Lesson 1Lesson 1Fundamentals of NutritionFundamentals of Nutrition

Mimi Giri, MD, Ph.D

Department of Endocrinology,

University Hospital of Ghent

Ghent, Belgium

CarbohydrateCarbohydrateNutrition and MetabolismNutrition and Metabolism

• Introduction & Sources of carbohydrate in the diet Introduction & Sources of carbohydrate in the diet

• StructuresStructures

• General functions of carbohydrate & EssentialityGeneral functions of carbohydrate & Essentiality

• Glucose from dietary carbohydrate:Glucose from dietary carbohydrate:

digestion, absorption, transport into cellsdigestion, absorption, transport into cells

• Glucose metabolism: glucose disposal & synthesis:Glucose metabolism: glucose disposal & synthesis:

• Glucose disposal: Glycolysis, TCA cycle, FFA Glucose disposal: Glycolysis, TCA cycle, FFA synthesis, NEAA synthesis; Glycogen synthesissynthesis, NEAA synthesis; Glycogen synthesis

• Glucose synthesis: purpose, glycogen breakdown and Glucose synthesis: purpose, glycogen breakdown and gluconeogenesisgluconeogenesis

• IntroductionIntroduction

Humans:Humans:

~ 50% of calories ingested as CHO (10 - 85%)

160 g starch, 120 g sucrose, 30 g lactose, 5 g glucose, 5 g fructose, trace maltose

• IntroductionIntroduction

Sources of carbohydrate:Sources of carbohydrate:

sucrose: sucrose: “sugar”

lactose: lactose: milk

maltose: maltose: beer

fructose: fructose: fruit, corn-syrup “processed foods”

starch (amylose & amylopectin): starch (amylose & amylopectin): wheat, rice, corn, barley, oats, legumes....

glycogen: glycogen: muscle and liver

• IntroductionIntroduction

Glucose:Glucose:

ATP synthesis: all tissues

RBC, tissues of eye, renal medulla, RBC, tissues of eye, renal medulla, brain, intestines, white blood cells, skin:brain, intestines, white blood cells, skin:

rely primarily on glucose as energy source in the fed state

In the In the fedfed state, glucose is primarily obtained state, glucose is primarily obtained from dietary carbohydrate (CHO)from dietary carbohydrate (CHO)

• StructuresStructuresMonosaccharides:

Glucose, fructose, galactoseGlucose, fructose, galactose

Dissacharides:

maltose: maltose: glucose + glucoseglucose + glucose

lactose: lactose: glucose + galactoseglucose + galactose

sucrose: sucrose: glucose + fructoseglucose + fructose

Polysaccharides:

amylose: amylose: glucose + glucose +.... glucose + glucose +.... (linear)

amylopectin: amylopectin: glucose + glucose +.... glucose + glucose +.... (branched)

glycogen: glycogen: glucose + glucose +...glucose + glucose +...(very branched)

• General functions of carbohydratesGeneral functions of carbohydrates

Energy: Energy: ATP synthesis (~ 4 kcal/g)

NEAA synthesis: NEAA synthesis: carbon skeleton

Fat synthesis: Fat synthesis: via acetyl-CoA

Glycogen synthesisGlycogen synthesis

TCA cycle intermediatesTCA cycle intermediates

Nucleotides: Nucleotides: sugar portion

GlycoproteinsGlycoproteins

GlycolipidsGlycolipids

Overview of Metabolism

acetyl-CoA

pyruvate ATP

ADP + Pi

polysaccharides

hexosespentoses

ADP + Pi

ATP

ADP + Pi

ATP

ADP + Pi

ATPATP

ADP + Pi

ADP + Pi

ATP

lipids

fatty acids

ATP

ADP + Pi

protein

amino acids

citric acidcycle

ureacycle ATP

ADP + Pi

urea

CO2

electron transportchain

oxidative phosphorylation

O2

ATP

e-

Overview of Catabolic Processes

CarbohydratesCarbohydrates FatsFatsProteinsProteins

Simple SugarsSimple Sugars Fatty acidsFatty acidsAmino acidsAmino acids

PyruvatePyruvate

Acetyl CoAAcetyl CoA

Oxidative phosphorylationOxidative phosphorylation

ATP

ATP

Citric acid cycleCitric acid cycle

Stage 1

Stage 2

Stage 3

GlycolysisGlycolysis

Use of Amino Acidsand Fatty Acids

Fats and protein can alsobe used by the bodyas a source of energy.

Not as easily used as carbohydrates.

Liver

glycogen

glucose-6-P

pyruvate

Liver

glycogen

glucose-6-P

pyruvate

Amino Acids

or

Fatty Acids

Amino Acids

or

Fatty Acids

• Essentiality of carbohydratesEssentiality of carbohydrates

metabolic need is for glucose: ~300 g/d in humans

- glucose can be made from most AAs (not Leu)

- glucose can be made from propionate (SCFA)

- glucose can be made from glycerol

- glucose cannot be made from fatty acids

CHO not strictly essential in dietCHO not strictly essential in diet

Relying solely on AAs etc. as precurser for glucose not prudent or practical (except for carnivores), so......

• Glucose from dietary carbohydrate: Glucose from dietary carbohydrate: DIGESTION, ABSORPTION & DIGESTION, ABSORPTION & TRANSPORT into cellsTRANSPORT into cells

MouthMouth

salivary amylase:salivary amylase:

- hydrolyzes 1-4 bonds in starch

- release: psychic (cephalic) stimuli

mechanical stimuli: food in mouthchemical stimuli: food on taste

buds

- little digestion

StomachStomach: Negligible

Stage One• Hydrolysis of food into smaller sub-units.

Handled bythe digestivesystem.

Handled bythe digestivesystem.

Stage One

• Salivary glands:Salivary glands:• Secrete amylase.• - digests starch.

• Stomach:Stomach:• Secretes HCl. • - denatures protein and pepsin.

• Pancreas:Pancreas:• Secretes proteolytic enzymes and lipases. • - degrades proteins and fats.

Stage One

• Liver and gallbladder:Liver and gallbladder:• Deliver bile salts.• - emulsify fat globules - easier to digest.

• Small intestine:Small intestine:• Further degradation.• Produces amino acids, hexose sugars, fatty acids

and glycerol.• Moves materials into blood for transport to

cells.

• CHO: Digestion, Absorption & TransportCHO: Digestion, Absorption & Transport

Small IntestineSmall Intestine

lumenlumen

brush borderbrush border

CHO Digestion: SMALL INTESTINECHO Digestion: SMALL INTESTINE

LUMENLUMEN

lumenlumen

digesta

CCKCCKpancreaspancreas

enzymesenzymes

CCK = cholecystekinin

Carbohydrate digestion: SMALL INTESTINECarbohydrate digestion: SMALL INTESTINE

LUMENLUMEN

lumenlumen

pancreaspancreas

enzymesenzymes

enzymesenzymes- -amylase

cuts 1-4 bond in starch:maltose, limit dex.efficient and fast acting enzyme

lumen (duodenum)lumen (duodenum)

Carbohydrate digestion: SMALL INTESTINECarbohydrate digestion: SMALL INTESTINE

Brush borderBrush border enzymes occur on brush border

maltase: maltase: cuts maltose

-limit dextrinase: -limit dextrinase: cuts 1-6 bond

lactase:lactase: cuts lactose

sucrase: sucrase: cuts sucrose

result:result: monosaccharidesmonosaccharidesglucose, galactose, fructose

• Carbohydrate: ABSORPTIONCarbohydrate: ABSORPTION

SITE OF ABSORPTIONSITE OF ABSORPTION

Jejunum & Ileum

GLUCOSE/GALACTOSEGLUCOSE/GALACTOSE

Absorbed by active transport- sugars move against conc- sugars move against concnn gradient gradient- requires ATP- requires ATP

Facilitated diffusion of glucose- glucose concentration must be lower in - glucose concentration must be lower in

enterocyteenterocyte

• Carbohydrate: ABSORPTIONCarbohydrate: ABSORPTION

FRUCTOSEFRUCTOSE

Carrier mediated facilitated diffusion- fructose conc must be lower in enterocyte- fructose conc must be lower in enterocyte

• CARBOHYDRATE TRANSPORTCARBOHYDRATE TRANSPORT- enterocyte to portal vein to liver

• GLUCOSE UPTAKE INTO CELLSGLUCOSE UPTAKE INTO CELLS- carrier mediated diffusion- stimulated by insulin (muscle, liver, adipocyte)

• Carbohydrate metabolism:Carbohydrate metabolism:

FRUCTOSEFRUCTOSE

liver:liver:

fructose F-6-P DHAP glycolytic

pathway

GALACTOSEGALACTOSE

liver:liver:

galactose gal-1-P G-1-P G-6-P

glucose

• Glucose metabolism:Glucose metabolism:glucose disposal & synthesisglucose disposal & synthesis

SIGNIFICANCESIGNIFICANCE

- Control blood glucose concentrations- Control blood glucose concentrations

in starvation, exercise, stress, refeeding...

4 - 6 mmol/L (humans): 10 mM after meal

high blood sugar: damage lens, kidney etc.

complications of diabetes

low blood glucose: brain damage & death

- Control rate of glucose utilization in tissues- Control rate of glucose utilization in tissues

• Control rate of glucose utilization in tissuesControl rate of glucose utilization in tissues

e.g. How does liver assess how much glucose is being used by muscle or brain?

e.g. When a high CHO meal eaten, rate of glucose absorption is high; to maintain normal blood glucose levels, the rate of glucose use in other tissues such as muscle must increase

Control & integration of glucose metabolism Control & integration of glucose metabolism (disposal & synthesis) among tissues is required(disposal & synthesis) among tissues is required

Liver plays a major role!!Liver plays a major role!!

Diet

Gut

Liver

Blood Glucose 4.5-5.5

mmol/L

Fat

Glycerol

Kidney

Urine BG >10mmol/L

Brain Glands & other tissues

Muscle

Amino AcidsLactic Acid

Liver as Glucostat

Factors affecting glucose concentration

• Hunger

• Glucose absorption from gut

• Hepatic glycogenolysis– Adrenaline

– Glucagon

• Gluconeogenesis in liver

• Insulin antagonist– Growth Hormone

– Cortisol

• Insulin destroying enzymes

• Satiety

• Glucose diffusion in ECF

• Muscular exercise

• Insulin Glucose oxidation Glycogen deposition Lipogenesis Gluconeogenesis

{ glucosuria – in diabetes}

Tend to raise Tend to lower

• Fate of glucoseFate of glucose

GLUCOSEGLUCOSE

ATP synthesisATP synthesisglycogen synthesisglycogen synthesis

FFA synthesisFFA synthesisNEAA synthesisNEAA synthesis

• Fate of glucose:Fate of glucose:glycolysis, TCA cycle & FFA synthesisglycolysis, TCA cycle & FFA synthesis

glucoseglucose

lactatelactatepyruvatepyruvate

FFA synthesisFFA synthesisacetyl-CoAacetyl-CoA

TCA cycleTCA cycle

ATPATPATPATP

ATPATPATPATP lots!!

ATP synthesis

• Fate of glucose: glycolysis & TCA cycleFate of glucose: glycolysis & TCA cyclepurpose & tissues

glucoseglucose

lactatelactatepyruvatepyruvate

FFAacetyl-CoA

TCA cycle

ATPATPATPATP

anaerobic glycolysisanaerobic glycolysis- RBCs, WBCs- kidney medulla- enterocytes- lens, cornea- skin- (skeletal muscle)

- make ATP (2 ATP/glucose)- make ATP (2 ATP/glucose)- maintain blood glucose- maintain blood glucose

• Fate of glucose: glycolysis & TCA cycleFate of glucose: glycolysis & TCA cyclepurpose & tissues

glucoseglucose

pyruvatepyruvate

acetyl-CoAacetyl-CoA

TCA cycleTCA cycle

ATPATPATPATP

ATPATPATPATP

aerobic glycolysisaerobic glycolysis- brain- liver- skeletal muscle- kidney cortex- etc.

- make ATP (32 ATP/glucose)- make ATP (32 ATP/glucose)- maintain blood glucose- maintain blood glucose

• Fate of glucose: glycolysis & TCA cycleFate of glucose: glycolysis & TCA cyclestimulation and inhibition

glucoseglucose

lactatepyruvatepyruvate

acetyl-CoAacetyl-CoA

TCA cycleTCA cycle

ATPATPATPATP

ATPATPATPATP

stimulationstimulation- high glucose- low ATP- insulin

inhibitioninhibition- high ATP- FFAs

FFA

• Fate of glucose: FFA synthesisFate of glucose: FFA synthesistissues, stimulation(generally only occurs if excess calories eaten)

glucoseglucose

pyruvatepyruvate

acetyl-CoAacetyl-CoA

TCA cycleTCA cycle TGTG

ATPATPATPATP

mainly:liverliveradipocytesadipocytes

stimulationstimulation- high glucose- high ATP **- insulin

FFAFFA

dietdiet

• Fate of glucose: NEAA synthesisFate of glucose: NEAA synthesis tissues, stimulation

glucoseglucose

pyruvatepyruvate

acetyl-CoAacetyl-CoA

TCA cycleTCA cycle ProteinsProteins

ATPATPATPATP

mainly:liverlivermusclesmuscles

stimulationstimulation- high glucose- high ATP **- insulin

NEAANEAA

dietdiet

• Fate of glucoseFate of glucose

GLUCOSEGLUCOSE

ATP synthesisATP synthesisglycolysisTCA cycle

glycogen synthesisglycogen synthesis

FFA synthesisFFA synthesisNEAA synthesisNEAA synthesis

• Fate of glucose: glycogen synthesisFate of glucose: glycogen synthesis

Liver & MuscleLiver & Muscle

glucose glycogen

LiverLiver

skeletalskeletalmusclemuscle

glucoseglucoseglucgluc

glycogenglycogen

SISI

glucoseglucoseglucoseglucose

glycogenglycogen

• Fate of glucose: glycogen synthesisFate of glucose: glycogen synthesisLiver & MuscleLiver & Muscleglucose glycogenstimulation:stimulation: high glucose (liver)high glucose (liver)

insulininsulinlow glycogen (muscle)low glycogen (muscle)

LiverLiver

skeletalskeletalmusclemuscle

glucoseglucoseglucgluc + ins+ ins

glycogenglycogen

SISI

glucoseglucoseglucoseglucose

glycogenglycogen

pancreaspancreas

insulininsulin(ins)(ins)

+ ins+ ins

• Fate of glucoseFate of glucose

GLUCOSEGLUCOSE

ATP synthesisglycogen synthesis

FFA synthesisNEAA synthesis

glucose utilizationglucose utilizationresult: decrease blood glucose level

regulate tissue glucose use

• Glucose synthesis: Glucose synthesis:

GLUCOSEGLUCOSE

gluconeogenesisglycogen breakdown

glucose synthesisglucose synthesispurpose: - maintain blood glucose level:

fasting, sustained exercise, stress,hypoglycaemia- regulation of tissue glucose use

tissues: liver, muscle, kidney

• Glucose synthesis: glycogen breakdown Glucose synthesis: glycogen breakdown (LIVER)(LIVER)

glycogen glucose immediate glucose immediate glucose sourcesource

stimulation:stimulation: low blood glucoselow blood glucoseadrenalin/glucagonadrenalin/glucagon

inhibition:inhibition: insulininsulin

LiverLiver

tissuestissues

glucoseglucoseglucoseglucose

glycogenglycogen

SISI

pancreaspancreas

glucagonglucagon

+ glucagon+ glucagon

glucoseglucose

COCO22

• Glucose synthesis: glycogen breakdown (muscle)Glucose synthesis: glycogen breakdown (muscle)

glycogen glycogen G-6-P (muscle) G-6-P (muscle) local use only

stimulation:stimulation: adrenalin (exercise/stress)adrenalin (exercise/stress)

skeletal muscleskeletal muscle

G-6-PG-6-P

glycogenglycogen

COCO22 lactate lactate

+ adr+ adr

G-6-P

note:glycogen

glucose

• Glucose metabolism: disposal & synthesisGlucose metabolism: disposal & synthesis

Liver: major role in regulation of blood glucoseLiver: major role in regulation of blood glucose

high blood glucose: glucose uptake

LiverLiver

glucoseglucoseglucoseglucose

glycogenglycogen

SISI

glucoseglucose

COCO22

+ i+ i

+ i+ i

+ i = stimulated by insulin+ i = stimulated by insulin

+ i+ i

FFAFFA+ i+ i

• Glucose metabolism: disposal & synthesisGlucose metabolism: disposal & synthesis

Liver: major role in regulation of blood glucoseLiver: major role in regulation of blood glucose

low blood glucose: glucose release

LiverLiver

glucoseglucoseglucoseglucose

glycogenglycogen

SISI

alaala lactatelactate alaninealaninelactatelactate

+g+g

+ g = stimulated by glucagon+ g = stimulated by glucagon

• Physiological importance of gluconeogenesisPhysiological importance of gluconeogenesis

low CHO diet, early starvation (no CHO intake),low CHO diet, early starvation (no CHO intake),

infection & trauma (high glucose need)infection & trauma (high glucose need)

LiverLiver

glucoseglucoseglucoseglucose

glycogenglycogen

SISI

brain &brain &anaerobicanaerobic

tissuestissues

gluconeo-gluconeo-genesisgenesis

LiverLiverSISI

• Regulation of glucose use among tissues and Regulation of glucose use among tissues and role of fatty acidsrole of fatty acids

e.g. fed state/high CHO dietglucose uptake and useglucose uptake and use

glucoseglucoseglucoseglucose

pancreaspancreas

insulininsulin(ins)(ins)

glucgluc + ins+ ins

glycogenglycogen ATPATP

+ ins+ ins

LiverLiver

skeletalskeletalmusclemuscle

SISI

• Regulation of glucose useRegulation of glucose use

glucoseglucoseglucoseglucose

pancreaspancreas

insulininsulin(ins)(ins)

glucgluc +ins+ins glucgluc

COCO22/ATP/ATPglycglyc ATPATP

+ins+ins??

fed state/high CHO dietglucose uptake and useglucose uptake and use

LiverLiver

skeletalskeletalmusclemuscle

SISI

adipocyteadipocyte

• Regulation of glucose useRegulation of glucose use

fed state/high CHO dietrole of fatty acidsrole of fatty acids

glucoseglucoseglucoseglucose

pancreaspancreas

insulininsulin(ins)(ins)

TGTG

FFAFFA- ins- ins

glucgluc + ins+ ins glucgluc

FFAFFA

COCO22/ATP/ATP

--

glycglyc ATPATP

• CHO metabolism:Vitamin & Mineral Co-CHO metabolism:Vitamin & Mineral Co-factorsfactors

glucoseglucose

lactatelactatepyruvatepyruvate

acetyl-CoAacetyl-CoA

TCA cycleTCA cycle

biotinbiotin (carboxylation)Thiamine: Vit BThiamine: Vit B11

Riboflavin: Vit BRiboflavin: Vit B22

(FAD)Niacin: Vit BNiacin: Vit B33

(NAD)pantothenic acidpantothenic acid (Acetly-CoA)

BB33

BB1,1,BB2,2,BB3,3,MgMg2+2+

pantothenic acidpantothenic acid

BB33

BB11, B, B33

biotinbiotinBB33

• IntroductionIntroduction• Symptoms and clinical featuresSymptoms and clinical features• Metabolic effects of insulin on CHO metabolismMetabolic effects of insulin on CHO metabolism• Metabolic effects on protein & fat metabolismMetabolic effects on protein & fat metabolism• Lack of insulin (diabetes mellitus)Lack of insulin (diabetes mellitus) - effect on glucose uptake, utilization & production - effect glucose production - effect on protein synthesis & protein breakdown - effect on TG breakdown (fat cells) - effect on ketone body synthesis (liver)

Diabetes Mellitus: Metabolism Diabetes Mellitus: Metabolism out of controlout of control

• IntroductionIntroduction

Diabetes MellitusDiabetes Mellitusor Type 1 (previously juvenile onset)Type 1 (previously juvenile onset)or insulin-dependent diabetes mellitus insulin-dependent diabetes mellitus (IDDM)(IDDM)

recognized as a disease for 2000 years

-cells of Islets of Langerhans (pancreas) damage: inadequate insulin production

Diabetes illustrates problems that arise when integration of metabolism is impaired:carbohydrate, protein & lipid metabolismcarbohydrate, protein & lipid metabolism

•Symptoms and clinical featuresSymptoms and clinical features

polyuriapolydipsiapolyphagiaweight lossdehydrationglycosuriaketosis/ketoacidosisunconsciousness/coma

•Metabolic effects of insulin on CHO metabolismMetabolic effects of insulin on CHO metabolismglucose uptake and usedecrease blood glucose

LiverLiver

skeletalskeletalmusclemuscle

SISI

glucoseglucoseglucoseglucose

insulin = insinsulin = ins

glucoseglucose +ins+ins glucgluc

COCO22/ATP/ATPglycoglyco

+ins+ins+ins+ins

AAs, lactateAAs, lactate

-ins-ins

•Metabolic effects of insulin on protein metabolismMetabolic effects of insulin on protein metabolism- stimulate amino acid uptake- stimulate protein synthesis- inhibit protein degradation

LiverLiver

skeletalskeletalmusclemuscle

SISI

AminoAminoAcidsAcids

AAsAAs

insulin = insinsulin = ins

AAsAAs +ins+ins aminoaminoacidsacids

proteinproteinproteinprotein

+ins+ins+ins+ins +ins+ins -ins-ins

•Metabolic effects of insulin on lipid metabolismMetabolic effects of insulin on lipid metabolism- stimulate triglyceride (TG) synthesis- inhibit triglyceride breakdown- inhibit ketone body synthesis

LiverLiverSISI

freefreefattyfattyacidsacids

AAsAAs

insulin = insinsulin = ins

FFAsFFAs

ketone bodiesketone bodies

-ins-ins

adipocyteadipocyte

TGTG

FFAFFA

-ins-ins+ins+ins

•Lack of insulin (diabetes mellitus)Lack of insulin (diabetes mellitus)

- effect on glucose uptake, utilization & production- effect on glucose uptake, utilization & production

- effect on protein synthesis & protein breakdown- effect on protein synthesis & protein breakdown

- effect on TG breakdown (fat cells)- effect on TG breakdown (fat cells)

- effect on ketone body synthesis (liver)- effect on ketone body synthesis (liver)

•Lack of insulin (diabetes mellitus):Lack of insulin (diabetes mellitus):effect on glucose uptake, utilization & productioneffect on glucose uptake, utilization & production

decreased glucose uptake and useincreased glucose production

increased blood glucoseincreased blood glucose

LiverLiver skeletalskeletalmusclemuscleSISI

AAs, lactateAAs, lactate

glucoseglucose glucoseglucose

AAsAAsglucglucfatfat

>10 mM glucose- glucosuria- polyuria- polydipsia- dehydration- coma

•Lack of insulin (diabetes mellitus):Lack of insulin (diabetes mellitus):effect on protein synthesis & protein breakdowneffect on protein synthesis & protein breakdown

decreased protein synthesisincreased protein breakdown

protein wastingprotein wasting

LiverLiver skeletalskeletalmusclemuscleSISI

AminoAminoAcidsAcids

AAsAAs aminoaminoacidsacids

proteinproteinglucoseglucoseAAsAAsglucglucfatfat

proteinprotein

•Lack of insulin (diabetes mellitus):Lack of insulin (diabetes mellitus):effect on TG breakdown & ketone body synthesis effect on TG breakdown & ketone body synthesis increased TG breakdown

weight lossweight lossincreased ketone body synthesis

metabolic acidosismetabolic acidosis

LiverLiverSISI

adipocyteadipocyte

TGTG

FFAFFAFFAFFAFFAFFA

ketonesketones KetonesKetonesAAsAAsglucglucfatfat

•Lack of insulin (diabetes mellitus):Lack of insulin (diabetes mellitus):SUMMARYSUMMARY

LiverLiver skeletalskeletalmusclemuscleSISI

AminoAminoAcidsAcids

AAsAAs aminoaminoacidsacids

proteinprotein

adipocyteadipocyteTGTG

FFAFFAFFAFFA

FFAFFA KBsKBs KetonesKetones

glucoseglucose glucoseglucose

AAsAAsglucglucfatfat

•Lack of insulin (diabetes mellitus): SummaryLack of insulin (diabetes mellitus): Summary

The normal flow of substrates following food intake is largely dependent on the secretion of insulin. Insulin exerts a potent, positive effect on anabolism, while inhibiting catabolic pathways. Diabetes is a vivid negative example that emphasizes the integration of metabolism and the importance of metabolic regulation to continuance of life.

from Advanced Nutrition & Human MetabolismGroff & Gropper 2000

. Fibre. Fibre

• Introduction, Definition & SourcesIntroduction, Definition & Sources• Type of fibre and propertiesType of fibre and properties

- cellulose, hemicelluloses, - cellulose, hemicelluloses, -glucans, pectins, -glucans, pectins, ligninlignin

- soluble vs. insoluble fibre- soluble vs. insoluble fibre• Physiological & Metabolic effectsPhysiological & Metabolic effects

- water holding capacity, binding of nutrients, - water holding capacity, binding of nutrients, fermentabilityfermentability

• SignificanceSignificance• Recommended intakesRecommended intakes

• IntroductionIntroduction

In humans, pre-1970’s fibre believed to have no nutritional value & antinutrient

Since 1970’s, fibre:

-- energy valueenergy value

-- gastrointestinal functiongastrointestinal function

-- nutrient availabilitynutrient availability

- prevention & treatment of many diseases- prevention & treatment of many diseases

• DefinitionDefinition

- - fibre is not a single entityfibre is not a single entity

- difficult to define- difficult to define

“Endogenous components of plant material in the diet that are resistant to digestion by enzymes produced by man.

They are predominantly non-starch polysaccharides and lignin and may include, in addition, associated substances.”

(Health and Welfare Canada)

• SourcesSources

Plant material

plant cell wall : 95% of fibre

cementing material in plants

legumes: legumes: beans, peasbeans, peas

forages: forages: alphalpha, timothy hay....alphalpha, timothy hay....

bran of cerealsbran of cereals: wheat, oats, corn, rice....: wheat, oats, corn, rice....

skin of fruits & vegetablesskin of fruits & vegetables

• Type of fibre & propertiesType of fibre & propertiesCelluloseCellulose

- structural component of cell walls

- linear polymer of -D-glucose

- forages, bran of grains

- high degree of crystallinity

fibrous & water insoluble

- monogastric animals lack cellulase in SI

cannot hydrolyze -1,4 linkage so indigestiblecolon: bacteria thus partly fermented

• Type of fibre & propertiesType of fibre & properties

HemicellulosesHemicelluloses

- polymers of: mannose, galactose, glucuronic acid, xylose, arabinose (5 & 6 carbon sugars)

with some branching

- forages, bran of cereals, legumes

- not very water soluble (depends on type)

- monogastric animals:

hemicelluloses are not digested in SI

partly digested in colon by bacteria

• Type of fibre & propertiesType of fibre & properties

-glucans -glucans (gum)

- cell walls of grasses

- bran coat of barley, oats

- glucose polymer: -1,4 and -1,3 (branched)

- water soluble

- monogastric animals:

not digested in SI

gummy and viscous

large intestine: rapidly fermented

• Type of fibre & propertiesType of fibre & properties

PectinsPectins

- structural component of plant cell walls

cementing material

- polymers of polygalacturonic acid, which may or may not have a methylester group

- fruit (skin), forages (alfalfa), rye,

- soluble in H2O & form gels (branched)

- monogastric animals:

pectins are not digested in SI

digested rapidly colon by bacteria

• Type of fibre & propertiesType of fibre & properties

LigninLignin

- NOT a carbohydrate

- structural component of plant cell walls

- aromatic polymer; polyphenolic (hydrophobic)

- insoluble in water

- not digestible in SI or by bacteria

Mucilages & algal polysaccharidesMucilages & algal polysaccharides

- carragenan, agar

- water soluble

- highly fermentable

• Type of fibre & propertiesType of fibre & properties

Dietary Fibre

SolubleSoluble

some hemicelluloses-glucanspectinsgums, mucilages

InsolubleInsoluble

some hemicellulosescelluloselignin

- solubility affects water-holding capacity, - solubility affects water-holding capacity, fermentability, nutrient adsorptionfermentability, nutrient adsorption

- these exert physiological & metabolic effects- these exert physiological & metabolic effects

• Physiological & Metabolic effectsPhysiological & Metabolic effects

water-holding capacitywater-holding capacity ability to hold water

faecal bulk faecal bulk colonic transit time (faster)colonic transit time (faster)reduce constipation

viscous & gel-formingviscous & gel-forming

mixing of digestive enzymes with food

nutrient diffusion rate

slower rate of absorption

SI transit time (slow passage) soluble fibreSI transit time (slow passage) soluble fibreincrease satiety

• Physiological & Metabolic effectsPhysiological & Metabolic effects

Adsorption or binding of nutrients by fibreAdsorption or binding of nutrients by fibre

- lignin, pectin, -glucan can bind some nutrients

bind and reduce absorption of bile acidsbind and reduce absorption of bile acids

cholesterol used for more bile acid synthesis

lower serum cholesterol

reduce Careduce Ca2+2+, Fe, Fe2+2+, Zn, Zn2+ 2+ absorptionabsorption

COO- bind divalent cations

pectins, hemicellulose

• Physiological & Metabolic effectsPhysiological & Metabolic effects

FermentabilityFermentability

- depends on fibre (esp. solubility)

- residence time

- bacteria population

Short chain fatty acids (SCFAs) are madeShort chain fatty acids (SCFAs) are made

acetate

propionate

butyrate

Gases: HGases: H22, CO, CO22, methane, methane

• Physiological & Metabolic effectsPhysiological & Metabolic effects

Short chain fatty acidsShort chain fatty acids

- absorbed

acetate (2 C) acetate (2 C) acetyl-CoA acetyl-CoA ATP or FFAsATP or FFAs

propionate (3 C)propionate (3 C) liver liver glucoseglucose

butyrate (4 C)butyrate (4 C) used as fuel for intestinal used as fuel for intestinal cellscells

Fibre that is fermented in can be a source of energy and glucose

• SignificanceSignificance

Fibre is not inertFibre is not inert

Energy Energy (< 4 kcal/g but > 0 kcal/g)

Disease prevention & treatmentDisease prevention & treatment

constipation/haemorroids/appendicitis

heart disease/plasma cholesterol

adult-onset diabetes/glucose absorption

obesity/satiety

Mineral deficiencyMineral deficiency

rare: intake low and fibre/phytate high

References

• Groff and Gropper, 2000. Advanced Nutrition and Human Metabolism