Caballero B. (ed.) Encyclopaedia of Food Science, Food Technology and Nutrition. Ten-Volume Set

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regulation of energy expenditure to maintain energy

balance. In this case, energy expenditure rises when

intakes are high and would otherwise lead to an

increase in energy stores, and decreases when intakes

are low and stores need to be conserved or used

efficiently. A consistent effect of high energy intakes

or low energy intakes is a change in body size. This

tends to buffer the effects of the inequality by altering

expenditure in the same direction as intake. However,

this is more of an obligatory response in energy ex-

penditure and less the facultative or adaptive re-

sponse, mentioned earlier. The main mechanism of

inefficient energy disposal in overeating has been sug-

gested to be uncoupled oxidative phosphorylation in

brown adipose tissue. The most recent suggestion is

that the role of the facultative response in the regula-

tion of energy balance may be secondary to its func-

tion in regulating the supply of essential nutrients in

nutrient-deficient or unbalanced diets.

0020 In undernutrition and during slimming the activity

of the sympathetic nervous system, essential for

brown adipose tissue thermogenesis, and protein syn-

thesis – an energetically expensive process – may be

reduced. However, in humans, by far the majority of

the savings in energy expenditure with undernutrition

occur owing to the smaller body size and reduced

volitional physical activity. The effect of reductions

of the metabolic rate of cells is less than 15% of the

total reduction. Similarly, the magnitude of DIT of

overfeeding at the rates seen in our societies and with

our diets is almost certainly low and unlikely to

exceed 10% of the extra energy ingested.

0021 A multitude of tertiary-level factors – behavioral,

social, and psychological – influence intake and

expenditure and, ultimately, energy balance. These

include the lifestyle factors referred to earlier, labor-

saving devices, availability of private transport,

shorter working hours, and inactive leisure. At the

same time, the constant availability of food, its var-

iety, and increased palatability and acceptance may

easily override control mechanisms evolved for other

diet types and nutritional circumstances. Median

weights and weights for height or age are increasing

in both Europe and North America, illustrating the

increased incidence of positive energy balance. Re-

duced physical activity and increased sedentary be-

haviors, such as watching television, contribute to

lower energy expenditure and are widely regarded

as having a role in the increased prevalence of over-

weight and obesity, but exactly what, it is difficult to

uncover. Longitudinal studies in the UK do not con-

sistently show falls in physical activity over the last 10

years, particularly in nonmanual households. There

are several dimensions to physical activity, which

affect different segments of the population differently.

0022It has been suggested that to avoid obesity popula-

tions should be physically active throughout life at a

PAL of 1.7–1.8. As present levels in adults may be

nearer 1.55, this would involve the adoption of

20 min vigorous activity per day, such as running or

team ball games, or 60 min per day of moderate

activity such as brisk walking or cycling. These are

clearly difficult to fit into most people’s daily lives and

a more appropriate strategy would be to perform

everyday activities in a more energy-expensive

manner, to walk instead of using fuelled transport,

to do activities standing instead of sitting, etc. Re-

cently, it has been suggested that fidgeting may play a

more important role in energy expenditure than was

previously thought. Training studies of the over-

weight but not obese suggest that increased physical

activity plus dieting is associated with weight loss of

only some 3 kg over 6 months. Women tend to be less

successful than men in reducing body weight and

fatness through exercise. It is not known if these

differences have physiological or behavioral origins.

0023One tenet of health and fitness is that body weight

should not increase in the adult years. However, data

from cross-sectional studies of 7000 male runners,

young and old, suggest that in modern society to

achieve this requires increasing physical activity

with age. Age-neutral body mass index (body weight

allowing for height) is not compatible with age-

neutral physical activity. Running distances needed

to increase 2 km week

1

for each increase of 1 year

of age. Again, such increases are not easy to adopt

and against the trend in the majority of even ardent

runners and joggers.

0024One objection to physical activity as a means of

achieving a more favorable energy balance that has

been raised is that physical activity and increased

energy expenditure cause energy intake to increase

with no net effect on energy balance and body weight.

The evidence suggests there often is compensation in

energy intake but not beyond the amount of energy

expended in exercise.

0025Although weight gain with age is commonplace, the

increment in body energy represents only a tiny pro-

portion of the energy throughput. Looked at in this

way, regulation and control are still quite accurate.

See also: Body Composition; Exercise: Metabolic

Requirements; Metabolic Rate

Further Reading

Ainsworth BE, Haskell WL, Leon AS et al. (1993) Compen-

dium of physical activities: classification of energy costs

of human physical activities. Medicine and Science in

Sports and Exercise 25: 71–80.

ENERGY/Energy Expenditure and Energy Balance 2107

Blaxter K (1989) Energy Metabolism in Animals and Man.

Cambridge: Cambridge University Press.

Blaxter K and Waterlow JC (1985) Nutritional Adaptation

in Man. London: John Libbey.

Bouchard C, Despres J-P and Tremblay A (1991) Genetics

of obesity and human energy metabolism. Proceedings

of the Nutrition Society 50: 139–147.

Department of Health (1991) Dietary Reference Values for

Food Energy and Nutrients for the United Kingdom.

Report on Health and Social Subjects, 41. London:

HMSO.

Durnin JVGA and Passmore R (1967) Energy, Work and

Leisure. London: Heinemann.

Ferro-Luzzi A and Martino L (1996) Obesity and physical

activity. In: Chadwick DJ and Cardew G (eds) The

Origins and Consequences of Obesity, pp. 207–266.

Chichester: Wiley.

Fox K (1999) Aetiology of obesity X: physical inactivity. In:

Obesity: Report of the British Nutrition Foundation

Task Force, pp. 116–132.Oxford: Blackwell Science.

Garrow JS (1974) Energy Balance and Obesity in Man.

Amsterdam: North-Holland.

McArdle WD, Katch FI and Katch VL (1996) Exercise

Physiology: Energy, Nutrition and Human Perform-

ance. Baltimore, MD: Williams & Wilkins.

Norgan NG and Ferro-Luzzi A (1996) Human adaptation

to energy undernutrition. In: Fregly MJ and Blatteis CM

(eds) Handbook of Physiology Section 4 Environmental

Physiology, pp. 1391–1409. New York: Oxford Univer-

sity Press.

Shetty PS (1999) Adaptation to low energy intakes: the

responses and limits to low intakes in infants, children

and adults. European Journal of Clinical Nutrition

53(suppl. 1): S14–S33.

Stock MJ (1999) Gluttony and thermogenesis revisited.

International Journal of Obesity 23: 1105–1117.

van Raaij J (1998) Energy. In: Mann J and Truswell SS (eds)

Essentials of Human Nutrition, pp. 73–90. Oxford:

Oxford Medical Publications.

Williams PT (1997) Evidence for the incompatibility of age-

neutral overweight and age-neutral physical activity

standards from runners. American Journal of Clinical

Nutrition 65: 1391–1396.

World Health Organization (1985) Energy and Protein

Requirements. Report of a Joint FAO/WHO/UNU

Expert Consultation. Geneva: World Health Organiza-

tion.

Energy Expenditure See Metabolic Rate

ENERGY METABOLISM

S Rubinstein-Litwak, Clarksville, MD, USA

Introduction

0001 All living organisms need energy to perform the most

basic of natural functions, that is, they need energy to

survive. Humans consume energy from the moment

they are conceived to the moment they cease to exist,

and considering that, according to the First Law of

Thermodynamics, ‘energy is not created or destroyed,

just transformed,’ where do humans obtain this much

needed energy? The answer to this question lies

within each cell of each individual organism.

0002 The group of chemical and biological reactions

involved in the process of obtaining and spending

energy is known as energy metabolism. There are

two major sources of free energy: food oxidation

and light absorption.

0003The input of energy needs to be constant and must

be converted into a highly accessible form to be used

for three major purposes:

0004performance of mechanical work in muscle con-

traction and other cellular movements;

0005active transport of molecules and ions;

0006synthesis of biomolecules that originate from

simple precursors, including macromolecules.

Metabolism

0007Metabolism is defined as the series of physicochem-

ical reactions that take place in cells with the purpose

of synthesizing, converting, utilizing, and cataboliz-

ing substrates. The primary goal of metabolism is to

form adenosine triphosphate (ATP), nicotinamide

adenine dinucleotide (NADH) and building blocks

for biosynthesis (i.e., amino acids, fatty acids, and

sugars). It is through this constant generation and

2108 ENERGY METABOLISM

consumption of metabolic substrates (i.e., ATP,

NADH,) that living organisms transform free energy

into channeled energy. Metabolism includes catabolic

and anabolic pathways that are almost always distinct.

During anabolic or degradative pathways, ATP is util-

ized, whereas during catabolic or biosynthetic path-

ways, ATP is generated. Most reactions of the human

metabolism are performed in the presence of enzymes,

which are protein molecules highly adapted and regu-

lated that catalyze said reactions. Many reactions also

require cofactors or coenzymes, most commonly vita-

min molecules. The amount of enzymes, the catalytic

activity of the enzymes, and the accessibility of sub-

strates present at the time of the reactions regulate the

metabolic process. The energy charge, defined as the

energy status of the cell based on the relative amounts

of ATP, adenosine diphosphate (ADP), and adenosine

monophosphate (AMP), plays a central role in meta-

bolic regulations. A low energy charge stimulates ATP-

generating pathways, while inhibiting ATP-utilizing

pathways. ATP is the only form of energy that can be

used directly by the cells; energy released as heat is lost

and cannot be utilized.

ATP–ADP Cycle

0008 The ATP–ADP cycle is the basis for energy exchange

in biological systems. ATP acts as the principal donor

of energy and has a very high turnover. When energy

is needed, ATP is hydrolyzed to ADP and ortho-

phosphate (Pi). If more energy is needed, ADP can

be further hydrolyzed to AMP and pyrophosphate

(PPi). ATP can also be regenerated from ADP during

oxidation of fuel molecules or when light is trapped

(i.e., photosynthesis) (Figure 1).

Metabolism of Food Molecules

0009 The energy in food becomes available only after the

macromolecules contained in it (carbohydrates, fat,

or protein) are transformed into less complex struc-

tures by undergoing a series of reactions. After adjust-

ment for net absorption and urinary losses, the energy

value of these substrates is estimated as 4 kcal g

1

for

carbohydrates, 4 kcal g

1

for proteins and 9 kcal g

1

for fat (16.8 kJ g

1

, 16.8 kJ g

1

, and 37.8 kJ g

1

respectively). Three stages in the generation of energy

from food oxidation have been described (Figure 2).

0010 Stage 1: Large molecules in food are broken down

into smaller units. No useful energy is generated in

this step.

0011 Proteins ! Amino acids

0012 Polysaccharides ! Simple sugars (i.e., glucose)

0013 Fats ! Glycerol þ fatty acids

0014 Stage 2: The recently formed smaller units are de-

graded once again, to yield a few simple units that

−

OHOH

−

O O

OHOH

−

OHOH

(b)

(a)

(c)

fig0001Figure 1 ATP metabolic path. (a) Adenosine triphosphate

(ATP); (b) adenosine diphosphate (ADP); (c) adenosine mono-

phosphate (AMP).

ENERGY METABOLISM 2109

play a central role in metabolism. Most molecules

are converted into acetyl coenzyme A (acetyl CoA).

During this step, some ATP is generated.

0015 Stage 3: During this step, 90% of the ATP is gener-

ated. It includes the citric acid cycle and oxidative

phosphorylation.

Carbohydrates

0016 Carbohydrates serve as energy stores, fuels, and

metabolic intermediates. When ATP is needed, poly-

saccharides can be rapidly mobilized to yield glucose,

which acts as a prime fuel for the generation of ATP.

Phosphorylated sugars are greatly involved in energy

production by acting as intermediate substrates in the

metabolic pathways. Glucose is the major form of

carbohydrate substrate andthepreferred energysource

for the brain, the renal cortex, and red blood cells.

0017 -Glycolysis Glycolysis includes a series of reactions

that convert glucose into pyruvate with a small pro-

duction of ATP. Reactions occur in the cytosol of the

cell. It represents the initial steps that lead to the

tricarboxylic acid cycle and the electron transport

chain. The glycolytic pathway has a dual role. On

one side, it degrades glucose to generate ATP, and on

the other, it provides building blocks for the synthesis

of cellular components. Glycolysis can be divided into

three stages that are presented in Figure 3.

0018 In the first stage, the substrate is trapped in the cell

to form a compound that can be readily cleaved

into phosphorylated three-carbon units from where

ATP is subsequently extracted. This consists of two

phosphorylations and one isomeration to convert

glucose into fructose 1,6-bisphosphate. In this step,

no energy is extracted, and two molecules of ATP

are used.

0019Glucose enters the cell through specific transport

proteins. Once in the cell, it is phosphorylated by

ATP to form glucose 6-phosphate.

0020Glucose 6-phosphate is isomerated into fructose

6-phosphate

0021Fructose 6-phosphate is phosphorylated by ATP,

forming fructose 1,6-bisphosphate.

0022In the second stage, some energy is generated. This

involves the conversion of fructose 1,6-bispho-

sphate into 3-phosphoglycerate and a molecule of

ATP.

0023Fructose 1,6-bisphosphate is split into glyceral-

dehyde 3-phosphate (which can be used in the

direct pathway) and dihydroxyacetone phos-

phate. With the help of an isomerase enzyme,

triose phosphate isomerase, the molecule of

dihydroxyacetone phosphate can be converted

into a second molecule of glyceraldehyde. The

result is the formation of two molecules of glycer-

aldehyde 3-phosphate from one molecule of fruc-

tose 1,6-bisphosphate.

0024Glyceraldehyde 3-phosphate is converted into

1,3-bisphosphoglycerate (1,3-BPG), whichis com-

bined with ADP to generate 3-phoshoglycerate

FATS

POLYSACCHARIDES PROTEINS

Amino acids

Glucose and

other sugars

Fatty acids and

glycerol

Acetyl CoA

CoA

Citric

acid

cycle

2 CO

−

ADPATP

Oxidative

phosphorylation

Stage

III

Stage

fig0002 Figure 2 Stages in the extraction of energy from food. From Stryer L (1995) Biochemistry, 4th edn. New York: W.H. Freeman, with

permission.

2110 ENERGY METABOLISM

plus ATP. This step represents the first ATP gen-

erating reaction in glycolisis.

0025 In the last stage, 3-phosphoglycerate is converted

into pyruvate, and a second molecule of ATP is

formed.

0026 The phosphoryl group in 3-phosphoglycerate is

rearranged to form 2-phosphoglycerate.

0027 2-Phosphoglycerate is dehydrated to form phos-

phoenolpyruvate.

0028 Phosphoenolpyruvate is converted into pyruvate.

During this reaction, the phosphoryl group is trans-

ferred to ADP to form a molecule of ATP.

The net reaction in the transformation of glucose into

pyruvate is:

Glucose þ 2Piþ2 ADP þ 2 NAD

2 pyruvate þ 2 ATP þ2 NADH þ 2H

þ 2H

Fat

0029 Dietary fat is primarily distributed as triacylglycer-

ols, which are highly concentrated stores of meta-

bolic energy. To be able to use fat as energy,

triacylglycerols need to be broken down to fatty

acids and glycerol. This is achieved by hydrolysis

with the help of a lipase, an enzyme that aids in the

degradation of fat molecules. Oxidation of fatty

acids takes place in mitochondria. Before entering

the mitochondrial membrane, long-chain fatty acids

in the outer membrane need to bind to coenzyme A

to form acyl CoA. The activated fatty acids are

carried across the inner membrane with the help of

carnitine. Once in the mitochondria, Acyl CoA goes

through a four-step process, called b-oxidation. First,

acyl CoA goes through oxidation by flavin adenosine

dinucleotide (FAD), then through a hydration, a

second oxidation by nicotinamide adenine dinucleo-

tide (NAD), and finally a thiolysis by CoA. The result

is the reduction of the carbon chain of the fatty acid

by two carbon atoms and the formation of acetyl

CoA, NADH and FADH

. Acetyl CoA then enters

the tricarboxylic acid cycle by binding to oxaloace-

tate, while FADH

and NADH transfer their elec-

trons to molecular oxygen by means of the electron

transport chain.

0030 The glycerol moiety that was liberated in the

degradation of triacylglycerols can also be further

metabolized by entering the glycolitic pathway

as a three-carbon compound yielding eventually

pyruvate.

Proteins

0031 Proteins need to be degraded to amino acids so the

body can use them. Most of the amino acids are used

for the synthesis of new proteins, while the remaining

amino acids are used for metabolic fuel. Amino

acids can be used as the precursors for the synthesis

of glucose, ketone bodies, and fatty acids. After the

amino group is removed and converted to urea, the

carbon chain of ketogenic amino acids is degraded

to acetyl CoA or acetoacetyl CoA, to form ketone

bodies. At the same time, glucogenic amino acids

are degraded to pyruvate or one of the intermedi-

ates of the TCA cycle; a-ketoglutarate, succinyl

CoA, fumarate, or oxaloacetate to synthesize

glucose.

Glucose

ATP

ADP

ATP

ADP

Herokinase

Glucose 6-phosphate

Phosphoglucose

isomerase

Fructose 6-phosphate

Phosphofructose-

kinase

Fructose 1,6-bisphosphate

Aldolase

Triose phosphate

isomerase

Dihydroxyacetone

phosphate

Glyceraldehyde

3-phosphate

Glyceraldehyde

3-phosphate

dehydrogenase

NAD

−

+ Pi

NADH + H

−

1,3-Bisphosphoglycerate

ADP

ATP

Phosphoglycerate

kinase

3-Phosphoglycerate

2-Phosphoglycerate

Phosphoenolpyruvate

Phosphoglycerate

mutase

Enolase

Pyruvate

kinase

ADP

ATP

Pyruvate

fig0003Figure 3 Glycolysis. From Stryer L (1995) Biochemistry, 4th

edn. New York: W.H. Freeman, with permission.

ENERGY METABOLISM 2111

Tricarboxylic Acid Cycle

0032 The tricarboxylic acid (TCA) cycle is also known as

the citric acid cycle or the Krebs cycle. It constitutes a

series of reactions that involve the decarboxylation of

pyruvate to form acetyl CoA, which in turn is fully

oxidized to carbon dioxide (CO

) and water (H

O).

These reactions take place in the mitochondria. The

TCA cycle represents the final common pathway for

the oxidation of fuel molecules.

0033 The link between glycolysis and the TCA cycle is

the oxidative decarboxylation of pyruvate to form

acetyl CoA. Coenzyme A is a heat-stable cofactor

that plays a central role within the molecule in

metabolism. It can deliver activated acyl groups for

degradation and energy generation as well as for

biosynthetic purposes.

Pyruvate þ CoA þ NAD

! Acetyl CoA þ CO

þ NADH:

The TCA cycle is graphically represented in Figure 4.

The start of the cycle includes the union of oxalo-

acetate (a four-carbon unit) with the acetyl group of

acetyl CoA (a two-carbon unit) to form citrate and

CoA. Citrate is then isomerized into isocitrate, which

undergoes the first oxidative decarboxylation of

the cycle to become oxalosuccinate and then a-

ketoglutarate. There then follows a second oxidative

decarboxylation that yields a molecule of succinyl

CoA. Succinyl CoA becomes attached to guanosine

diphosphate (GDP), resulting in the formation of suc-

cinate, guanosine triphosphate (GTP) and CoA. This

is the only step in the cycle that directly yields a high-

energy phosphate bond.

0034 Succinate is oxidized to fumarate, which in turn is

hydrated to form malate. The final step in the cycle is

the regeneration of oxaloacetate from malate. The

electrons that are released during the cycle are

transferred to NAD

and FAD to be transported in

oxidative phosphorylation.

0035 The net reaction of the TCA cycle is:

Acetyl CoA þ 3 NAD

þ FAD þ GDP þ Pi

þ 2H

O ! 2CO

þ 3 NADH þ FADH

þ GTP

þ 2H

þ CoA

Oxidative Phosphorylation

0036 Oxidative phosphorylation is also known as the

electron transport chain. It includes the reactions

that result in the synthesis of ATP from ADP þ Pi.

Heat can also be generated when ATP production is

uncoupled from the respiratory chain.

Synthesis of ATP

0037Oxidative phosphorylation constitutes the major

source of ATP in aerobic organisms. During the oxi-

dation of fuel molecules, FADH

and NADH play a

central role as the major electron carriers taking the

electrons to the ultimate acceptor, oxygen (O

). The

transfer of electrons from NADH and FADH

to O

takes place in the inner membrane of the mitochon-

dria. During this transfer, a number of protons are

pumped out of the mitochondrial matrix, forming a

proton gradient. Finally, with the help of ATPase, an

ATP-synthesizing complex, the protons flow back

into the matrix generating the necessary energy to

generate ATP.

0038The electrons are transferred from NADH to O

through a chain of three large protein complexes.

Each complex is an electron-driven proton pump

that contains multiple oxidation–reduction centers.

The electron carrying groups that take the electrons

from NADH and FADH

to O

are flavins, iron–

sulfur clusters, hemes and copper ions (Figure 5).

0039Complex I, also known as NADH-Q reductase,

involves the first process through which the electrons

from NADH are transferred. NADH binds to a flavo-

protein, flavin mononucleotide (FMN), transferring

its two high potential electrons and losing its

hydrogen molecules. The result is FMNH

and

NAD

. From there, the electrons are transferred to

coenzyme Q, also known as ubiquinone Q, on their

way to complex III. Coenzyme Q is also the entry

point for the electrons of FADH

to the chain. While

some energy is lost as heat, ATP is also formed in a

coupled reaction by bonding ADP þ Pi. Complex III,

also known as cytochrome reductase or cytochrome

b, is the second proton pump in the electron transport

chain. In this step, the electrons from coenzyme Q are

transferred to cytochrome b and then to cytochrome

c, a water-soluble protein, on their way to complex

IV. During the transfer, some protons are once again

pumped out of the mitochondrial membrane. A

second coupled reaction results in the formation of

ATP. Complex IV, also known as cytochrome oxidase

or cytochrome a, plays a role in the transfer of the

electrons from cytochrome c to O

. In the final step,

the electrons bind to O

to form H

0040The net reaction from each glucose molecule that

enters glycolysis and proceeds through the TCA cycle

and oxidative phosphorylation is:

2112 ENERGY METABOLISM

Glucose þ 6O

þ 36 ADP þ 36 Pi ! 6CO

þ 36 ATP þ 6H

Generation of Heat

0041 When there is not enough energy to transform

ADP into ATP, mitochondrial electron transport is

uncoupled from ATP synthesis by a proton leak. The

result is the release of energy as heat. Uncoupling

proteins (UCP) are known to be responsible for

the leak that sometimes occurs during oxidative

phosphorylation. Three uncoupling proteins have

been identified. Thermogenin or UCP1 present in

brown adipose tissue, UCP2 present in several tissues,

and UCP3 mainly present in skeletal muscle. UCP

COOH

Pyruvate

CoA

NAD

NADH + H

TPP

(CoA)

Acetyl CoA

CoA

COOH

ISOCITRATE

NAD

NADH+H

ALPHA-

KETOGLUTARATE

(CoA)

CoA

SUCCINATE

GTP

GDP

FADH

FAD

FUMARATE

MALATE

OHH

NADH + H

NAD

OXALOACETATE CITRATE

SUCCINYL CoA

fig0004 Figure 4 Tricarboxylic acid cycle.

ENERGY METABOLISM 2113

play a role in energy metabolism by limiting the syn-

thesis of ATP and dissipating energy as heat, thus

reducing the efficiency of energy production.

Summary

0042 As described in the previous paragraphs, humans

obtain their energy from food. Once in the body, the

macromolecules found in food undergo a series of

degenerative reactions that yield the necessary sub-

strates to promote the continuation of a process

known as energy metabolism. The result of this very

precise series of chemical and biological reactions is

the transformation of energy in its free form into

energy that can be fully utilized by the human body.

Carbohydrates are degraded to simple sugars, fat to

fatty acids and proteins to amino acids. Eventually,

the complete oxidation of these molecules yields

acetyl CoA, which acts as a link to the TCA cycle.

0043In the TCA cycle, acetyl CoA is fully oxidized to

and H

O. Throughout the cycle, hydrogen

atoms and their electrons are released. The hydrogen

atoms are then bound to other compounds, resulting

in the production of three molecules of NADH, one

FADH

, and one GTP. These new molecules contain

the energy originally found in acetyl CoA. For the

production of ATP, NADH and FADH

carry the

electrons from the TCA cycle through an electron

transport chain known as oxidative phosphorylation.

The process ends with the production of ATP and

O. An alteration in oxidative phosphorylation

can impair the production of ATP and dissipate

energy as heat instead. Uncoupling proteins are

responsible for this.

See also: Amino Acids: Metabolism; Carbohydrates:

Digestion, Absorption, and Metabolism; Metabolism of

Sugars; Fatty Acids: Metabolism; Tricarboxylic Acid

Cycle

Further Reading

Lehninger AL (1975) Biochemistry, 2nd edn. New York:

Worth Publishers.

Linder MC (1991) Nutritional Biochemistry and Metabol-

ism. New York: Appleton & Lange.

Ricquier D and Bouillaud F (2000) The uncoupling protein

homologues: UCP1, UCP2, UCP3, StUCP and AtUCP.

Biochemistry Journal 345: 161–179.

Rubinstein S (1998) Energy metabolism. In: Sadler MJ

Strain JJ and Caballero B (eds) Encyclopedia of Human

Nutrition. pp. 682–687. London: Academic Press.

Schrauwen P, Walder K and Ravussin E (1999) Human

uncoupling proteins and obesity. Obesity Research

7(1): 97–105.

Stryer L (1995) Metabolic energy: generation and storage.

In: Biochemistry, 4th edn, pp. 443–652. New York: WH

Freeman and Company.

NADH-Q reductase

Flavoprotein

ADP + Pi

ATP

ADP + Pi

ATP

ADP + Pi

ATP

Coenzyme Q

COMPLEX I

COMPLEX III

COMPLEX IV

FADH

Cytochrome reductase

Cytochrome b

Cytochrome oxidase

Cytochrome a

Cytochrome c

2H + O H

NADH

fig0005 Figure 5 Oxidative phosphorylation.

2114 ENERGY METABOLISM

ENTERAL NUTRITION

V A Stallings, The Children’s Hospital of Philadelphia,

Philadelphia, PA, USA

Enteral Feeding

0001 The nutritional status of hospitalized patients has

received much interest since studies in the 1970s

and 1980s indicated that up to 50% of surgical and

medical pediatric and adult patients have some

clinical or biochemical evidence of malnutrition.

(See Protein: Deficiency.)

0002 The four main groups of patients who generally

require nutrition support are:

0003 Patients with existing moderate-to-severe malnu-

trition indicated by weight loss in excess of 10%,

muscle wasting, peripheral edema and/or albumin

less than 30 g l

1

0004 Patients with mild-to-moderate malnutrition who

are at-risk of becoming further nutritionally com-

promised as a result of their medical condition.

0005 Patients with a normal nutritional status but who,

as a result of their medical condition, would not

be able to commence normal feeding of adequate

nutrient intake for a length of time appropriate for

age and disease status, thereby potentially leading

to a state of malnutrition.

0006 Pediatric patients who are unable to maintain a

normal pattern of growth and development, or

who require nutrition support to promote an

increased rate of growth (catch-up growth).

In order to prevent and treat malnutrition, the early

identification of the ‘at-risk’ patient is very important.

(See Malnutrition: The Problem of Malnutrition.)

Providing Enteral Nutrition Support

Oral Feeding

0007 Patients who cannot safely consume solid food may

take blenderized food. Patients who are able to take

some amount of food but cannot maintain an ad-

equate nutritional status may require oral dietary sup-

plements. There are two main types of dietary

supplements:

0008 Modular, i.e., single nutrient supplements such as

protein, fat, carbohydrates, vitamins, or minerals.

There are several formulations of each type of nu-

trient. For example, protein may be provided as

intact proteins, protein hydrolysates, or individual

amino acids, and fats as long-chain fats, including

essential fatty acids and medium-chain trigly-

cerides.

0009Complete, i.e., balanced nutrient supplements

which contain all the nutrients and may be taken

as the whole meal, part of a meal, or a snack.

There are a vast number of liquid and semisolid com-

mercial nutritional products that may be used for

enteral feeding. These products may be designed for

a specific age group (i.e., infant, adult) or specific

medical condition (i.e., premature infant, pulmonary

failure, renal failure).

Enteral Tube Feeding

0010Enteral tube feeding is the preferred route of diet

administration for all patients with a functioning

gastrointestinal tract who, for a variety of reasons,

do not take adequate nutrition from food and/or oral

dietary supplements. In recent years, research and

clinical experience has led to many technical advances

in the formulation and presentation of enteral formu-

las and feeding equipment. As a result, technology-

assisted enteral support is now widely used. The most

commonly used routes for providing enteral nutrition

are via nasogastric and gastrostomy feeding tubes.

0011-Nasogastric feeding Fine-bore feeding tubes are the

tubes of choice as they are narrow, softer, flexible,

and more comfortable for the patient than the previ-

ously used large-bore nasogastric tubes. The use of

fine-bore feeding tubes has reduced many of the

common nasal tube complications such as rhinitis,

esophagitis, pharyngitis, esophageal strictures, and

erosions.

0012Fine-bore feeding tubes are inserted per nasally

with a wire stylet to facilitate passage. The correct

position of the tube may be confirmed by aspiration

of the gastric contents and testing for acidic pH, or

by auscultation of the epigastrium as air is injected

into the stomach via the feeding tube. Radiological

confirmation of the correct position of the nasogas-

tric tube is required in patients who have an impaired

gag reflex, those who are semiconscious or un-

conscious, and other high-risk patients including

infants.

0013Nasogastric feeding may not be suitable for

patients who are at-risk of regurgitation and/or pul-

monary aspiration of the feed, and nasoduodenal or

nasojejunal feeding tubes should be considered for

these patients. Enteral feeding tubes with small

weighted tips (3–5 g) are available to facilitate tube

passage postpylorically for feeding directly into the

ENTERAL NUTRITION 2115

duodenum or the jejunum. Figure 1 shows weighted

fine-bore nasoenteral tubes (Corpak Medsystems,

USA) and two types of unweighted nasogastric feed-

ing tubes. In some patients, endoscopic placement of

the feeding tube may be undertaken to ensure rapid

and correct placement.

0014 -Gastrostomy feeding Patients who require long-

term or permanent enteral feeding should be con-

sidered for gastrostomy feeding tube or gastrostomy

button (a smaller appliance which is almost flush with

the skin) placement. The technique of percutaneous

endoscopic gastrostomy (PEG) is a well-established

procedure for providing enteral nutrition support.

Although the feeding gastrostomy may be placed sur-

gically, PEGs compare favorably, with a lower mor-

bidity and cost; the surgical gastrostomy requires a

laparotomy and a general anesthetic, whereas the

PEG is performed under local anesthesia using a

fiber-optic endoscope. A range of PEG kits are avail-

able for infants, children, and adults. A feeding

jejunostomy may be considered as the means of

providing early postoperative nutrition support in

selected patients and may be used for short- or long-

term support.

Techniques of Administration of Enteral

Tube Feeding

0015 Enteral formulas are usually given from a reservoir

(plastic bag) via appropriate tubing to connect to the

feeding tube (nasogastric, gastrostomy, jejunostomy).

The formula is infused either by gravity or by mech-

anical peristaltic pump to ensure a selected and steady

delivery rate. The enteral feeding administration set

should be changed at least every 12 h to minimize the

risk of infectious complications. The method of con-

tinuous feeding by a pump saves nursing time and

ensures that the prescribed amount and rate of for-

mula are provided. Bolus feeding is considered more

physiological, but this method of enteral nutrition has

a greater incidence of side-effects, such as regurgita-

tion, distention, and diarrhea.

0016Intermittent enteral tube feeding during the day or

the administration of continuous overnight (8–12 h)

infusion can be of benefit to patients who may be able

to take small quantities of food. This is common

practice when patients are being transitioned for

total intravenous nutrition support for conditions

such as short-bowel syndrome.

Enteral Formulas Tube Feeding

0017In the past, regular hospital food was blenderized,

but these preparations were too viscous for most

feeding tubes. Further dilutions lowered the nutrient

density, and the resulting blended feed was often

nutritionally inadequate. The problems of ensuring

nutritional quality while avoiding microbial con-

tamination of these feeds, along with the time

taken for their preparation, has led to the increa-

sed use of commercially prepared ‘ready-to-feed’

enteral formulas in most hospital and home care

settings.

Types of Enteral Formulas

0018The four main groups of commercially available

enteral diets are polymeric, predigested, disease-

specific, and modular. The selection of the most ap-

propriate enteral formulas requires consideration of

the patient’s age, nutritional status, disease process,

and the specific nutritional requirements.

0019-Polymeric formulas Polymeric formulas are indi-

cated for the majority of patients with normal or

near-normal gastrointestinal function. The dietary

constituents in polymeric enteral formula generally

are as follows: energy – carbohydrate as glucose poly-

mers, fat as long-chain triglycerides; nitrogen – whole

protein; vitamins; minerals;andtrace elements.(See

Carbohydrates: Requirements and Dietary Import-

ance; Energy: Measurement of Food Energy; Fats:

Requirements; Minerals – Dietary Importance; Pro-

tein: Requirements; Vitamins: Overview.)

0020Most standard polymeric diets have an energy

density of 4.2 kJ (1 kcal) ml

1

and a nitrogen concen-

tration of 5–7gl

1

. Some patients may require the

energy and nitrogen-dense formulations which con-

tain 8–10 g of nitrogen per liter and possess an energy

density of 6.3 kJ (1.5 kcal) ml

1

or more. Polymeric

diets containing dietary fiber are available and may

promote the regulation of bowel function in some

enterally fed patients. The use of enteral formulas

containing fiber has been suggested in the elderly,

those who require long-term nutritional support,

and patients with neurological conditions and enteral

fig0001 Figure 1 Fine-bore nasoenteral tubes (courtesy of Corpak

Medsystems, USA).

2116 ENTERAL NUTRITION