Assessment Statements
 H.2.1 State that digestive juices are secreted into the alimentary canal
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by glands, including salivary glands, gastric glands in the stomach wall,
the pancreas and the wall of the small intestine.
H.2.2 Explain the structural features of exocrine gland cells.
H.2.3 Compare the composition of saliva, gastric juice and pancreatic
juice.
H.2.4 Outline the control of digestive juice secretion by nerves and
hormones, using the example of secretion of gastric juice.
H.2.5 Outline the role of membrane-bound enzymes on the surface of
epithelial cells in the small intestine in digestion.
H.2.6 Outline the reasons for cellulose not being digested in the
alimentary canal.
H.2.7 Explain why pepsin and trypsin are initially synthesized as
inactive precursors and how they are subsequently activated.
H.2.8 Discuss the roles of gastric acid and Helicobacter pylori in the
development of stomach ulcers and stomach cancers.
H.2.9 Explain the problem of lipid digestion in a hydrophilic medium
and the role of bile in overcoming this.
Secretion of digestive juices
 digestive juices are secreted
into the alimentary canal by
glands
 These glands includes;
 salivary glands,- secrets saliva
 gastric glands in the stomach
wall,- secret gastric juice
 pancreas, - secrets pancreatic
juice
 wall of the small intestine, secrets intestinal juice
Structural features of exocrine gland cells
 Exocrine glands secrets into a
space, lumen or duct
 The clustered secretary cells of an
exocrine gland, arranged around
the space into which secretion
takes place, are called acini (sing.
acinus)
 Secretory cells have a distinctive
structure, the cyrtoplasm is
packed with:
 rough endoplasmic reticulum
(rER) which synthesis of proteins
to be packaged for export
 many mitochondria – the
source of the ATP necessary for
the protein synthesis
 several Golgi apparatus –
processing & packaging proteins
from rER
 nucleoli in the nucleus –
synthesis ribosomes for rER
Group of acini with their ducts connecting together
TEM of secretory cells of the exocrine glands of
the pancreas
By use of a table, compare the
composition of saliva, gastric
juice & pancreatic juice.
Active ingredients, conditions required & outcome
Secretion
and gland
Saliva
salivary
glands
gastric
juice
gastric
glands
pancreatic
juice
pancreas
Site of
action
mouth
stomach
pH
6.5
–
7.5
2.0
small
7.0
intestine
enzymes &
non-enzyme
components
substrate or effect
product
Amylase
mucus
Starch
lubricates
maltose
Pepsin
rennin (young
mammals only)
hydrochloric acid
Proteins
coagulates milk
protein
creates acidic
environment that
kills bacteria
polypeptides
Amylase
proteases (trypsin
& chymotrypsin)
peptidases
Starch
proteins
Maltose
Polypeptides
peptides &
amino acids
Lipases
Triglycerides
nucleases
nucleotides
polypeptides
fatty acids &
Glycerol
pentose sugars,
Pi & bases
Control of gastric juice secretion by
nerves & hormones.
Control of gastric juice secretion by nerves
& hormones
 chemoreceptors & stretch
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 sight & smell of food initiate
release of gastric juice before
food is taken into the mouth
 i.e. before food reaches stomach,
gastric juice is already secreted
by reflex action
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receptors in gastric mucosa detect
presence of food in the stomach
impulses from these receptors are
sent to brain, which sends
impulses to gastric glands
causing the release more gastric
juice
impulses are also sent to
endocrine glands in gastric
mucosa to release gastrin into the
blood stream
gastrin stimulates gastric glands to
increase secretions of gastric juice
gastric juices contains
hydrochloric acid & pepsinogen
low pH of stomach & hormones
inhibits gastrin production
through negative feedback
mechanism
The control of gastric secretion
Role of membrane-bound enzymes
 some digestive enzymes such as
maltase are immobilised in the
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plasma membrane of epithelial
cells on the surface of intestinal
villi
enzyme immobilisation is when the
enzyme molecule is attached to a
fixed surface
being fixed to the membrane of the
gut epithelium is more efficient
since the enzyme is not removed
(reused) & can be linked to
secondary functions such as
membrane transport
maltose binds into the active site of
maltase on the cell membrane
enzyme.
maltose is hydrolysed into glucose
molecules which are immediately
absorbed into epithelial cells & pass
into blood capillary
Reasons for cellulose not being
digested in the alimentary canal
 cellulose exists in plant cell
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walls
it is insoluble in water, causing
a problem with it’s digestion
humans do not have enzyme
cellulase thus they are not
able to digest cellulose
cellulose makes up the
roughage or dietary fibre that
is an essential component of
our diet
eventually, cellulose is egested
along with other undigested
materials as faeces
Synthesis & activation of Pepsin & Trypsin
 pepsin and trypsin are
protease enzymes
 if they were produced in an
active form they would
digest the exocrine cells
that make them
 thus they are produced in
an inactive form
(precursors), pepsinogen
& trypsinogen
 pepsinogen is activated by
HCl while trypsinogen is
activated by enterokinase
Helicobacter pylori (H. pylori)
 Helicobacter pylori is a bacterium
which enters the stomach &
survives by attaching to receptors
on the plasma membrane of the
cells of the stomach mucosa, below
the mucus lining
 in stomach, the bacteria are
protected from strong acidity by:
 the mucus layer that lines the
inner surface;
 secreting the enzyme urease
which neutralized the acidic
environment of the stomach by
converting urea into the basic
ammonia and buffer bicarbonate
 bacteria cells can't be destroyed by
the body’s immune system because
the mucus layer prevents antibodies
from reaching the bacteria
Roles of gastric acid & Helicobacter pylori in the
development of stomach ulcers & stomach cancers.
 about 80 % of gastric ulcers
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are caused by Helicobacter
pylori (H. pylori)
H. pylori is a bacterium which
causes gastritis i.e.
inflammation of stomach
lining
stomach ulcers are open sores
in the stomach wall lining
prolonged presence of ulcers
may lead to the formation of
tumours
cancer of the stomach is a
malignant tumour in the
stomach wall
 H. pylori survives in the stomach
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mucosa by producing urease
which neutralizes gastric acid
colonization by H. pylori opens up
& weakens the protective mucus
lining for digestive attack by
gastric acid (HCl), causing ulcers
linking H. pylori to stomach ulcers
was a paradigm shift in medicine
cause was previously thought to be
stress, lifestyle, or diet
H. pylori is now thought to be
primary cause of gastric ulcers & is
now treated as infectious disease
Problem of lipid digestion in a hydrophilic
medium & the role of bile in overcoming this
 lipids are strongly
 bile is a strongly alkaline
hydrophobic & resist
break-up into small
droplets in a hydrophilic
(aqueous) medium
 lipid molecules tend to
coalesce forming droplets
of fat
 lipase is water soluble but
has an active site to which
its hydrophobic substrate
binds
yellow green, mucous fluid
containing the bile salts,
bile pigments & cholesterol
 bile’s main role is to
emulsify fats i.e. break
fats into tiny droplets
which enormously
increases their surface area
therefore increasing the
rate at which it digest lipid
 bile also neutralises the
acidity of the chyme
Emulsification of fats
 bile salts are molecules with
both hydrophilic & hydrophobic
properties
 tiny spheres of lipid are formed,
with the hydrophobic part of
bile salts embedded in their
surfaces, and the hydrophilic
parts exposed to interact with
water & prevent lipid molecules
from coalescing with each other
 the droplets in this condition,
known as micelles, remain
suspended in an aqueous
medium.
 this process is called
emulsification
Revision Questions
 Explain the structural
 Discuss the roles of gastric
features of exocrine gland
cells.
[4]
 Compare gastric juice and
pancreatic juice.
[3]
 Outline the control of the
secretion of gastric juice by
nerves and hormones.
[4]
 Outline the reason for one
named substance found in
food not being digested and
absorbed by humans.
[2]
acid and Helicobacter
pylori in the development
of stomach ulcers and
cancers.
[5]
 Explain why trypsin is
initially synthesized as an
inactive precursor and how
it is activated.
[3]
 State two components of
bile.
[2]
 Explain the role of bile in
lipid digestion.
[2]