FUNCTION OF THE GI TRACT

1. Ingestion

Motility mechanical breakdown of

food, propulsion of food through gut

2. Digestion

Secretion secretion of enzymes,

water & ions

3. Absorption
Control of motility and secretion by
nervous system and hormones

4. Egestion

Innervation of GI tract
Located
In the submucosa (submucosal or Meissners plexus ) and between
circular and longitudinal muscle layers (myenteric or Auerbachs
plexus).
Excitatory Acetylcholine

Substance P

Control

Inhibitory VIP , nitric oxide

Motility Myenteric plexus

Secretion Submucosal plexus
Through release of neurotransmitters

Excitatory - Acetylcholine

Properties of GI smooth muscle

5-10m

200m
Form hollow tubes not contracting against skeleton
Form a syncitium electrically couple, joined by gap junction contractions
synchronous
Actin:myosin ratio 15:1 (skeletal muscle 2:1)
Contractile elements not arranged in sarcomeres not striated
Stimulated by neurotransmitter released from varicosities
Have slow wave activity.

0
M
e

-60
Tension

Acetylcholine
Membrane
Potential (mV)

-60
Tension

Slow waves in GI smooth muscle

Slow waves are changes in resting membrane potential IE
3-12 cycles per minute depending on area of GI tract 3/min in
stomach, 12/min small intestine.
Always present but do not always cause contractions.
Frequency of contractions dictated by frequency of slow waves.
Slow wave frequency and height modulated by body temp &
metabolic activity
Intrinsic & extrinsic nerves (increased by Ach, SP; decreased by
noradrenaline, No. VIP). Circulating hormones (esp. CCK,
motilin)

Contraction of GI smooth muscle

Calcium activates contraction
OUT

Depends on influx of calcium

from extracellular space
through calcium channels

Ca2

IN

Calcium-calmodulin complex
activates myosin light chain
kinase
(Ca2)4-Calmodulin

Inactive myosin
light chain kinase
MUSCLE
CONTRACTION

Contraction explained by
sliding filament theory

Active myosin light

chain kinase
Myosin (PO4)2

Innervation of the GI tract

2. Extrinsic nerves
Parasympathetic innervation
Via preganglionic fibres in vagus and pelvic nerves
-

Synapse on ganglionic neurons in enteric nervous system

Excitatory through release of acetylcholine

Parasympathetic nervous system

Postganglionic fibres from coeliac, superior and inferior
mesenteric system.
Inhibitory through release of noradrenaline

Parasympathetic n.s.

Sympathetic n.s.

Vagal nuclei

CNS
Preganglionic Fibres
Preganglionic fibres

Sacral spinal
cord

Sympathetic
ganglia
Postganglionic fibres

Enteric nervous System

Myenteric
Submucosal
plexus
plexus

Smooth
Muscle

Secretory
cells

Endocrine
cells

Blood
vessels

Effect of different stimuli on

muscle contraction
Stimulus

Effect on muscle
more depolarised smooth

1.
2.
3.

Stretch of GI tract wall

Acetylcholine release
Parasympathetic stimulation

muscle, more excitable

4.
5.

Noradrenaline release
Sympathetic stimulation

more hyperpolarised smooth

Leads toaction potential

generation and smooth

muscle contraction.

muscle, Less excitable and

fewer contractions .

Musculature of the GI tract

All smooth muscle except :
Upper third of oesophagus striated
Middle third of oesophagus mixed
External anal sphincter striated

Areas of striated muscle are areas that

are under conscious control.

GASTRIN
3 Main forms polypeptides
II
G34
III G17
mins
IV G14
I
G45
V
G4

- T
T

= 15 mins
= 2-3

Produced by G cells in Antral part and duodenal bulb.

Physiological Actions
Gastric Acid
Gastrin Pepsin
Also insulin + glucagon after a meal
Gastric motility ++
Gastro-oesophageal sphincter.
Release
Amino Acids
Peptides
Distention of
Stomach
Vagus
Catecholamine

Luminal
Acids

G Cell

Secretin
Glucagon
Gastric Inh
Peptides
Intestinal inh.
Peptides

CHOLECYSTOKININ - PANCREOZYMIN
SECRETED BY UPPER SMALL INTESTINE
STRUCTURE
Amino Acids
CCK 39, 33, 12, 8, 4
C5 terminal amino acids similar to Gastrin
ACTIONS
1. Gall Bladder contraction
2. Pancreatic juice - rich in enzymes
3. INHIBIT gastric emptying
4. Augments pyloric sphincter tone to delay gastric emptying
5. Enterokinase Secretion
6. Augments action of secretion
7. Glucagon
SECRETION
Peptides / amino acid in intestine
FA > 10 carbon in duodenum
+ve feed back with protein or fat digestion

SECRETIN
Produced by small intestine
Amino acid structure glucagon
T = 5 mins.
Action HCO3Pancreatic Juice
Water Content
Augments CCK action
Gastric HCl
Insulin secretion

GIP
43 amino - residues
Secretion duodenum + jejunum
Stimulated by glucose + fat in duodenum
ACTION - insulin Secretion
Inhibit gastric motility + secretion

VIP
28 amino acid
T 2 mins.
In blood + gut
Stimulates Electrolytes & H2O of intestinal secretions.
Dilate blood vessels
Gastric acid secretion

GI motility
There are many types of contractions in different
Areas of the GI tract. Some muscles contract and
relax in seconds
- phasic contractions

peristalsis
segmentation
Some maintain contractions over minutes or hours
- tonic contractions

sphincters.

GI motility controlled by both humoral and neural

Mechanisms
1. Extrinsic nervous system
Paraymp = acetylcholine release = increased contraction

2.

Intrinsic nervous system

Receptors in GI tract/stretch = Ach, SP release = increased contraction

3.

Hormones

Only hormones known to have physiological effects on motility are

motilin = increased gastric and intestinal motility
cholecystokinin = decreased gastric emptying

Gastric motility
Fundus acts as food store
Body and antrum mix food
Pylorus contracts to limit exit of chyme

1. Relaxtion of fundus
(vagovagal reflex

3. Pylorus contracts
4. Mixing by
retropulsion
2.Contraction
of body
and antrum

GASTRIC EMPTYING FACTORS

CNS
- Anxiety
Sympathetic
- Drugs

NATURE OF FOOD
Volume
Solid or Liquid

Vagus
pH
food
Gastrin

Tonicity
Fat content
Protein
content

Slow waves in the stomach cause

contraction without action potential

Em

Tension
4s

Control of gastric motility

Vagovagal reflex - Fundal relaxation
Myenteric plexus - Slow waves
contractions

Parasympathetic - inc contraction force

and freq

Sympathetic -

dec contraction force

and freq

Control of gastric emptying

Chyme only empties from stomach when particle size is small
Enough to pass through polyrus

Most important mechanism is strong stomach contractions

Contractions stimulated by :
1.
2.

Presence of food
Gastrin

But control of stomach emptying by these factor is fairly weak

solids

liquids

Time

Control of gastric emptying

Most control of stomach emptying is done through
Inhibitory mechanisms in the duodenum and jejunum
Through nervous reflexes and hormones
Inhibitory reflexes - direct - myenteric plexus
indirect via extrinsic nerves

Neural reflexes stimulated by :

Distension, irritation, acidity, high osmolality,
Protein/fat.
Fats and acids also stimulate release of humoral factors which
Reduce gastric emptying
Cholecystokinin stim. By fats
Secretin stim. By acids.

Gastric motility on fasting

Migrating Motor Complex
Occurs on fasting I.e. after digestion and absorption of last meal, to
clear undigested food particles.
Peristatic contractions sweep down stomach and duodenum
pylorus relaxes.
Pattern of contraction approx every 90 min. on fasting

Slow peristatic waves sweeping whole of GI tract

Thought to be controlled by motilin

Control of intestinal motility- neuronal

Mixing segmentation
frequency set by slow waves (12/minute dudenum)
additional control myeneteric plexus

Propulsion peristalsis
Local reflex stretch causes relaxation distal and
contraction proximal (Bayliss-Starling law of the intestines)
moves bolus through intestines.
Intestino-intestinal reflex extrinsic nerves
Local stretch in one area inhibits contractions in rest of bowel

Reflex control of gut activity

CNS
Parasympathetic and
Sympathetic efferents
Splanchnic
And vagal
Afferents

Myenteric
plexus

Parasympathetic
and sympathetic
efferent

Submucosal
plexus
Local efferents

Local afferents

Chemoreceptors
mechanoreceptors in
gut wall

Gut wall muscle

Endocrine cells
Secretory cells
Blood vessel

Absorption of electrolytes and water

Na+ low

Na+

high

K+

diffusion

Na+

ATP

Na+

Cl-

Na+ also absorbed

In active transport
Processes eg
Glucose, amino
Acids, H+ ions

Osmosis

Aldosterone stimulates Na+ absorption

H2O

Disorder of fluid absorption

consequence - diarrhoea
Hyperosmotic chyme e.g. high intake of
artificial sugars or high acid content.
Infection e.g. cholera
Colon can absorb 7L water per day but if small
Intestine secretes more than this, result is
Diarrhoea.

Reflex

Stimulus

Effect

gastroenteric
Stomach distension
Sl activity
gastrocolic
Distension,emptying
Colonic
duodenocolic distension
motility
enterogastric
Chyme
stomach
acid/protein/fat
emptying
irritant
vagovagal
Food in stomach
intestointestinal distention

Fundal relax.
relaxation

Clinical problems with motility

Gastric emptying
too slow = gastric carcinoma or
ulceration (vagotomy)
Results in nausea and vomiting, diarrhoea, cramps.
Patients seek help for difficulty swallowing (oesophageal scarring)
or dental erosion.
too fast = usually found in patients with
duodenal ulcer
Dont know if cause or effect overwhelms protective defences of
duodenum

VOLUME OF G.I.T. SECRETIONS

Saliva
Gastric Juice
Pancreatic Juice
Bile
Intestinal Juice

1000ml
3000ml
1000ml
1000ml
3000ml

TOTAL

9000ml

DAILY EXCRETION OF ELECTROLYTES

IN GIT SECRETIONS
Na

Cl

Saliva
Gastric J
Pancreatic J
Bile
Intestinal J

200
150
70
100
300

10
20
3
4
15

100
250
50
50
300

Mmol/day

820

52

750

GASTRIC SECRETION
William Beaumont first identified actions of gastric
Juice, hydrochloric acid content, mucus secretion,
and observed gastric motility directly in 1825.
Protection of mucosa
mucus
bicarbonate
Digestion and absorption of food, control of motility
acid
gastrin
pepsinogen
cholecystokenin
intrinsic factor
histamine

Oxyntic gland mucosa

secretes
mucus
acid from parietal cells
Pepsinogen from peptic
cells
Intrinsic factor from
parietal cells in humans
(peptic cells in other
species.

Pyloric gland mucosa secretes

Endocrine cells
throughout mucosa
secretes
mucus
histamine
gastrin from G cells

Gastric secretions
Mucus

pH<2

pH7
HCO3 -

Physical/Chemical
barrier to attach by
gastric juice:
Stimulated by :
- Ach
- Mechanical stim
- Chemicals(ethanol)
If breached e.g.
hypersecretion of
acid
ulceration

Parietal cell - secreting

Tubulovesicles fuse with
canaliculus, increased surface area
and numbers of H+K+ATP ase
increases acid secretion into lumen
of gut.

H+
Acid secretion is against a 3
million fold concentration
gradient
H+ inside = 4x 10-8M
H+ outside = 0.1 M
NEEDS ENERGY

Blood

Parietal cell

Lumen
At rest 70mV
Secretion 40mV

K+

K+

HCO3-

HCO3-

ATP

H+

H+
H2CO3
Na+

Na+

K+

Na+

H2O + CO2

ATP

Na+
ATP

K+

ClCl-

ClATP

H2O

H2O

ClH+

K+
Na+

Gastric secretions
Pepsinogen

Inactive precursor of pepsin which

initiates protein digestion
Is not necessary for complete
digestion of dietary protein
pancreatic enzymes are sufficient
active only when the pH < 3.5
Released by Ach

Pesinogen
Acid

pepsin

Gastric secretions
Intrinsic factor

Only gastric secretion that is

Essential for health

Secreted from parietal cells in humans, chief cell in other

Species.

Forms a complex with vitamin B12 in the gut

The complex is resistant to digestion & therefore enables

Absorption of vitamin B12

Lack of intrinsic factor causes Vit B12 deficiency

(Pernicious anaemia) as all the Vit B12 is digested and
Therefore none can be absorbed

HCl SECRETION
CELL
INTERSTITIAL

JUICE

Cl

Cl
CO2 + H2O
c.A.
H2O CO3
HCO3- + H+
K
OH-

H+
H2O

Gastric hormones
Gastrin
Release from G-cells in the pyloric glands is stimulated by
Distension of stomach causes gastrin releasing
peptide (GRP) release from submucosal plexusGRP causes gastrin release

Presence of amino acids in stomach stimulates

chemoreceptors local reflexes cause gastrin release.

Release inhibited by pH<2 I.e. during active acid secretion

Released into blood form G-cells and acts on parietal cells to stimulate
Acid production and cell growth.
Also acts on enterochromaffin-like cells ion the lamina propria to release
histamine

Gastric secretion
Control is in 3 phases

Cephalic phase entirely dependent on the vagal nerve accounts

for 10% - 15% total volume of secretion
acid secretion stimulated by sight, smell, chewing
and swallowing
Oral/nasal chemoreceptors
vagal nucleus
Ach + GRP
Release
acetylcholine + gastrin + histamine = acid secretion
1.

Vagal
afferents

2.

Gastric phase accounts for at least 50% of gastric

secretion
Controlled by local reflexes, vagovagal reflexes and hormones
Distension of stomach
local mechanoreceptors
acetylcholine
and gastrin release
acid and pepsinogen secretion
Amino acids/peptides
local chemoreceptors
gastrin release
acid and pepsinogen secretion

3.

Intestinal phase - about 5% of secretion

Primarily hormonal denervated stomach will be stimulated
to secrete acid by protein in duodenum
Hormone still unknown
Very small number of G-cells in duodenum also release gastrin in response
to amino acids.

Inhibition of gastric secretion

All mechanisms for the inhibition of acid secretion act to ensure effective
digestion of food.
1. Control by the stomach
Fall in pH<3 in the stomach inhibits gastrin secretion.
2. Control by duodenum
pH<3 nervous reflexes inhibits both acid secretion and gastric emptying
pH<3, fatty acids, hyperosmotic solution causes release of hormones.
a) secretin released by acid inhibits acid secretion directly and also
inhibits release of gastrin.
b) gastric inhibitory peptide released by fatty acids and has direct effect on
parietal cells to inhibits acid secretion.

Secretion of the small intestine,

pancreas and liver
Small Intestine
many villi on surface of intestine
crypts/glands of Lieberkuhn between villi epithelial cells have
brush border.
Secretions are from cells within the crypts of Lieberkuhn and fall
Into two groups
secretions into the lumen (from enterocytes)
secretions into the blood (from endocrine cells)

Secretion into the lumen - mucus

Brunners glands
Compound mucus glands,
Secreting

First protection
For duodenum
From acid

- alkali
- mucus

Secretion
Stimulated by
Para-sympathetics
Inhibited by
Sympathetics
?stress related
ulceration

Pancreas

Secretions into the lumen-aqueous

Absorption of nutrients and
Secretion occurs at brush
Border in mature
enterocytes

Secretion moves up and out

Of the crypts, mixes with
Chyme and washes over the
Villi into the lumen

Water and electrolyte

Secretion from
Undifferentiated enterocytes
In the bottom of crypts

Intestinal secretions
Small intestine
Mucus/alkali secretions mucosal protection
Aqueous secretions
under local nervous control
some minor hormonal control (secretin, CCK)
Large intestine
Secretion primarily consists of mucus. Can also secrete water
In response to irritation

Secretions from the intestines enzymes

and hormones
Digestive enzymes not secreted from small intestine
From pancreas or found on enterocytes
except enterokinase secreted from duodenal
mucosa.
Hormones secreted from endocrine cells in mucosa
Stimulated by activation of chemoreceptors in response to
Constituents of food and act to stimulate production of digestive
Secretions from the other organs
Gastrin - duodenum stomach
Cholecystokinin Sl pancreas
Secretin Sl pancreas

Pancreatic secretions
Endocrine insulin & glucagon
Exocrine enzymes and bicarbonate
essential for digestion
almost under separate hormonal control

Key hormones in stimulation of secretion are :

Cholecystokinin (CCK)
Secretin
Both released from the small intestine

Cholecystokinin
CCK

Stomach
duodenum

I Cells
Peptides
Amino acids, H+

FAT

Pancreas

Pancreatic enzymes
Essential for digestion - essential for life

Acinar cells
Proteases

Lipases Amylases

Inactive form
Active enzymes
Activated in gut

SECRETIN

FAT H+

HCO3S cells

SECRETIN

Bicarbonate secretion
Lumen

Blood
CO2

H2O

CO2

H2CO3
HCO3-

ClNa+

H2O

HCO3-

H+

H+

ATP

ClNa+

Na+

H2O

Pancreatic secretion
- secretion in 3 phases
Cephalic phase - only 10-15% of total secretion
activation of vagal efferents stimulates enzyme
release
Gastric phase - only present in some species
NOT SIGNIFICANT IN HUMANS
Intestinal phase - majority of secretion
combination of hormones CCK and secretin
results in maximal enzyme and bicarbonate
release

Intestinal phase of secretion

VAGUS
CCK

Peptides
Amino acids

Fat, H+

Secretin

HCO3-

Enzymes

ACH

Functions of bile

emulsification of facts
increased absorption of lipids into
enterocytes.
cholesterol excretion (only route)
excretion of breakdown products of
haemoglobin (bilirubin)

Secretion and storage of bile

Constituents of bile
Water
Bile Salts
Bilirubin
Cholesterol
Fatty acids
Lecithin

Liver

Gallbladder

98%
1%
0.04%
0.1%
0.12%
0.04%

92%
6%
0.3%
0.3-0.9%
0.3-1.2%
0.3%

Function and fate

Of bile acids - the
Enterohepatic
circulation

Liver
Secretion

Portal vein
GallbladderStorage &
concentration

Bile acids almost totally

Reabsorbed in terminal illeum.
20% excreted daily. Inhibition of
Reabsorption results in
Synthesis of new bile acids and
Lowering of cholesterol levels.

Common
Bile duct

Duodenum
Digestion &
emulsification

Ileum
Absorbption of
Bile acids

Secretions of the intestine, pancreas

and liver-summary
Small intestine
mucus and fluid involved in protection and absorption
hormones control of pancreatic and bile secretions.
Pancreatic secretions
Bicarbonate for neutralisation of acids, optimises
conditions for enzyme action
Enzymes for digestion
Liver
-

bile for emulsification of fat

Digestion of carbohydrate, protein and fats by catalytic

hydrolysis
enzymes are either luminal (e.g. from salivary glands
or pancreas) or membrane bound

Digested nutrients / fluids absorbed through the brush

Border by
active transport

diffusion passive
facilitated
solvent drag

Carbohydrate digestion
-

Initiated by salivary amylase from salivary glands

majority by pancreatic amylase in small intestine
pH optimum 7, activated by Cl- ions

1,4 bonds give straight chains

1,6 bonds give branched chains

Amylase can only hydrolyse 1,4

bonds branched chains cannot be
broken down by amylase

Carbohydrate digestion
Starch
Glycogen
Luminal digestion
amylase

-dextrins, di-&
trisaccharides
Membrane digestion
e.g. sucrase, lactase

Glucose, galactose
fructose

Humans do not have

Cellulase-cellulose makes
Up most of undigested fibre
In diet

Absorption of simple sugars

Limiting step on simple sugar availability is rate of
Absorption large excess in small intestine.
Majority absorbed in duodenum and jejunum

Digested at membrane so available for transport

Fructose absorbed by facilitated diffusion
Glucose/galactose absorbed passively (small quantities)
Under anaerobic conditions and actively absorbed by same
Carrier when O2 available.
Deficiencies of brush border enzymes cause osmotic diarrhoea
Human Sl can absorb up to 10kg sucrose per day

Absorption of glucose

K+ Low

Glu

Na+

ATP
Na+

Na+

Glu

Glu

Na+

diffusion
Glu
Facilitated transport

Na+

Protein Digestion begins in stomach

Pepsin inactive precursor pepsinogen
Active @ pH 2-3, inactive pH>5
Secretion stimulated by acetylcholine or acid
Only protease which can break down collagen
Action terminated by neutralisation by
Bicarbonate in duodenum
N.B. All proteases (stomach & pancreatic) secreted as inactive
Precursors. Most protein digestion occurs in the duodenum/
Jejunum.

Activation of pancreatic proteases

Enterokinases

Trypsinogen

Trypsinogen
Chymotrypsinogen
Proelastase
Procarboxypeptidase

Trypsin

Trypsin
Chymotrypsin
Elastase
Carboxypeptidase

Active proteases inactivated by trypsin

Protein
Di/tri
peptides

Transporters

Amino acids

Peptides

Peptidases
aminopolypeptidase

Cytoplasmic peptidase

Amino acids

Transporters

Absorption of peptides and amino acids

Transport at the brush border
1.
Active transport by carrier.
2.
Mostly dependent on Na+ gradient co-transport similar to that
for glucose.
3.
Some amino acids (basic, and neutral with hydrophobic side
chains) are absorbed by facilitated diffusion.
Protein assimilation affected by :

Pancreatitis, congenital protease deficiencies, deficiencies of specific

Transporters.

Digestion of fats
Fat stim CCK release
Gallbladder contraction
Bile salts emulsify fact
large surface area for
enzymatic action

Lecithin important for

Emulsification
Pancreatic lipase
- water soluble
- acid labile
- extremely active and
secreted in large quantities

1m

Absorption of vitamins
Vitamin
A
B1
B2
Niacin
C
D
E
K
Folic Acid
B6
B12

Soluble in fat

Soluble in water

Calcium absorption
Skin
Liver
Parathyroid
hormone

Kidney

Ca2+

Vit D3
25, OH-D3

1,25 (OH)2D3

CBP
Ca2+

Ca2

Absorptive capacity of the

intestine
Actual
500g
100g
50-100g
amino
acids
7 8L

Capacity
Carbohydrate
Fat
Protein

Water

10g
500g
700g

20+ L

Iron absorption transferrin

mediated uptake
Fe

Fe
Fe

Ferritin
Fe
Fe
Fe

TF

Fe2+ + plasma transferrin

Digestion and absorption

Digestion by hydrolysis
Importance of pancreatic enzymes
Types of membrane bound enzymes
Mechanism of absorption :
Carbohydrates, fats, proteins, electrolytes, water, special cases

Effect of disturbances in digestion /

absorption.

Nutrition and control of food

intake
Control of appetite, hunger and satiety
Nutritional requirements
Essential fatty acids

Essential amino acids

Carbohydrates
Vitamins, minerals

Special cases, pregnancy & lactation

Malnutrition & dental relevance

Experimental evidence that hunger

and satiety are controlled centrally
lateral nucleus feeding centre
Electrical stimulation hyperphagia
Destruction aphagia
Endogenous control of feeding
Low plasma glucose and amino acids
Input from olfactory (smell), gustatory (taste) and
Visual primary afferents

Ventromedial nucleus satiety centre

Stimulation refusal to eat
Destruction uncontrolled eating, obesity
Endogenous control of feeding
Also responds to low plasma [glucose] and
[amino acids] BUT IN OPPOSITE WAY
Other inputs : stomach distension, plasma CCK
& insulin all stimulate
Amphetamines potentiate neurotransmitter effects in the VMN and
Suppress feeding

Regulation of food intake

Glucose (GI & plasma)
Amino acids
Lipids (CCK)

+
Ventromedial nucleus
satiety centre

Feeding

+
Lateral nucleus
feeding centre

Regulation of appetite food choice

Controlled by dietary need (exp.animals)
Controlled by limbic system (amygdala)
acting on hypothalamus
Area of brain involved in emotional control

Lesions abolish food choice

Major control in humans (developed world)
probably taste rather than dietary need,

Body
Temperature
-Energy
available

Long term

Glucostatic
Aminostatic
lipostatic

Control of food intake

Hormones
CCK,
Insulin,
glucagon

Short term
What stops you eating

Gl distension
Oral meter

NUTRITION
We require
proteins (essential amino acids)
fats (but Western diet fats too high)
vitamins
Carbohydrate
minerals
50%
Intake (normally 3000-6000k cal
Per day & depends on
Geography
Occupation

Protein
15%

Fat 35%

Nutrition what we need and why ?

Amino acids protein synthesis
Essential, conditionally essential, non-essential plus
Extra
Protein requirements 0.6g/kg adult per day
More in growth & repair e.g. infants, infection, pregnancy

Protein required due to turnover in tissues

In growth or wasting, tissues which turn
over protein fastest will alter most in mass
I.e. Liver, gut, white cells

Loss of protein = loss of function

Nutrition What we need and why

Essential fatty acids

Barriers skin and gut waterproofing &
lubrication
Nervous development low fat diet in infants
poor myelination
Cellular signals precursors for inflammatory
mediators immune function
inflammation
platelet aggregation

Nutrition what we need and why

Fatty acid deficiency in animals failure to grow linolenic acid
skin & kidney lesions
Linoleic and arachidonic acids reverse
other deficiencies.
BODY CANNOT MAKE THESE FATTY ACIDS

ESSENTIAL

Nutrition what we need and why

Carbohydrates
- non-essential
except for non-starch polysaccarhides (fibre).
Insufficient fibre results in poor blood glucose and lipid control, increased
Gut infection and incidence of cancer.

- preferred source of energy

- Sucrose most cariogenic substance

Vitamins
Deficiency becoming more common in
Some urban populations in UK
Vit D - rickets
Vit C - scurvy

Long history of recognised importance Deficiency disease

e.g. beri-beri (B1; 2000BC), scurvy
(C; in sailors 1400 AD)

Vitamins requirements and deficiencies

1.
Vitamin

Water soluble
Recommended daily intake (mg)

B1 (Thiamine)
Riboflavin
Niacin
C
Folic acid
B12
B6
Panthothenic acid

1.5
1.8
20
45
0.4
0.003
2
unknown

Deficiency
Beri-beri
Pellagra
Scurvy
Anaemia, spina bifida
Pernicious anaemia

Not stored in body deficiency leads to rapid clinical symptoms.

Most important ones in terms of dentistry are :
B12 (fiboflavin) important for cellular metabolism in mouth, cornea & skin
deficiency glossitis, angular stomatitis, corneal vascularisation
photophobia
Vitamin C
necessary for collagen formation
deficiency (scurvy) = gingival oedema & bleeding, delayed healing,
brusing.

Vitamins requirements and deficiencies

2.

Fat soluble

Vitamin

Recommended daily intake

Deficiency

5000 IU

400 IU

E
K

15 IU
70g

Blindness, dry mucous membrane, abortion

growth failure.
Rickets, poorly calcified dentition, delayed
eruption
Foetal resorption
Poor clotting

Particularly important in dentistry :

Vitamin A - 500,000 new cases per year in developed countries
Vitamin D - may be prevalent in racial groups moving from sunny to
temperature climates

Minerals and trace elements

Mineral/trace element Recommended daily intake

Required for

Iron
Calcium
Cobalt
Iodine
Copper
Zinc
Fluorine

Oxygen carriage haemoglobin

Calcification, cell excitability
part of Vitamin B12
thyroid function
ossification
immune response
prevention of caries

10-20mg
800-1200mg
150g
15mg
1ppm drinking water

Ion deficiency anaemia. May present with pale mucous membranes.

Fairly common particularly in women (pregnancy).
Calcium deficiency - rare except in vegetarians
Iodine = extremely rare as salt is iodinated
Deficiency of trace elements extremely rare as requirements are so low

FASTING
A.

6 24 hours
Liver Glycogen
glucose insulin (100g)
Major source - free fatty acids from ADIPOSE TISSUE
Gluconeogenesis
glucose
Small amount of acetoacetate, B OH butyrate
Major response due to insulin

B.

2 4 days
Liver Glycogen depleted
Glyconeogenesis ++ from amino acids mainly from muscle, glycerol
from adipose tissue + lactate from Rbc
FA

Ketones in liver

Hormones Insulin
Cortisol & adrenaline
Glucagon & this peaks at 4 days.

FASTED STATE > 2 WEEKS

1. Ketone Bodies formed as main source of energy
mainly in LIVER

2. Gluconeogenesis
3. Insulin conc. Tends to be low
Cortisol be responsible fo
High levels
Adrenaline
Glucagon levels
Gluconeogenesis.

and may r reduced levels of

Take home message

Energy in = energy out
Avoid faulty diet balanced diet few deficiencies
Special care in special circumstances
Less fat, more CHO
(watch the sucrose!)

Extra care in :

Less meat, more fish

(EFF)

Pregnancy more
Energy & protein plus
Fe, Ca, Vit D, etc etc

More exercise
Enough Fe & Ca
Fluorides (?)

Weaned infants Protein, fatty acids, vit

C etc.etc.