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

LocatedIn the submucosa (submucosal or Meissner’s plexus ) and

between circular and longitudinal muscle layers (myenteric or Auerbach’s plexus).

Excitatory – Acetylcholine

Substance P

Control Inhibitory – VIP , nitric oxide

Motility – Myenteric plexusSecretion – Submucosal plexus Excitatory - Acetylcholine

Through release of neurotransmitters

Properties of GI smooth muscle

5-10µm

200µmForm hollow tubes ⁂ not contracting against skeletonForm a syncitium – electrically couple, joined by gap junction contractions ⁂

synchronousActin:myosin ratio 15:1 (skeletal muscle 2:1)Contractile elements not arranged in sarcomeres not striated ⁂Stimulated by neurotransmitter released from varicositiesHave slow wave activity.

0

0

-60Tension Acetylcholine0

-60

Tension

Me

Acetylcholine

Mem

bran

eP

ote n

ti al (

mV

)M

embr

ane

Pot

entia

l (m

V)

Tension

Tension

0

-60

0

-60

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 activityIntrinsic & extrinsic nerves (increased by Ach, SP; decreased by noradrenaline, No. VIP). Circulating hormones (esp. CCK, motilin)

Myosin –(PO4)2

Calcium activates contraction

OUT Depends on influx of calcium

from extracellular spaceIN Ca2 through calcium channels

Calcium-calmodulin complex

activates myosin light chain kinase

(Ca2)4-Calmodulin

Contraction explained by sliding filament theory

Inactive myosin Active myosin lightlight chain kinase chain kinase

MUSCLE CONTRACTION

Contraction of GI smooth muscle

Innervation of the GI tract

2. Extrinsic nervesParasympathetic 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 Sympathetic cord ganglia

Postganglionic fibres

Enteric nervous System Myenteric Submucosal plexus plexus

Smooth Secretory Endocrine BloodMuscle cells cells vessels

Effect of different stimuli onmuscle contraction

Stimulus Effect on musclemore depolarised smooth

1. Stretch of GI tract wall muscle, more excitable2. Acetylcholine release Leads toaction potential3. Parasympathetic stimulation generation and smooth

muscle contraction.

4. Noradrenaline release more hyperpolarised smooth5. Sympathetic stimulation muscle, Less excitable and

fewer contractions .

Musculature of the GI tract

All smooth muscle except :

Upper third of oesophagus – striatedMiddle third of oesophagus – mixedExternal anal sphincter – striated

Areas of striated muscle are areas that are under conscious control.

GASTRIN

3 Main forms polypeptides II G34 - T ½ = 15 mins III G17 T ½ = 2-3 mins IV G14 I G45 V G 4 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 Luminal Peptides Acids Distention of Secretin Stomach G Cell Glucagon Vagus Gastric Inh Peptides Catecholamine 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 ½ = 5 mins. Action HCO3

- Pancreatic 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 ½ 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 andrelax in seconds

- phasic contractions peristalsissegmentation

Some maintain contractions over minutes or hours

- tonic contractions sphincters.

GI motility controlled by both humoral and neuralMechanisms1. Extrinsic nervous systemParaymp = acetylcholine release = increased contraction

2. Intrinsic nervous systemReceptors in GI tract/stretch = Ach, SP release = increased contraction

3. HormonesOnly hormones known to have physiological effects on motility are

motilin = increased gastric and intestinal motilitycholecystokinin = decreased gastric emptying

Gastric motility

Fundus acts as food storeBody and antrum mix food 1. Relaxtion of fundusPylorus contracts to limit exit of chyme (vagovagal reflex

3. Pylorus contracts

4. Mixing by retropulsion

2.Contractionof bodyand

antrum

GASTRIC EMPTYING FACTORS

CNS NATURE OF FOOD - Anxiety Vagus Volume Sympathetic Solid or Liquid - Drugs pH Tonicity food Fat content Protein Gastrin content

Slow waves in the stomach causecontraction without action potential

Em

Tension

4s

Control of gastric motility

Vagovagal reflex - Fundal relaxation

Myenteric plexus - Slow waves –contractions

Parasympathetic - inc contraction forceand freq

Sympathetic - dec contraction forceand freq

Control of gastric emptying

Chyme only empties from stomach when particle size is smallEnough to pass through polyrus Most important mechanism is strong stomach contractions

Contractions stimulated by :

1. Presence of food2. Gastrin

But control of stomach emptying by these factor is fairly weak

solids

liquids

Time

Prop

ortio

n in

sto

mac

h

Control of gastric emptying

Most control of stomach emptying is done throughInhibitory mechanisms in the duodenum and jejunumThrough 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 whichReduce gastric emptyingCholecystokinin stim. By fatsSecretin 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 – segmentationfrequency set by slow waves (12/minute dudenum)additional control myeneteric plexus

Propulsion – peristalsisLocal reflex – stretch causes relaxation distal andcontraction proximal (Bayliss-Starling law of the intestines)

moves bolus through intestines.

Intestino-intestinal reflex – extrinsic nervesLocal stretch in one area inhibits contractions in rest of bowel

Reflex control of gut activity

CNS

Parasympathetic and Sympathetic efferents Parasympathetic

and sympathetic

Splanchnic efferent And vagalAfferents Myenteric Submucosal

plexus plexus

Local efferents Local afferents

Gut wall muscle Chemoreceptors Endocrine cells

mechanoreceptors in Secretory cells gut wall Blood vessel

Na+ low Na+ high

K+

diffusion Na+

ATP

Na+ Cl-

Na+ also absorbedIn active transportProcesses egGlucose, amino

Acids, H+ ions Osmosis H2O

Aldosterone stimulates Na+ absorption

Absorption of electrolytes and water

Disorder of fluid absorptionconsequence - diarrhoea

• Hyperosmotic chyme e.g. – high intake ofartificial sugars or high acid content.

• Infection e.g. cholera

Colon can absorb 7L water per day but if smallIntestine secretes more than this, result isDiarrhoea.

Reflex Stimulus Effect

gastroenteric Stomach distension Sl activitygastrocolic Distension,emptying Colonicduodenocolic distension motilityenterogastric Chyme stomach

acid/protein/fat emptying irritant

vagovagal Food in stomach Fundal relax.

intestointestinal distention relaxation

Clinical problems with motilityGastric emptying

too slow = gastric carcinoma orulceration (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 withduodenal ulcer

Don’t know if cause or effect – overwhelms protective defences of duodenum

VOLUME OF G.I.T. SECRETIONS

Saliva 1000ml Gastric Juice 3000ml Pancreatic Juice 1000ml Bile 1000ml Intestinal Juice 3000ml TOTAL 9000ml

DAILY EXCRETION OF ELECTROLYTES IN GIT SECRETIONS

Na K Cl Saliva 200 10 100 Gastric J 150 20 250 Pancreatic J 70 3 50 Bile 100 4 50 Intestinal J 300 15 300 Mmol/day 820 52 750

GASTRIC SECRETION

William Beaumont first identified actions of gastricJuice, hydrochloric acid content, mucus secretion,and observed gastric motility directly in 1825.

Protection of mucosamucusbicarbonate

Digestion and absorption of food, control of motilityacid gastrinpepsinogen cholecystokeninintrinsic factor histamine

Oxyntic gland mucosasecretesmucusacid from parietal cellsPepsinogen from

pepticcellsIntrinsic factor fromparietal cells in humans(peptic cells in otherspecies.

Endocrine cellsPyloric gland mucosa secretes throughout mucosa

secretes mucus histamine gastrin from G cells

Gastric secretions• Mucus

Physical/ChemicalpH<2 barrier to attach by

gastric juice:

Stimulated by :- Ach

pH7 - Mechanical stim HCO3

- -

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+

ATP H2O + CO2 Na+ Na+

K+ K+ ATP

Cl-

Cl- Cl-

ATP

H2O H2O

conc

entra

tion

Na+

K+

Cl-

H+

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 < 3.5Released by Ach

Pesinogen pepsin

Acid

Gastric secretions

• Intrinsic factor

- Secreted from parietal cells in humans, chief cell in otherSpecies.

- Forms a complex with vitamin B12 in the gut

- The complex is resistant to digestion & therefore enablesAbsorption of vitamin B12

Lack of intrinsic factor causes Vit B12 deficiency (Pernicious anaemia) – as all the Vit B12 is digested andTherefore none can be absorbed

Only gastric secretion that isEssential for health

HCl SECRETION

CELL INTERSTITIAL JUICE

Cl Cl CO2 + H2O c.A. H2O CO3

HCO3- + H+

K

OH- H+

H2O

Gastric hormones• GastrinRelease from G-cells in the pyloric glands is stimulated by• Distension of stomach causes gastrin releasing

peptide (GRP) release from submucosal plexus-GRP causes gastrin release

• Presence of amino acids in stomach stimulateschemoreceptors – 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 stimulateAcid production and cell growth.

Also acts on enterochromaffin-like cells ion the lamina propria to releasehistamine

Gastric secretionControl is in 3 phases

1. 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 + GRPRelease acetylcholine + gastrin + histamine = acid secretion

Vagalafferents

2. Gastric phase – accounts for at least 50% of gastric secretion

Controlled by local reflexes, vagovagal reflexes and hormones

Distension of stomach local mechanoreceptors acetylcholineand gastrin release acid and pepsinogen secretionAmino acids/peptides local chemoreceptors gastrin releaseacid and pepsinogen secretion

3. Intestinal phase - about 5% of secretion

Primarily hormonal – denervated stomach will be stimulatedto secrete acid by protein in duodenumHormone still unknown

Very small number of G-cells in duodenum also release gastrin in response to amino acids.

Inhibition of gastric secretionAll mechanisms for the inhibition of acid secretion act to ensure effectivedigestion of food.

1. Control by the stomachFall in pH<3 in the stomach inhibits gastrin secretion.

2. Control by duodenumpH<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 intestinecrypts/glands of Lieberkuhn between villi epithelial cells have“brush border”.

Secretions are from cells within the crypts of Lieberkuhn and fallInto two groups

secretions into the lumen (from enterocytes)secretions into the blood (from endocrine cells)

Secretion into the lumen - mucusPancreas

Pancreas

First protectionFor duodenumFrom acid

Brunner’s glandsCompound mucus glands,Secreting

- alkali - mucus

SecretionStimulated byPara-sympathetics

Inhibited bySympathetics

?stress relatedulceration

Secretions into the lumen-aqueous

Absorption of nutrients andSecretion occurs at brushBorder in matureenterocytes

Secretion moves up and outOf the crypts, mixes withChyme and washes over theVilli into the lumen

Water and electrolyteSecretion fromUndifferentiated enterocytesIn the bottom of crypts

Intestinal secretions

Small intestineMucus/alkali secretions – mucosal protectionAqueous secretions

under local nervous control some minor hormonal control (secretin, CCK)

Large intestineSecretion 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 duodenalmucosa.

Hormones – secreted from endocrine cells in mucosa

Stimulated by activation of chemoreceptors in response toConstituents of food and act to stimulate production of digestiveSecretions from the other organs

Gastrin - duodenum stomachCholecystokinin – Sl pancreasSecretin – Sl pancreas

Pancreatic secretions

Endocrine – insulin & glucagonExocrine – enzymes and bicarbonate

essential for digestionalmost under separate hormonal control

Key hormones in stimulation of secretion are :

Cholecystokinin (CCK)

Secretin

Both released from the small intestine

ENZYMES

Pancreas

Stomachduodenum

PeptidesAmino acids, H+

FAT

I Cells

CCKCholecystokinin

Pancreatic enzymes

Essential for digestion - essential for life

Acinar cells

Proteases Lipases Amylases

Inactive form Active enzymes

Activated in gut

SECRETIN

FAT H+

HCO3-

S cells

SECRETIN

ATP

Bicarbonate secretionLumen

BloodH2O CO2 CO2

H2CO3

HCO3- HCO3

-

H+ H+

Cl- Cl-

Na+ Na+ Na+

H2O H2O

Pancreatic secretion

- secretion in 3 phasesCephalic phase - only 10-15% of total secretion

activation of vagal efferents stimulates enzyme release

Gastric phase - only present in some speciesNOT SIGNIFICANT IN HUMANS

Intestinal phase - majority of secretioncombination of hormones CCK and secretinresults in maximal enzyme and bicarbonate release

Intestinal phase of secretion

VAGUS

CCK

PeptidesAmino 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 Liver Gallbladder

Water 98% 92%Bile Salts 1% 6%Bilirubin 0.04% 0.3%Cholesterol 0.1% 0.3-0.9%Fatty acids 0.12% 0.3-1.2%Lecithin 0.04% 0.3%

Liver –Secretion

Function and fateOf bile acids - theEnterohepaticcirculation

Bile acids almost totallyReabsorbed in terminal illeum.20% excreted daily. Inhibition ofReabsorption results in Synthesis of new bile acids andLowering of cholesterol levels.

Portal vein

Gallbladder-Storage &concentration

CommonBile duct

DuodenumDigestion &emulsification

Ileum –Absorbption ofBile acids

Secretions of the intestine, pancreasand 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 glandsor pancreas) or membrane bound

Digested nutrients / fluids absorbed through the brushBorder by

active transportdiffusion – passive facilitatedsolvent 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 1,4bonds – branched chains cannot bebroken down by amylase

Carbohydrate digestionStarch

Glycogen

-dextrins, di-& trisaccharides

Glucose, galactose

fructose

Luminal digestion amylase

Membrane digestione.g. sucrase, lactase

Humans do not haveCellulase-cellulose makesUp most of undigested fibreIn diet

Absorption of simple sugarsLimiting 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 sameCarrier when O2 available.

Deficiencies of brush border enzymes cause osmotic diarrhoea

Human Sl can absorb up to 10kg sucrose per day

Absorption of glucose

Na+

Na+

Glu

Glu

Glu

Na+

ATP

K+ Low Na+

Na+

diffusion

Facilitated transport

Glu

Protein Digestion begins in stomach

Pepsin – inactive precursor pepsinogenActive @ pH 2-3, inactive pH>5Secretion stimulated by acetylcholine or acidOnly protease which can break down collagenAction 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 Trypsin

TrypsinogenChymotrypsinogen

ProelastaseProcarboxypeptidase

TrypsinChymotrypsin

ElastaseCarboxypeptidase

Active proteases inactivated by trypsin

TransportersPeptidases

aminopolypeptidase Transporters

Cytoplasmic peptidase

Amino acids

Protein

PeptidesDi/tripeptides

Amino acids

Absorption of peptides and amino acids

Transport at the brush border1. 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 specificTransporters.

Digestion of fats

Fat stim CCK release Gallbladder contraction

Bile salts emulsify fact large surface area for enzymatic actionLecithin important forEmulsificationPancreatic lipase

- water soluble- acid labile- extremely active and secreted in large quantities 1µm

Absorption of vitaminsVitamin Soluble in fat Soluble in water

A B1

B2 Niacin C

D E K Folic Acid B6 B12

Calcium absorption

Skin Vit D3

Liver 25, OH-D3

Kidney 1,25 (OH)2D3

Parathyroid’hormone

Ca2

CBPCa2+

Ca2+

Absorptive capacity of theintestine

Actual Capacity

500g Carbohydrate 10g 100g Fat 500g

50-100g Protein 700g amino acids 7 – 8L Water 20+ L

Iron absorption – transferrin mediated uptake

Fe2+ + plasma transferrin

Ferritin

Fe Fe

Fe

Fe

Fe

Fe

TF

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 foodintake

Control of appetite, hunger and satietyNutritional requirements

Essential fatty acidsEssential amino acidsCarbohydratesVitamins, minerals

Special cases, pregnancy & lactationMalnutrition & dental relevance

Experimental evidence that hungerand satiety are controlled centrally

lateral nucleus – feeding centreElectrical stimulation hyperphagiaDestruction aphagia

Endogenous control of feedingLow plasma glucose and amino acids Input from olfactory (smell), gustatory (taste) andVisual primary afferents

Ventromedial nucleus – satiety centre

Stimulation refusal to eatDestruction uncontrolled eating, obesity

Endogenous control of feedingAlso responds to low plasma [glucose] and[amino acids] BUT IN OPPOSITE WAYOther inputs : stomach distension, plasma CCK& insulin all stimulateAmphetamines potentiate neurotransmitter effects in the VMN and Suppress feeding

Regulation of food intake

Glucose (GI & plasma)Amino acidsLipids (CCK)

Ventromedial nucleus ‘satiety centre’

Lateral nucleus‘feeding centre’

++-

- -Feeding

Regulation of appetite – food choice

• Controlled by dietary need (exp.animals)• Controlled by limbic system (amygdala)

acting on hypothalamusArea of brain involved in emotional control

• Lesions abolish food choice• Major control in humans (developed world)

probably taste rather than dietary need,

Long termBody Temperature-Energyavailable

GlucostaticAminostaticlipostatic

Control of food intake

Short termWhat stops you eating

Hormones –CCK,Insulin,glucagon

Gl distensionOral ‘meter’

NUTRITION

We requireproteins (essential amino acids)fats (but Western diet fats too high)vitaminsminerals Carbohydrate

50% Protein15%

Fat 35%

Intake (normally 3000-6000k calPer day & depends on

Geography

Occupation

Nutrition – what we need and why ?Amino acids – protein synthesis

Essential, conditionally essential, ‘non-essential’ plusExtra

Protein requirements – 0.6g/kg adult per dayMore in growth & repair e.g. infants, infection, pregnancy

Protein required due to turnover in tissuesIn growth or wasting, tissues which turnover protein fastest will alter most in massI.e. Liver, gut, white cells

Loss of protein = loss of function

Nutrition – What we need and why

• Essential fatty acidsBarriers – skin and gut waterproofing &

lubricationNervous development – low fat diet in infants

poor myelinationCellular signals – precursors for inflammatorymediators immune function

inflammation platelet aggregation

Nutrition – what we need and why

Fatty acid deficiency in animals -failure to grow – linolenic acidskin & kidney lesions

Linoleic and arachidonic acids reverseother 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, increasedGut infection and incidence of cancer.

- preferred source of energy- Sucrose most cariogenic substance

VitaminsDeficiency becoming more common inSome urban populations in UK

Vit D - ricketsVit 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. Water solubleVitamin Recommended daily intake (mg) Deficiency

B1 (Thiamine) 1.5 Beri-beriRiboflavin 1.8Niacin 20 PellagraC 45 ScurvyFolic acid 0.4 Anaemia, spina

bifidaB12 0.003 Pernicious anaemiaB6 2Panthothenic acid unknown

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 solubleVitamin Recommended daily intake Deficiency

A 5000 IU Blindness, dry mucous membrane, abortiongrowth failure.

D 400 IU Rickets, poorly calcified dentition, delayederuption

E 15 IU Foetal resorptionK 70g Poor clotting

Particularly important in dentistry :Vitamin A - 500,000 new cases per year in developed countriesVitamin D - may be prevalent in racial groups moving from sunny to

temperature climates

Minerals and trace elementsMineral/trace element Recommended daily intake Required for

Iron 10-20mg Oxygen carriage – haemoglobinCalcium 800-1200mg Calcification, cell excitabilityCobalt part of Vitamin B12

Iodine 150g thyroid functionCopper ossificationZinc 15mg immune responseFluorine 1ppm drinking water prevention of caries

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 and may r reduced levels of

Gluconeogenesis.

‘Take home message’Energy in = energy outAvoid ‘faulty’ diet – balanced diet few deficienciesSpecial care in special circumstances

Less fat, more CHO(watch the sucrose!)

Extra care in :

Less meat, more fish(EFF)

Pregnancy – moreEnergy & protein plusFe, Ca, Vit D, etc etc

More exercise

Enough Fe & Ca

Fluorides (?)

Weaned infants -Protein, fatty acids, vitC etc.etc.