Lecture 1 - Overview of Gut Physiology
1. Understand the structure of the GI tract
Hollow tube stretching from mouth to anus, 4.5m long (9m in cadaver when
smooth muscle is no longer contracting)
Accessory digestive organs:
o Salivary glands
o Exocrine pancreas
o Liver (gall bladder)
Oesophagus Stomach Small intestine (duodenum, jejunum, ileum) Large
intestine (ascending, transverse, descending and sigmoid colon) Rectum Mucosa
o Innermost layer of GI tract, surrounding the lumen.
o Divided into: epithelium, lamina propria, muscularis mucosae.
o Structure of mucosa consists of invaginations of secretory glands or
folded in order to increase surface area (i.e. villi).
o Dense layer of irregular connective tissue with large blood vessels,
lymphatics and nerves branching into mucosa and muscularis.
o Contains submucosa plexus (Meissner’s), part of enteric nervous
system, situated on the inner surface of muscularis externa.
o Two layers of smooth muscle:
Inner circular layer squeezes the tract.
Outer longitudinal layer which shortens tract.
o Coordinated contractions of the 2 smooth muscle layers is peristalsis.
o Between the two muscle layers is the myenteric plexus (Auerbach’s).
o Consists of several layers of connective tissue.
o Covered by thin squamous epithelial cell layer, mesothelium.
o Together forming a serosa (serous membrane).
2. Understand its basic digestive processes
Note: The GIT is a major interface between microbes and the immune system.
Primary function of the GI system is for the transfer of nutrients, water and
electrolytes from the food we eat into the body’s internal environment.
Not regulated according to body homeostasis.
Maximizes absorption regardless of whether nutrients are needed.
Four basic digestive processes:
Absorption 3. Identify the major cell types in the GI tract
a. Muscle cells
Propulsion or mixing of contents
Two types of muscle cells in the gut
o Skeletal muscle – oesophagus
o Smooth muscle
Circular muscle, longitudinal muscle and muscularis
Sphincters: valves that regulate emptying of organs.
Afferent – sensory signals from the intestine.
Efferent – autonomic nervous system.
o Enteric Nervous System
o Sympathetic inhibits motility and closes sphincters
o Parasympathetic increases motility.
c. Epithelial cells
A mucosal epithelium constitutes the physical barrier between the
lumen and the body. Mucous secretions contribute to the barrier.
Functions include secretion, absorption, lubrication, protections. Also
an important endocrine organ.
Motility of the GIT
Contraction of the gastrointestinal smooth muscle is an involuntary process.
Movement of organ walls propels food/liquid along the GIT and mix contents.
Segmentation is the contraction of circular muscle in order to mix the food
without propelling food along the GIT.
Peristalsis is the coordinated contraction of the circular and longitudinal
muscle to propel food down the GIT.
Motility – peristalsis
The propulsive contractile movements of the oesophagus, stomach and intestine are
The circular muscle produces a narrowing
The longitudinal muscle contracts, shortening the organ and moving the
narrowed portion, and the food within, down the length of the organ. Gastrointestinal secretions
A total o 7L of secretions enter the GIT each day.
These secretions are produced by the:
o Salivary glands
o Stomach – gastric
o Small intestine
Mechanical and Chemical Digestion
Digestion is the process where the food we ingest is converted by chemical and
mechanical means into the nutrients required by the body to survive.
Mechanical: change in size and consistency of contents.
Chemical: enzymatic and chemical breakdown of food components into
smaller units that can be absorbed across the GIT mucosa.
Absorption – general
The movement of small molecules across the wall of the small and large intestine
through osmosis, active transport and diffusion.
Sugar – carbohydrate (monosaccharides) Small intestine
Fat – lipids (monoglycerides)
Protein (amino acids, small peptides)
Absorption of water and electrolytes Small & large
Absorption of minerals and vitamins intestine Gastrointestinal immune system
The largest component of the immune system
o Eosinophils, neutrophils, macrophages, T calls, B-cells, mast cells
o Gut exists in a state of physiological inflammation
o Antigens, bacteria, physical damage
o Maintain protection while tolerating commensal microbes.
Microbial flora of the gut
Largest population of bacteria inhabit the gastrointestinal tract. Several factors
determine the final composition of an individual’s microbiota:
Mother’s microbiota composition
Protection by commensal bacteria
Antibiotics may create a niche for enteric pathogens
Balanced microbial community Antibiotics
Increased species diversity Decreased species diversity
Increased TLR signaling Altered TLR signaling
Immune development and tolerance Immune dysregulation
Gram +ve, spore forming, toxin producing bacillus
20-50% carriage rate in hospital patients; 3% carriage rate in healthy
Emerging treatments by stool sample transplant Lecture 2 – Swallowing and the events that follow
1. Learn about the swallowing reflex
The Cephalic Phase
Preparation of GI tract for a meal
Stimuli – cognitive, olfactory, visual
Auditory – classic conditioning experiments e.g. Pavlov
o Pairing auditory stimulus to presentation of food; auditiory stimulus
along salivary secretion.
Activaiton of dorsal motor nucleus of the vagus (DMV) in brainstem.
Neural components of cephalic phase
Activation of the DMV leads to increased activity in parasympathetic efferent
innervation of the GI tract
Salivary secretion (cranial nerve IX/glossopharyngeal nerve)
Gastric acid secretion (cranial nerve X/vagus nerve)
Pancreatic enzyme secretion (cranial nerve X)
Gallbladder contraction and relaxation of sphincter of Oddi (cranial nerve X)
Mastication – Chewing
o Incisors and canines exert a cutting/tearing action
o Molars perform a grinding function
o Food in the mouth causes a reflex relaxation and dropping of the jaw.
o Initiates a stretch reflex and rebound closure of the jaw.
o The food bolus again activates relaxation and the cycle repeats.
Neural control is largely from the motor branch of the 5 cranial nerve
(trigeminal) controlled by areas of the brain stem.
Salivary gland locations
1. Parotid (next to ear)
2. Submandibular (under jaw)
3. Sublingual (under tongue)
Functions of secretions
Secrete 1.5L /day of saliva. Responsible for:
Lubrication, oral hygiene, neutralize pH, initiate carbohydrate digestion.
Composition: mostly water (99.5%), 0.5% electrolytes and organic
compounds. Organic Composition of Saliva
Two major proteins:
o α-amylase initiates carbohydrate breakdown.
o Mucin glycoproteins act as lubricant and barrier.
Also present in small amounts:
o Lingual lipase – initiates lipid breakdown.
o Lactoferrin (antibacterial actions)
o Lysozyme (antibacterial actions)
o Muramidase (antibacterial actions)
o Immunoglobulins (IgA)
Salivary gland acinar cells
Serous acinar cells: secrete a watery product containing α-amylase but
Mucus acinar cells: secrete a viscous product containing mucin glycoproteins.
Stimuli for salivation
Salivatory nuclei in the brain stem
Positive stimuli for the salivatory nuclei include:
o Taste and tactile stimuli from the tonge
o Sight and small of food
Parasympathetic fibres stimulate secretion from salivary glad via muscarinic
Control of salivary secretion
Secretion from salivary acinar cells is primary under control of the autonomic
Parasympathetic: acetylcholine (Ach) acting on muscarinic M receptors.
Sympathetic: noradrenaline (norepinephrine) acting on α- and β- receptor
Some medications of anti-cholinergic actions that can block stimulation of
saliva secretion leading to dry mouth (side effect). SWALLOWING
Complex mechanism involving voluntary and involuntary phases as well as sharing
of the upper airways.
Phases of swallowing
Voluntary phase: oral – food moved by tongue pushing upwards and
backwards towards pharynx.
o Pharyngeal – mechanoreceptors initiate closure of the trachea,
relaxation of the upper esophageal sphincter (UES) and initiation of a
primary peristaltic wave. Involves swallowing centre in medulla (brain
stem) and several cranial nerves (vagus, trigeminal and
o Esophageal – conduction of food to the stomach is assisted by gravity,
primary and secondary peristaltic waves, opening of the LES and
receptive relaxation of the stomach. All of this involves local enteric
neural reflexes and extrinsic parasympathetic reflexes.
Step by step:
1) Swallowing centre inhibits respiratory centre in brain stem.
2) Elevation of uvula prevents food from entering nasal passages.
3) Position of tongue prevents food from re-entering mouth.
4) Epiglottis is pressed down over closed glottis as auxiliary mechanism to
prevent food from entering airways.
Regions of the stomach
Fundus: near the gastro-esophageal junction, mainly for storage.
Body: larges portion of the stomach and contains parietal and chief cells.
Antrum: most distal portion of the stomach, most endocrine cells are found
in the antrum.
Surface area of the stomach increased by folds in wall – rugae.
Folds in the mucosa – glands and pits.
Glands contain several cell types:
o Mucosa – mucus secreting
o Parietal – acid secreting
o Chief – pepsinogen secreting
o Endocrine cells – hormone secreting Functional anatomy of the stomach
Oxyntic gland area
o Body and fundus, upper 80%
o Acid secreting parietal cells
Pyloric gland area
o Atral region, lower 20%
o Gastrin secreting G cells
Mucous neck cells
Mucous neck cells secrete mucins – viscous and sticky glycoproteins.
Mucins are stored in large granulaes in the apical cytoplasm of the mucous
Maintenance of the protective mucus layer requires continuous secretion of
Surface epithelial cells
The surface epithelial cells are tall columnar epithelial cells.
Gastric epithelial cells secrete a watery fluid containing a high concnetraion
of HCO .3-
The high HCO concnetration helps buffer the pH of the mucus layer.
Mucins and HCO tog3ther form a protective barrier that prevents acid and
pepsins from damaging the gastric mucosa. Lecture 3 – The gastric phase of digestion
Lines the body and fundus of the stomach. These glands constitue 80% of the
stomach and secret:
Acid (H , proton)
Pepsin (as pepsinogen)
Mucus (and HCO ) 3
Lines the antrum of the stomach and secretes:
Functions of Gastric Secretions
o Required to convert pepsinogen to pepsin.
o Bacteriostatic (stops bacterial growth)
o Initiates digestion of protein together with pepsin.
Mucus lubricates and protects against physical damage.
Mucus plus HCO ma3ntains a near neutral pH at the lining of the stomach.
Intrinsic factor (IF) is critical for the absorption of vitamin B12 in the
terminal small intestine (ileum).
Parietal cells secrete both acid and intrinsic factor (required for absorption
of Vit B12).
Parietal cells have a distinct triangular morphology with an abundance of
mitochondria, intracellular vesicles and canalicular structures.
Control of intrinsic factor secretion
Required for transport of vitamin B12. Uptake takes place in terminal ileum.
Lack of B12 leads to pernicious anemia.
Failure to secrete IF is associated with a lack ofk parietal cells and chlorydia
(lack of acid secretion). Parietal cell acid production
1) Vesicles with proton pumps (H+/K+ ATPase) waiting for stimulation.
2) Mitochondria provide energy for active transport.
3) Proton pumps relocate to the cell membrane and pump H+ into lumen.
4) K+ channels exist in the apical membrane to return K+ to the lumen.
5) Carbonic anhydrase converts water and CO to H2and HCO 3-
6) HCO i3 exchanged for Cl- at the basal membrane.
7) Cl- leaves the cell through apical Cl- channels.
Stimulation of gastric acid secretion
Secretion of acid by parietal cells is stimulated by:
Acetylcholine released from the vagus nerve and enteric neurons acting
through muscarinic M re3eptors
o Can stimulate acid release directly or via gastrin and histamine
Gastrin is released from G cells in the antrum in response to acetylcholine.
o Gastrin acts via gastrin-cholecystokinin receptors.
Histamine released from enterochromaffin-like cells acts through histamine
o Histamine release can be stimulated by both gastrin and ACh.
Digestive phases and regulation of gastric secretion
1) Cephalic phase via vagus
2) Parasympathetics excite pepsin and acid production
3) Gastric phase:
a. Locat nervous ENS secretory reflexes.
b. Vagal reflexes.
c. Gastrin-histamine stimulation.
4) Intestinal phase:
a. Nervous mechanisms
b. Hormonal mechanisms
Cephalic phase of acid secretion
20-30% of maximal secretory response to a meal
Occurs before food reaches the stomach
Driven by taste and smell through mechano- and chemoreceptors and by
Mediated by branches of the Vagus
o Parasympathetic nerve Ach gastrin increased acid secretion
Has be studied by sham feeding (via oesophageal and gastric fistulas) Gastric phase of acid secretion
Greater than 50 of maximal secretory response
Food enters the stomach buffering the pH to approx. 6 which dis-inhibits
gastring release (the brake is off).
Distension of the stomach walls via mechanoreceptors initiate short (ENS)
and long (vago-vagal) reflexes.
G cells are also directly stimulated by digested protein (amino acids), calcium
and caffeine (not blocked by vagotomy).
Gastrin release is:
o Increased by gastrin-releasing peptide (GRP) from the ENS
o Inhibited by release of somatostatin (SS) from the D cells
Intestinal phase of acid secretion
Approx. 5% of maximal secretory response
There is evidence that amino acids contribute to gastrin release (from the
intestinal mucosa) and possible a role for other unidentified hormones.
The intestinal phase is more important in inhibiting acid secretion and
Interdigestive phase of acid secretion
Acid secretion rate is approximate 10% of maximal secretory response.
Stomach contains a low volume of gastric juice at pH less than 2.0.
A low pH inhibits gastrin release from the G cells and thus limits excessive
Inhibition of gastric secretion
Gastric luminal pH
Acid solutions in the duodenum
Digestive products in the duodenum
Hyperosmotic solutions in the duodenum
Secretion of acid by parietal cells is inhibited by the hormone somatostatin:
Somatostatin released from endocrine “D cells” in both the antrum and body
regions of the stomach
o Antral D cells are stimulated by low luminal pH
o Antral somatostatin inhibits release of gastrin from G cells
o Body D cells are stimulated by neural and hormonal mechanisms
o Somatostatin can act on enterochromaffin like cells (ECL) to block
histamine release or directly on parietal cells to block acid release. Chief Cells
Secrete pepsinogen but not acid.
Pepsinogen is activated by low pH (less than 3) and converted to pepsin.
Pepsins are endopeptidases that initiate protein digestion by hydrolysis.
Control of pepsinogen secretion
Pro-enzyme released from peptic (chief) cells.
Strongest stimulus is vagally-mediated (via ENS and Ach release). Release
will occur in the cephalic and gastric phases.
H+ stimulates a local enteric (ENS) cholinergic reflex to release pepsinogen.
Low pH 3-5 is required to activate pepsin (and pepsin will activate pepsin)
and greater than pH 5 is inhibitory.
Motor functions of the stomach
4 events in the process of gastric filling and emptying:
1) Receiving and providing temporary storage of foods and liquids.
2) Mixing of food and liquid with gastric secretory products including pepsin
3) Grinding of food to reduce particle size to enhance digestion and permit
passage through the pylorus.
4) Regulating the exit of material from the stomach into the duodenum.
Neurally-mediated relaxation of (upper) stomach
Accommodation: food volume increases without pressure increases.
Depends on parasympathetic input to enteric nerves.
Vagotomy was used as a weight loss strategy.
Pyloric region of the stomach
Contributes to the mechanical reduction of particle size and mixing
Movements have three stages
o Propulsion: bolus is pushed toward the pylorus.
o Grinding: the antrum churns the trapped material.
o Retropulsion: bolus is pushed back into the proximal stomach.
All together this is called the “pyloric pump”
Content of meal influences rate of gastric emptying
The rate is greater if the meal is:
-Liquid, non-nutrient, carbohdrate > protein > fat, neutral > acid.
Regulation of gastric emptying
Promotes Emptying Inhibits emptying
-Gastric chyme volume Cholecystokini (CCK) Enterogastric reflexes
Distension or irritation of duodenum,
protein and fat digestion products.
Esophageal protective mechanisms for resisting the corrosive effects of acid:
A certain amount of acid reflux is normal while excess exposure can be
Saliva acts to neurtralize acid.
Protective action of mucus.
Barrier function of the lower esophageal sphincter.
Helicobacter pylori and gastric ulcers
Only known bacteria that can thrive in acidic environment of the stomach.
Estimated 66% of worlds population are infected with H. pyloria.
o 70% are asymptomatic.
o Symptomatic people develop stomach ulcers.
H. pylori excretes the enzyme urease
o Urea ---urease---> (NH3 + HCO3-)
A ‘basic cloud’ protects the bacteria from the acidic stomach environment but
the ammonia is toxic to the gastric epithelial cells.
H. pylori also produces other enzymes including protease, catalase and
phospholipases - damage gastric cells initiating an inflammatory response.
Helicobacter pylori and gastric ulcers
Antibiotic therapy now common.
Standard ulcer therapy is triply therapy:
o Omeprazole (proton pump inhibitor to reduce acid damage during
Other treatments include histamine (H2) receptor antagonists. Lecture 4: Small Intestinal Physiology 1
Understand how structure and function of the small intestine are linked.
Appreciate the different type of small intestinal motility.
Understand the roles of the pancreas in nutrient digestion.
Major functions of the small intestines
Movement of food (mixing and propulsion)
Absorption of nutrients is the main function of the small intestine.
The small intestine absorbs nutrients after extensive digestion by luminal
and brush border enzymes.
Anatomical divisions of the small intestine
The small intestine (bowel)
o Duodenum (first 5%)
o Jejunum (middle 40%)
o Ileum (final 55%)
The bile and pancreatic ducts enter the small intestine in the duodenum
(ampulla of Vater)
Absorption of nutrients is the major function of the small intestine (mostly in
jejunum and ileum) Surface are for nutrient digestion
and absorption is maximized
Inner surface contains folds
(plicae circulares) on which
villi are positioned.
Each enterocyte is lined by a
“brush border” containing
Actin filaments allow for
What determines the movement patterns of the GI tract?
Optimal time of exposure to various segments of the GI tract is essential for
effective digestion and absorption.
Motility provides both mixing and propulsion.
GIT function is highly regulated by neural, hormonal, local chemical and
physical factors. ‘Slow waves’ in smooth muscle
Smooth muscle shows continual oscillations in membrane potential called
o Frequency decreases down the intestine:
3/min in stomach
12/min in duodenum, 8/min in ileum, 3/min in colon
Thus there is a gradient from top of the small I. to large I.
o Peridically the slow waves give rise to “spike potentials”
These are slow Ca++ mediated action potentials (APs).
o This increases cytoplasmic Ca++ and gives rise to smooth muscle
Generation of slow waves
Interstitial cells of Cajal (ICC)
o Contained within the smooth muscle layers.
o Some ICC act as pacemakers.
Contain specialized ion channels that underlie this activity.
o Other ICC transfers excitability to the smooth muscle cells.
Act through gap junctions.
Spread the excitation more widely.
Suited to the function of sphincters Underlying electrical activity can be either:
o Repetitive spike potentials
o Sustained depolarization
May need inhibitory transmission (ATP, NO, VIP) to relax some smooth
Ileocacal sphincter controls movement of chyme from small to large intestines
1) Pressure and chemical irritation relax sphincter and excite peristalsis
2) Fluidity of contents promotes emptying
3) Pressure or chemical irritation in cecum inhibits peristalsis of elium and
A wave-like movement of muscles in the GI tract, characterized by the alternate
contraction and relaxation of the muscles that propel the contents downward.
Mediated by the local, intrinsic enteric nerves (ENS) and is not affected by
vagotomy or sympathectomy.
Moves contents down the GIT.
A non-propulsive mixing motility seen especially in the small intestine. Segmental
rings of contraction chop and mix the ingested materials to enhance digestion.
Fasting patterns of motility: MMC
Fasting state exhibits the Migrating Motility Complex (MMC).
Contractile wave periodically moving down the GI tract from the mid-
stomach to the ileum and on to the colon.
Associated with increased levels of the motilin.
Interrupted by feeding.
Digestion in the small intestine
Breakdown of nutrients/macromolecules to enable transport to
o Enzymatic digestion
o Sugar, protein and fats
o Pancreatic enzymes are key
Functional roles of the pancreas
Pancreas has both endocrine and exocrine functions
Endocrine functions: important for metabolic control (insulin production)
Exocrine functions: important for gastrointestinal function. Pancreatic digestive enzyme secretion
Pancreas has the highest rate of protein secretion of any organ.
Each day the pancreas delivers 5-15g of protein to the small intestine.
The pancreas secretes over 20 proteins.
Most of these proteins are digestive enzymes secreted in an inactive form.
Secretin and the birth of endocrinology
Pavlov believed that the pancreas was exclusively regulated by the nervous
Bayless and Starling denervated the pancreas and still observed pancreatic
secretions in response to acid.
Removed mucosa, stimulated with acid, collected supernatant
o Supernatant caused pancreatic secretion
o Active ingredient “secretin”, the first hormone.
The lesson, as always: beware dogma.
Structure of pancreatic exocrine glands
Exocrine glands are made up of acini which are clusters of cells that
synthesize and secrete protein (e.g. enzymes) into the ducts.
The acini contain secretory acinar cells while the ducts contain duct
epithelial cells which secrete bicarbonate.
Pancreatic HCO sec3etion
1. H 2 diffuses across the cell membrane, CO is 2ormed as a by-product of
2. Cytoplasmic carbonic anhydrase (CA) catalyses the conversion of CO and 2
- - +
OH to HCO an3 H . 3. H leaves the cell via the basal Na /H exchanger.
4. HCO se3retion into the duct lumen occurs via the Cl /HCO exchanger3-
5. Outward rectifying Cl channels in the apical membrane return the Cl into
6. Na /K ATPase removes the accumulating Na +.
Composition of pancreatic juice
Two distinct components of pancreatic juice:
o Duct cells: watery alkaline secretion rich in HCO . 3-
o Acinar cells: digestive enzymes.
Pancreatic HCO ac3s to neutralize the acidic stomach contents as they enter
the small intestine.
Pancreatic digestive enzymes complete the digestion of protein,
carbohydrates and fats
o Broken down into small constituent molecules that can be absorbed.
Pancreatic digestive enzymes
o Trypisonigen enteropeptidase Trypsin
o Chymotrypsinogen trypsin Chymotrypsin
o Procarboxypeptidase trypsin Carboxypeptidase
o Pancreatic amylase
o Pancreatic lipases Proenzyme/active Activating agent Product
TRYPSINogen Enteropeptidase Peptides
CHYMOTRYPSINogen Trypsin Peptides
ProELASTASE Trypsin Peptides
ProCARBOXYPEPTIDASE B Trypsin Amino acids
Phase Stimulant Regulatory Pathway % of max
Cephalic Sight, small, taste,Parasympathetic 25
Gastric Distension Parasympathetic, hormones, H + 10-20
Intestinal Amino acids, fatty Intestinal hormones (e.g. secretin 50-80
acids, H & cholecystokinin)
Digestive Enzymes Lecture 5 Small Intestinal Physiology II – Nutrient digestion/absorption
Objective: Understand how nutrient components of a meal are digested/absorbed.
Carbohydrates in the diet
60% complex carbohydrates – starch
30% disaccharides – sucrose and lactose
10% monosaccharides – glucose and fructose
Monosaccharides can be absorbed across the small intestine epithelium therefore
for most of the carbohydrate in the diet digestion has to take place first. Digestion of carbohydrate
Takes place in the lumen of the gut.
Luminal digestion of starch to disaccharide by salivary and pancreatic
Further broken down by the action of amylases that are expressed by the
Brush border digestion of disaccharides to monosaccharides by
Sucrose sucrase glucose fructose
Lactose lactase glucose galactose
Maltose maltase 2 glucose
Enzymes for CHO digestion
Absorption of carbohydrates
The monosaccharide products of carbohydrate digestion (glucose, fructose,
galactose) are absorbed by the small intestine in a two-step process.
1) Across the apical cell membrane
a. Glucose and galactose
i. Na+/glucose co-transporter (SGLT1)
b. Fructose facilitated sugar transporter (GLUT5)
2) Across the basal cell membrane
Monosaccharide absorption Abnormalities of CHO digestion or absorption
Lactose intolerance: genetic or acquired conditions where the enzyme lactase is
deficient. NOT an allergy. Controlled by dietary modification or exogenous enzymes.
Lactose = “milk sugar”
Lactose accumulates in the gut
o Acts as an osmolyte (osmotic laxative – traps water in lumen)
o Acts as nutrient for bacteria
o Accumulation of gas and water lead to irritation, bloating, diarrhea.
Lactose intolerance is actually a deficiency of the enzyme lactase. ot enough lactase
to break lactose into glucose and galactose. The excess lactose then acts as an
osmotic stimulant. It can also act as a substrate for bacterial growth leading to
bacterial overgrowth that can produce gas. This leads to feelings of bloating and
Protein in the diet
The protein requirements of the body
o Adult 0.6g/kg body weight per day; child 3-4g/kg body weight/day
Average diet – 90g protein per day
o 10-30g from gastrointestinal secretions including proteases produced
o 3g albumin.
o Stomach production of pepsin.
During first six months of life some protein uptake by phagocytosis (passive
immunity from mother to child). Digestion of protein
4 major pathways:
1) Luminal proteases from the stomach and small intestines can hydrolyse
proteins to peptides and amino acids (30%).
2) Brush border enteropeptidase digest the peptides to amino acids.
3) Peptides are absorbed and broken down to individual amino acids by
4) Peptides are absorbed and cross directly into the blood stream.
Absorption of amino acids
1) Across apical cell membrane
a. Na+ dependent amino acid co-transporter
b. H+ dependent peptide co-transporter
2) Across basal cell membrane
a. Mainly an amino acid co-transporter which is Na+ INdependent
Apical transport of amino acids
At lease 7 transport systems in the apical membrane.
o For groups of amino acids (e.g. acidic/basic amino acids).
The pre-dominant amino acid transporter is the Na+-dependent amino acid
o Driven by the inward directed Na+ gradient.
Small peptides (3-6 amino acids)
Small peptide uptake occurs via the H+/peptide co-transporter (Pept1) o An active process driven by the H+ gradient.
o Most small peptides are broken down in the enterocyte by
cytoplasmic peptidases to single amino acids.
Basal transport of amino acids
o 90% of absorbed amino acids