can undergo modifications and conformational changes
in the endoplasmic reticulum before being transported
to the Golgi complex where further post-translational
modification (glycosylation), sorting, and concentration
occur.19
Digestive enzymes are then transported to the
zymogen granules. A given zymogen granule has
various pancreatic proteins mixed in relative proportions
depending on their rates of synthesis. The rate of
synthesis of a particular enzyme is related to the type
of diet. For example, dietary increase in carbohydrates
50
will result in increased expression of amylase compared
to other pancreatic enzymes. Zymogen granules then
move towards the apical membrane of acinar cells via
microtubules and await appropriate neurohormonal
stimulus to trigger exocytosis.20
Facilitated by microvilli covering apical surface of
acinar cells, exocytosis is a process where the zymogen
granule fuses with the apical surface and allows its
contents to be released in the ducts.21 This entire process
takes less than 1 hour allowing the pancreas to be ready
for the next meal by repeating synthesis and packaging
of enzymes.
Cellular Regulation of Enzyme Secretion
At the cellular level, secretion of pancreatic juice can be
divided into organic and inorganic secretions. Organic
secretions containing pancreatic enzymes occurs
by regulating acinar cells, and inorganic secretions
containing bicarbonate and other electrolytes occurs
by regulating ductal cells. Hormonal regulation of
acinar and ductal cells is explained in this section and
the integrated neurohormonal control of pancreatic
secretion is discussed later.
Acinar Cells
Acinar cells express receptors on their basolateral
membranes for the following hormones: cholecystokinin
(CCK), acetylcholine (ACh), gastrin-releasing
peptide (GRP), vasoactive intestinal peptide (VIP),
and secretin.22,23 These receptors are divided into two
groups based on their mode of stimulating acinar cells
(Figure 1). VIP and secretin activate adenylate cyclase,
which increases cellular cAMP and facilitates enzyme
secretion through cAMP dependent protein kinase A.
The other group consisting of acetylcholine, GRP, and
CCK lead to an increase in intracellular free calcium
concentrations via stimulating cellular metabolism of
membrane phosphoinositides.24 This phospholipase
C-dependent pathway is the primary stimulus for
significant acinar secretion, with cAMP-dependent
signaling playing a secondary role.
Ductular Cells
Ductular cells contribute the fluid and bicarbonate
components of pancreatic juice. Bicarboanate is
predominantly derived from plasma rather than
intracellular metabolism. Both the apical and
basolateral membranes have polarized epithelial cells
(continued on page 52)
PRACTICAL GASTROENTEROLOGY  •  DECEMBER 2014
The Physiology of the Pancreas

DISEASES OF THE PANCREAS, SERIES #9

(continued from page 50)

and membrane transport proteins that help with ion
transportation (Figure 2). Ductal cells are very sensitive
to secretin and VIP, both of which increase intracellular
cAMP, which in turn leads to opening of CFTR chloride
channels initiating secretion.14,15 Bicarbonate enters
through the sodium-bicarbonate cotransporter on the
basolateral membrane and exits through the CFTR
channel on the apical membrane.25 Concomitantly, the
sodium-potassium pump keeps the intracellular sodium
low thus creating a continual electrochemical force
and driving bicarbonate into the ductal cell through
the sodium-bicarbonate cotransporter. Water and
sodium ions follow paracellularly in response to the
electrochemical gradient across the epithelium.

Organ Physiology Figure 1.

Exocrine pancreatic secretion happens during two
states: fasting (interdigestive) and after ingestion of a
meal (digestive). The interdigestive pattern of secretion
begins when the stomach is empty. Secretory activity
related to eating (digestive state) occurs in phases:
cephalic (20-25%), gastric (10%), and intestinal
(approximately 60%-70%). Pancreatic secretion is
activated by a combination of neural and hormonal
effectors.

Interdigestive Secretions
The interdigestive pancreatic secretions are governed by
the cholinergic nervous system, motilin, and pancreatic
polypeptide. Secretions follow the cyclical pattern of
the migrating myoelectric complex (MMC) [26, 27].
Enzyme secretion occurs every 1 to 2 hours and is
associated with the periods of increased motor activity
in the stomach and duodenum. In addition to pancreatic
enzyme secretion, there is increased secretion of
bicarbonate and bile (secondary to partial gallbladder
contraction) into the duodenum. The pancreatic
secretion during the interdigestive phase is integral to
the “housekeeping” function of the MMC to clear the
stomach and small intestine of debris including bacteria
between meals.26
Digestive Secretions
Secretion with ingestion of a meal is divided into
three phases: cephalic, gastric, and intestinal. During
the cephalic and gastric phases, secretions are low in
volume with high concentrations of digestive enzymes,
reflecting stimulation primarily of acinar cells. This
Figure 2.
stimulation arises from cholinergic vagal input during
the cephalic phase, and vago-vagal reflexes activated
by gastric distension during the gastric phase. Gastric
distention predominantly causes secretion of enzymes
with little secretion of water and bicarbonate.28
The intestinal phase begins when chyme leaves
stomach and enters the small intestine. During the
intestinal phase, ductular secretion is strongly activated,
resulting in the production of high volumes of pancreatic
juice with decreased concentrations of protein, although
the total quantity of enzymes secreted during this
phase is actually also markedly increased. Ductular
secretion during this phase is driven primarily by the
endocrine action of secretin on receptors localized to

52 PRACTICAL GASTROENTEROLOGY  •  DECEMBER 2014

 The Physiology of the Pancreas

DISEASES OF THE PANCREAS, SERIES #9

Table 2. Pancreatic Function Tests

Indirect/Non-Invasive Tests:
• Do not require IVS or tubes
• Detection of severe exocrine pancreatic dysfunction
• Insensitive for detecting mild or moderate pancreas dysfunction

Test Description Utility

Fecal fat Measure fat content in stool Provides quantitative measurement
after ingesting meals with a of steatorrhea
known amount of fat

Fecal chymotrypsin or Measure chymotrypsin or Widely available test

Elastase
NBT-PABA
(N-benzoyl-l-tyrosyl-p-
aminobenzoic acid) and
Fluorescein dilaurate
elastase in stool
*no oral ingestion needed
Measure PABA or fluorescein in
serum or urine after oral ingestion
of NBT-PABA or fluorescein
dilaurate with a meal
High clinical utility
Easier to obtain than stool samples
Unreliable in patients with small bowel
mucosal disease

Direct/Invasive tests:
• Most sensitive and specific
• Require duodenal intubation and IV administration of hormones
• Not widely available

Test Description Utility

Secretin Measure volume of pancreas Detects mild, moderate,
secretion and or severe exocrine
bicarbonate secretion into the pancreatic dysfunction
duodenum after IV secretin
Cholecystokinin Measure duodenal Detects mild, moderate,
output of amylase, trypsin, or severe exocrine
chymotrypsin, and lipase after pancreatic dysfunction
IV cholecystokinin
Indirect/Invasive Tests:
• No IV administration of hormones
• Requires duodenal intubation, oral ingestion, and normal small bowel
• Not widely available

Test Description Utility

Lundh test meal Measure duodenal trypsin Detects moderate or severe pancreatic
concentration after ingestion of dysfunction
a test meal

PRACTICAL GASTROENTEROLOGY  •  DECEMBER 2014 53

The Physiology of the Pancreas
DISEASES OF THE PANCREAS, SERIES #9
the basolateral pole of duct epithelial cells. The inputs to
the acinar cells during the intestinal phase include CCK
as well as neurotransmitters including acetylcholine
(ACh), GRP, and VIP.29-31 The large magnitude of the
intestinal phase is also attributable to amplification by
so-called enteropancreatic reflexes transmitted via the
enteric nervous system.
CCK is released from the upper small intestinal
mucosa by digestion products of fat, protein, and starch.
CCK is a potent stimulus of acinar secretion, acting
both directly on CCK-B receptors localized to the
basolateral membranes of acinar cells (Figure 1), and via
stimulation of vagal afferents close to its site of release
in the duodenum, thereby evoking vago-vagal reflexes
that stimulate acinar cell secretion via cholinergic and
noncholinergic neurotransmitters (the latter including
both GRP and VIP).32 In addition to its effects on the
pancreas, CCK coordinates the activity of other GI
segments and draining organs, including contraction
of the gallbladder, relaxation of the sphincter of Oddi,
and the slowing of gastric motility to retard gastric
emptying and thereby control the rate of delivery of
partially digested nutrients to more distal segments of
the gut.33 Finally, CCK modulates the activity of secretin
in a synergistic fashion by markedly potentiating the
effect of secretin as an agonist of pancreatic ductular
secretion of bicarbonate.31
The other major regulator of pancreatic secretion is
secretin, which is released from S cells in the duodenal
mucosa by gastric acid, with a pH threshold of 4.5.34
When the meal enters the small intestine from the
stomach, the volume of pancreatic secretions increases
rapidly, shifting from a low-volume, protein-rich fluid to
a high volume secretion in which enzymes are present
at lower concentrations (although in greater absolute
amounts, reflecting the effect of CCK and neural
effectors on acinar cell secretion). As the secretory
rate rises, the pH and bicarbonate concentration in
the pancreatic juice rises, with a reciprocal fall in the
concentration of chloride ions.34 These latter effects on
the composition of the pancreatic juice are mediated
predominantly by the endocrine mediator, secretin.35
After the meal, trypsin is free and inhibits intestinal
CCK release and pancreatic enzyme secretion. This
process is known as feedback inhibition and this effect
of trypsin is mediated by intraluminal CCK-releasing
factors (CCK-RF) present on the intestinal epithelium.36
In the presence of a meal the digestive proteases are
occupied and CCK-RF promotes CCK release and more
54
digestive enzyme secretion. However, after digestion of
a meal when there is an excess of digestive proteases
in the intestinal lumen, CCK-RF is in turn digested and
inactivated so that its ability to augment CCK release
and stimulate further pancreatic enzyme secretion
ceases (Table 2).
SUMMARY
The pancreas is a complex organ that plays a critical
role in the digestion process. Understanding the cellular
physiology of acinar and ductal cells lends to grasping
the concepts of pancreatic exocrine secretions in various
phases of digestion. Knowledge of normal pancreatic
secretory functions can help clinicians order appropriate
tests, which eventually assist in diagnosing specific
pathologies. n
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https://market.android.com/details?id=com.texterity.android.PracticalGastroApp
http://www.amazon.com/gp/product/B00820QCSE

56 PRACTICAL GASTROENTEROLOGY  •  DECEMBER 2014