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REVIEW
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Nutrients, satiety, and control of energy intake1

Angelo Tremblay and France Bellisle

Abstract: In the context of the worldwide epidemic of obesity affecting men and women of all ages, it is important to understand
the mechanisms that control human appetite, particularly those that allow the adjustment of energy intake to energy needs.
Satiety is one important psycho-biological mechanism whose function is to inhibit intake following the ingestion of a food or a
beverage. According to the classical theories of appetite control, satiety is influenced by macronutrient intake and/or metabo-
lism. Satiety also seems to be modified by micronutrients, non-nutrients, and some bioactive food constituents. Under optimal
conditions, satiety should be well connected with hunger and satiation in a way that spontaneously leads to a close match
between energy intake and expenditures. However, the current obesity epidemic suggests that dysfunctions often affect satiety
and energy intake. In this regard, this paper presents a conceptual integration that hopefully will help health professionals
address satiety issues and provide the public with informed advice to facilitate appetite control.

Key words: appetite, satiation, obesity, weight loss.

Résumé : Dans le contexte de l’épidémie mondiale de l’obésité touchant les femmes et les hommes de tous âges, il est important
de comprendre les mécanismes de contrôle de l’appétit humain et particulièrement ceux des ajustements de l’apport énergé-
tique aux besoins énergétiques. La satiété est un important mécanisme psychobiologique dont la fonction est d’inhiber l’apport
alimentaire consécutivement à la consommation d’un aliment ou d’une boisson. D’après les théories classiques du contrôle de
l’appétit, la satiété subit l’influence de l’apport en macronutriments et/ou du métabolisme. La satiété semble aussi sous
l’influence des micronutriments, des ingrédients non nutritifs et de quelques constituants alimentaires bioactifs. Dans des
For personal use only.

conditions optimales, la satiété devrait être bien connectée à la faim et à la sensation de plénitude de manière à installer
spontanément une connexion nette entre l’apport et la dépense énergétique. Toutefois, l’épidémie actuelle d’obésité indique
une dysfonction de la satiété et de l’apport énergétique. Dans cette optique, cet article présente une intégration conceptuelle qui
devrait aider, on l’espère, les professionnels de la santé à aborder la question de la satiété et à communiquer au public de sages
conseils pour faciliter le contrôle de l’appétit. [Traduit par la Rédaction]

Mots-clés : appétit, rassasiement, obésité, perte de poids.

Introduction ories of appetite control to recently proposed conceptual paradigms.

In the context of the worldwide epidemic of obesity affecting
men and women of all ages, it is important to understand the
mechanisms that control human appetite, particularly those that
allow the adjustment of energy intake to energy needs. While
hunger and numerous environmental cues stimulate eating, sati-
ety is one important psycho-biological mechanism whose func-
tion is to inhibit intake following the ingestion of a food or a
beverage. The intensity and duration of this post-ingestive inhibi-
tion are determined by several factors, including the nutrient
composition of the foods or drinks consumed. Depending on its
nutrient content, a food exerts a certain “satiating power”; in
other words, it has a particular “satiating efficiency”. Enhancing
the specific “satiating power” of foods might be a way to increase
the intensity and duration of the post-meal inhibition of appetite
and, perhaps, facilitate the control of energy intake.
The present review examines classic notions and recent develop-
ments in the field of satiety research. Definitions and methods used
for the assessment of satiety are presented in the first section. Then,
we address the role of macronutrients in satiety, from classical the-
Other sections are devoted to the role of micronutrients in satiety
and the contribution of non-nutrients and bioactive food constitu-
ents. The developing field of satiety induced by the gut microflora
and its diet-induced variations is also addressed. Finally, we discuss
the conceptual transfer that can be offered to health professionals.
Satiation and satiety: definitions and current
knowledge
In mammals, including humans, eating is a patterned activity.
Under ethological conditions, eating patterns are often deter-
mined by the intermittent availability of food sources. In many
human societies, and particularly in developed areas of the world,
the supply of food has ceased to be uncertain and food is now
easily available at any time. Even under circumstances of constant
access to food, however, humans as well as laboratory animals do not
eat continuously. Periodic signals trigger meal onset, whereas other
signals bring consumption to an end and then inhibit further intake
for a certain time before the cycle starts again. Much research in the
field of appetite has been devoted to the identification of critical

Received 11 December 2014. Accepted 25 March 2015.

A. Tremblay.* Department of Kinesiology, PEPS, Room 0234, Université Laval, Quebec City, QC G1V 0A6, Canada.
F. Bellisle. Department of Kinesiology, PEPS, Room 0234, Université Laval, Quebec City, QC G1V 0A6, Canada; Unité d’Épidémiologie Nutritionnelle,
UMR U557 INSERM, U1125 INRA, CNAM, Université Paris 13, 74 rue Marcel Cachin, 93017 Bobigny, France.
Corresponding author: Angelo Tremblay (e-mail: angelo.tremblay@kin.ulaval.ca).
*All editorial decisions for this paper were made by Wendy Ward and Terry Graham.
1This paper is the first recipient of the Award for Nutrition Translation, which was granted by the Canadian Nutrition Society in conjunction with Canadian

Science Publishing and the Editorial Staff of APNM.

Appl. Physiol. Nutr. Metab. 40: 971–979 (2015) dx.doi.org/10.1139/apnm-2014-0549 Published at www.nrcresearchpress.com/apnm on 13 May 2015.
 972
Fig. 1. The Satiety Cascade. CCK, cholecystokinin; GLP-1, glucagon-like peptide-1; PYY, peptide YY. (From Blundell 2010, reproduced with
permission of Academic Press, © 1987 Elsevier.)
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For personal use only.
signals that trigger and inhibit intake. It has become obvious, partic-
ularly in the human situation, that such signals are the result of
complex processes involving physiological as well as sensory, cogni-
tive, environmental, and social factors.
Pioneer studies of animal behavior postulated the existence of
two related mechanisms that contribute to the inhibition of food
intake: satiation and satiety (Le Magnen 1971). Satiation was de-
fined as a set of complex processes that progressively inhibit the
motivation to eat during an eating event. At the beginning of a
meal, eating occurs under the combined stimulatory influences of
physiological factors (hunger), sensory cues (olfactory, gustatory,
visual, somesthetic), and numerous other factors linked to the
environment, such as time of day and the social situation (de
Castro 2010). Progressively, as food is ingested, internal inhibitory
influences (sensory, cognitive, gastric, hormonal, neural) develop
and finally bring ingestion to an end. This mechanism, satiation,
determines meal size (Le Magnen 1992).
Satiety is the inhibitory mechanism that takes place after the
end of an eating episode and prevents the return of hunger for a
variable duration. In animal models with constant access to food
sources, satiety is recognized as a powerful mechanism that al-
lows the matching of intake to energy needs via the adjustment of
the postprandial interval to the energy content of the previous
meal (Le Magnen 1992). In the human situation, however, meal-
times are set by cultural norms, and satiety mechanisms cannot
adjust intake to needs through the modulation of postprandial
intervals, although they could do so by inhibiting intake at the
next socially determined eating occasion. In efficient appetite
control, hunger, satiation, and satiety occur in succession and
allow the adjustment of energy intake to energy needs. The pres-
ent epidemic of obesity shows that many things can go wrong in
appetite control when powerful and ubiquitous stimulatory influ-
ences override inhibitory mechanisms.
The Satiety Cascade
The interplay of post-consumption factors that contribute to the
inhibition of intake is illustrated in the Satiety Cascade, first de-
Appl. Physiol. Nutr. Metab. Vol. 40, 2015
scribed more than 25 years ago (Blundell et al. 1987) and subse-
quently modified to integrate new findings (Fig. 1) (Blundell 2010).
Sensory factors such as taste, smell, and texture of foods stimulate
intake at the onset of an eating episode; as eating progresses,
sensory-specific habituation develops to the ingested foods
(Hetherington and Havermans 2013; Rolls et al. 1981), while signals
from the gastrointestinal tract (gastric distention, drop in stomach
ghrelin, release of hormones and peptides, and others) and the rise
in glycemia progressively undermine the motivation to eat and bring
eating to an end. After satiation is reached for the specific sensory
characteristics of a particular food, other foods with different sen-
sory aspects retain their stimulatory power and maintain consump-
tion until satiation signals are sufficiently powerful to counter the
sensory appeal of all food options. Palatability antagonizes satiation:
highly palatable meals in free-living subjects can be 44% larger than
neutral or unpalatable meals (de Castro et al. 2000).
Other factors such as cognitive influences (expectations about the
satiating effects of the foods, beliefs, attention or distraction at the
time of eating) also contribute to satiation (Bellisle and Dalix 2001;
Bellisle et al. 2004; Brunstrom 2011; Mitchell and Brunstrom 2005).
Even non-food-related cognitions play a role. For example, a demand-
ing cognitive task carried out before a meal has been shown to in-
crease energy intake at mealtime without increasing perceived
hunger (Chaput and Tremblay 2007). In this context, preprandial
mental work increases glycemic instability and cortisolemia, which
can disturb satiating effects (Chaput et al. 2008). Evidence of impair-
ments in satiation has also been observed in short sleepers who
display hormonal adaptations (Chaput et al. 2007; Spiegel et al. 2004)
that likely allow increased energy intake to occur before the devel-
opment of satiation signals (Brondel et al. 2010).
Following the end of a meal, numerous influences contribute to
the inhibition of further intake for a certain time (de Castro 2010).
The intensity and duration of post-intake satiety depend on the
weight, volume, energy and nutrient content, and energy density
of the meal, among other factors (Keller et al. 2013). Cognitions,
for example beliefs about the satiety value or the energy load of
the last meal, also contribute to the modulation of satiety (Cassady
Published by NRC Research Press
 Tremblay and Bellisle
et al. 2012; Wansink et al. 2005). “Sensory-specific satiety” inhibits
the intake of any food sharing the sensory characteristics (the
smell, the taste, and even the shape and the color) of ingested
foods in the hours or days following consumption (Hetherington
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et al. 1989). Caloric beverages often induce less post-intake inhibi-
tion of subsequent intake than comparable solid energy loads,
a satiety deficit that can induce “passive overconsumption”
(Almiron-Roig et al. 2013; Mattes 2006).
Sensory and cognitive factors exert an inhibitory influence after
the end of a meal, in parallel with a succession of physiological
post-ingestive and post-absorptive signals. Eating with attention
reinforces post-meal satiety (Bellisle et al. 2004), and so does the
cued recall of the foods consumed earlier on the same day (Higgs
et al. 2008). The volume of the previous meal exerts satiety effects
in the early phase of satiety (owing to gastric distension signals),
whereas nutrient contents exert their influence during the post-
absorptive phase. Although in humans the duration of the post-
prandial interval cannot be solely determined by the energy load
ingested at the previous meal, food intake diaries obtained over
7 consecutive days revealed how previous intake inhibits later
consumption: the weight of food remaining in the stomach at the
time of meal onset (in other words, at the end of the satiety cas-
cade of events) is one significant influence determining the size of
the next meal (de Castro 2010).
As illustrated in the Satiety Cascade, many metabolic satiety
factors originate from the periphery of the organism (Woods
2013). Such signals can be neural, for example when the nutrient
chemoreceptors and stretch receptors in the gastrointestinal tract
respond to the presence of food and send signals to the brain.
For personal use only.
Hormonal signals such as leptin, insulin, glucagon, and ghrelin
modulate appetite and satiety. Numerous other “satiety peptides”
and “satiety hormones” are secreted in the gastrointestinal tract
following food consumption: cholecystokinin (CCK), glucagon-
like peptide-1 (GLP-1), gastric inhibitory peptide (GIP), and peptide
YY (PYY), among others.
The Satiety Cascade also illustrates how the brain receives and
integrates various signals from the periphery of the organism, the
“internal milieu”. The brain integrates signals reflecting energy
input and energy expenditures and acts as a “homeostatic regula-
tor”, adjusting intake to needs to maintain the body energy bal-
ance (Berthoud 2002). One of the key features of the homeostatic
regulator is the alternation between hunger and satiety states.
Recent data suggest that the homeostatic adjustment of energy
intake and expenditure becomes more difficult to achieve when
energy expenditure is significantly decreased by interventions
such as a weight-reducing program. Indeed, the management of
this homeostatic process represents a significant challenge for
weight-reduced individuals whose energy expenditure may be de-
creased much below the level predicted by normal variations in
body weight (Doucet et al. 2001; Leibel et al. 1995). In this regard,
we have reported a significant positive relationship between ther-
mogenic adaptation in post-obese individuals and the increase in
their hunger level (Tremblay et al. 2013), suggesting that the pre-
cise alternation between hunger and satiety states may be more
difficult after a substantial weight loss. As discussed in the follow-
ing sections, a decrease in energy expenditure is also associated
with other biological adaptations influencing satiety.
Satiation and satiety: one or two processes?
Many of the inhibitory influences active in satiety are also pres-
ent in satiation. It is then legitimate to ask how distinct these
processes are. There is one obvious behavioral reason to distin-
guish satiation from satiety: satiation inhibits an ongoing intake
behavior, whereas satiety inhibits all potential ingestive re-
sponses for a certain time. Satiation processes occur while inges-
tion is taking place, whereas satiety processes prevent ingestion.
Satiation and satiety processes were originally inferred from the
973
observation of food intake patterns in laboratory rats whose epi-
sodic meal intake suggested an alternating hunger/satiety cycle
(Le Magnen 1971). The onset and cessation of meal intake clearly
required specific explanatory hypotheses, whereas the observa-
tion of inter-meal intervals of variable duration suggested the
influence of distinct underlying factors.
Clearly, some influences are limited to the time of eating, for
example the early responses of the “cephalic phase of digestion”,
the drop in gastric ghrelin, and environmental cues (social con-
text, distraction), while others develop well after meal termina-
tion (post-absorptive metabolic effects). Nevertheless, many satiety
factors are present at the time of consumption and continue to
affect behavior in the hours that follow meal termination: cogni-
tive and sensory factors, the rise and later decline of glycemia,
gastric and hormonal responses, etc.
Despite a certain degree of overlap between satiation and sati-
ety influences, the distinction of the two concepts is useful. First,
it allows consideration of the specific factors that actually inhibit
ongoing consumption as opposed to preventing or delaying inges-
tive responses. Second, as the recent literature on claims suggests,
satiety and satiation processes can be manipulated independently
by various means to influence total intake and body weight con-
trol (Blundell 2010). Two approaches or strategies can be envis-
aged. In the “satiation strategy”, a food can be tailored to provide
less energy for a given weight or volume, for example by the use of
ingredients with reduced energy density (Blundell 2010). This
strategy would decrease the energy load of meals. An alternative
“satiety” strategy would aim to strengthen the satiety efficiency of
foods via the use of satiety-enhancing ingredients such as fibres
and proteins (Blundell 2010).
Measuring satiety effects
The inhibition of intake that follows an eating event can be
quantified in different ways. One classic approach, used in many
pioneer studies of free feeding in laboratory animals, consists of
measuring the duration of the spontaneous interval that sepa-
rates one meal from the beginning of the next one; satiety is then
quantified as a duration (Le Magnen 1971). The duration of post-
meal intervals has also been assessed in human studies of satiety
(Himaya et al. 1997; Melanson et al. 1999). Satiety can also be
measured as the decrease in intake observed at the next eating
occasion following an inter-meal interval of fixed duration. This
approach is typical of the preload paradigm, widely used in both
animal and human studies (Kissileff 1985). It presents the inhibi-
tion of intake in terms of a reduction of amounts consumed rela-
tive to a control condition. In human consumers, satiety can also
be assessed as changes in the intensity of various subjective sen-
sations that follow eating, for example hunger, fullness, desire to
eat, or prospective consumption; satiety is then presented as a
score (Flint et al. 2000). Typically, ratings of hunger, fullness, etc.
are obtained at regular intervals during the postprandial interval,
from 30 min up to 5 h or more, and reflect the time-related
changes in post-meal appetite.
A “Satiety Index” can be computed based on the model of the
glycemic index (GI) (Holt et al. 1995): the area under the curve
(AUC) of satiety ratings (rather than glycemic values) following the
ingestion of a food is measured and compared with the AUC of
satiety ratings obtained following the consumption of a reference
food. The “Satiety Quotient” corresponds to the difference in hun-
ger ratings before and after consumption of a food, divided by the
weight or the energy load of the food ingested (Drapeau et al.
2007). In many studies, different indices of satiety are used in
combination.
For all these aspects of satiety, rigorous measurement princi-
ples have been established (Chapelot 2013). The reliability and
validity of experimental tools to assess satiety have been con-
firmed. Both the Satiety Index and the Satiety Quotient have been
Published by NRC Research Press
 974
shown to predict future consumption (Drapeau et al. 2005, 2007).
Under controlled laboratory conditions, the reproducibility of satiety
effects on further ad libitum energy intake is high (Gregersen et al.
2008). The Visual Analogue Scales (VAS) classically used to assess
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the intensity of satiety sensations can generate highly reproduc-
ible satiety profiles over repeated presentations of the same meal
conditions (Flint et al. 2000). A recent analysis of 23 randomized
controlled studies showed that VAS scores recorded for 30 min to
5 h following the intake of a preload significantly predict energy
intake at the next meal (Sadoul et al. 2014). Electronic devices,
such as the validated hand-held Electronic Appetite Rating System
(Gibbons et al. 2011), now facilitate the acquisition of repeated
ratings over the postprandial period. Taken together, these obser-
vations suggest that even if there is no standardized clinical best
practice for the measurement of satiety, the use of VAS scores has
high relevance. Indeed, as indicated above, it offers a simple and
valid tool to predict variations in energy intake in different con-
texts, for example in the management of a diet-based weight-
reducing program.
Macronutrients and satiety: from classical theories
of appetite to recent conceptual paradigms
Early theories of appetite control were built around the notion
of “homeostasis”, or in other words, the stability of the organism’s
internal milieu. According to these early perspectives, homeo-
static mechanisms trigger and then inhibit intake to ensure that
the intake of energy or nutrients matches bodily needs. These
theories postulated that some regulated physiological parameter
would be actively maintained within a narrow range by the brain.
For personal use only.
Such regulation requires that a signaling mechanism informs the
brain of the current status of the regulated parameter. The brain,
in turn, via a feedback loop, corrects the fluctuations of the regu-
lated factor by generating the states of hunger or satiety that
trigger or inhibit consumption.
Many of the classic theories of appetite control have focused on
the bodily status of one macronutrient. The glucostatic theory
(Mayer 1953) posits that eating is triggered by a decrease in the
availability of glucose to tissues. Glucosensitive neurons in the
brain monitor the blood glucose level and generate signals that
stimulate or inhibit food intake. According to this view, the in-
crease in the blood glucose level after a meal is the critical factor
underlying satiety. Experimental manipulations of glycemia in
human subjects confirmed this hypothesis (Gielkens et al. 1998).
In contrast to the notion that hyperglycemia induces satiety, en-
hanced satiety sensations (van Amelsvoort and Weststrate 1992),
delayed onset of hunger (Benini et al. 1995), and/or decreased ad
libitum energy intake (Ludwig et al. 1999) have been reported
following the intake of low-GI foods or meals that induce modest
post-intake rises in glycemia (Brand-Miller et al. 2002). This field
remains controversial, and conflicting reports suggest that the GI
is not a reliable predictor of satiety effects (Geliebter et al. 2013).
Many factors could potentially account for the diverging results,
such as the difficulty of predicting the GI of a meal from the GI of
its food components (Dodd et al. 2011) or the concurrent influence
of other nutrients or hormonal responses (Chapman et al. 1998).
Resolving the controversy is beyond the scope of the present re-
view, but it is mentioned here as an illustration of the present-day
relevance of the glucostatic theory. The impact of carbohydrate
(CHO) intake on satiety is not limited to the effects of available
CHO but also depends on the presence of fibre (soluble and insol-
uble), which has been shown to enhance satiety (Holt et al. 1992).
The aminostatic theory (Mellinkoff et al. 1956) holds that amino
acids and their metabolites are the crucial agents determining
satiety. Early experimental tests showed that the intake of pro-
tein, which elevates serum amino acid concentrations, reduced
hunger sensations and food intake in human subjects (Mellinkoff
et al. 1956). Over the years, evidence has accumulated suggesting a
Appl. Physiol. Nutr. Metab. Vol. 40, 2015
nutrient-specific hierarchy of satiating power, with protein show-
ing the highest potency (protein > CHO > fats) (Veldhorst et al.
2008). This conception finds an echo in current works on the high
satiating value of protein-rich functional foods (Lluch et al. 2010).
Several mechanisms could contribute to the high satiating value
of dietary proteins. Gastrointestinal responses to dietary proteins
reach the brain via an indirect neural pathway (mainly via the vagus
nerve) and a direct humoral pathway (Johnstone 2013). The pres-
ence of amino acids in the gastrointestinal tract induces the re-
lease of the satiating hormone CCK, which is released before the
end of the meal and could therefore contribute to both satiation
and satiety (Tomé et al. 2009; Woods 2013). In addition, the gas-
trointestinal tract responds to the presence of amino acids by
releasing other anorexigenic substances such as GLP-1 and PYY
(Lejeune et al. 2006; Moran and Dailey 2011).
The lipostatic theory (Kennedy 1953) proposes that body weight,
or more precisely the body fat mass, is the regulated parameter.
This theory was reinforced by the discovery of the hormone lep-
tin, which is secreted by the body adipose tissue and informs the
brain of the current body adiposity (Zhang et al. 1994). A homeo-
static regulation of the body fat mass by the brain would explain
why attempts at weight loss are often followed by a return to the
pre-dieting body weight.
Experimental and clinical evidence in support of all these the-
ories has accumulated. These approaches seem to offer comple-
mentary perspectives on the control of food intake rather than
mutually exclusive options.
In a more recent paradigm proposed by Flatt (1996), the orga-
nism’s CHO stores (in the form of liver and muscle glycogen) are
the regulated parameter. According to this model, the body’s reg-
ulatory functions strive to maintain nutrient balance rather than
energy balance, since “energy” is an abstract notion without phys-
iological equivalent. While the fat and protein (muscle) reserves
are abundant in the body, the glycogen reserve varies between
1.0 and 1.5 times the amount of CHO consumed and oxidized
during a typical day, representing about 1000–2000 kcal. Given its
small size in relation to its turnover and the importance of main-
taining adequate blood glucose levels, the glycogen reserve is reg-
ulated within narrow limits by potent mechanisms (key enzyme
activity and hormonal signals) to adjust glucose oxidation to CHO
availability. Glycogen is maintained at levels sufficient to prevent
hypoglycemia and maintain usual physical activity. Glycogen
stores vary between individuals and also in response to environ-
mental conditions. For example, they tend to be higher on high-
CHO diets than on low-CHO diets. When the range within which
glycogen levels are maintained rises, daily fat oxidation is likely to
decrease, promoting fat accumulation and contributing to the
development of overweight or obesity (Flatt 2004).
In this regard, the Respiratory Quotient-Food Quotient (RQ-FQ)
concept described by Flatt (1987) represents an interesting integra-
tion of the glucostatic and lipostatic theories of appetite control.
Accordingly, we have found that after obese individuals have lost
enough body weight to reach a state of resistance to further loss of
body fat, mild hypoglycemia is observed (Tremblay et al. 1999).
Moreover, this hypoglycemia is a significant predictor of body
weight regain in weight-reduced obese patients followed over
1.5 years after weight loss (Boulé et al. 2008). This suggests that the
altered glycemia–body fat relationship may make the achieve-
ment of satiety more difficult in weight-reduced obese individuals
reaching a lower energy balance status. Even if the RQ-FQ concept
is based on substrate (protein, lipid, CHO) gradient effects, its
clinical implications are consistent with studies documenting an
impact of fat loss on hormonal and neural factors influencing
satiety and energy balance. For instance, Rosenbaum et al. (2010)
showed that a substantial fat loss promotes a decrease in leptine-
mia and sympathetic nervous system (SNS) activity associated
with an increase in hunger. Thus, fat loss modifies appetite con-
trol via biological effects that must be counteracted if one wishes
Published by NRC Research Press
 Tremblay and Bellisle
to postpone the occurrence of resistance to further loss of body
weight/fat. As discussed further in this paper, a major challenge
for health professionals and food producers is the development of
foods, beverages, and menus favoring appetite-reducing effects
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that can at least partly compensate for the opposite effects in-
duced by weight loss.
Under isoenergetic conditions, the macronutrient content of
foods modulates satiety effects. A hierarchy of satiating power has
been documented (Poppitt et al. 1998). Protein induces the maxi-
mum satiety, followed by CHO and then by fat, for which a rela-
tive “satiety deficit” has been documented. For example, Lawton
et al. (1993) showed that obese individuals displayed significant
overconsumption when exposed to a high-fat meal compared
with a high-CHO meal. The weak satiety efficiency of dietary fats
could be accounted for by their high energy density and/or their
palatability-enhancing effects: in many foods, taste, aroma, and
texture are improved by fat, which stimulates overconsumption
with relatively poor post-intake satiety. In addition, hormonal
factors contribute to the hierarchy of nutrient-associated satiat-
ing potency. For example, the hormone ghrelin, an appetite-
stimulating substance, is present in high concentrations in the
stomach before a meal and drops to a low level at the end of the
meal while hunger feelings are totally suppressed. The postpran-
dial drop in ghrelin is more profound after a CHO-rich meal than
after ingesting dietary fats (Gibbons et al. 2013).
Alcohol induces lower satiety than food macronutrients, per-
haps because of its liquid form and its disinhibiting effect (Mattes
1996). In fact, in the context of ad libitum food intake, alcohol
calories simply add to the energy intake from solids, suggesting
For personal use only.
that alcohol intake exerts no inhibitory effect on the ingestion of
food (Tremblay and St-Pierre 1996; Tremblay et al. 1995).
Micronutrients: a potential role in satiety
Classical theories of appetite control are based on mechanisms
related to macronutrient and energy metabolism. However, there
is no reason to exclude a role for micronutrients in the control of
appetite and energy intake. This viewpoint is consistent with the
existence of a calcium-specific appetite control mechanism (Tordoff
2001): calcium-deprived animals display a preferential calcium in-
take when given the opportunity. Following a 6-week low-calcium
diet, rats were able to selectively ingest calcium-containing bev-
erages to compensate for the imposed deficiency (Paradis and
Cabanac 2005).
The existence of a calcium-specific appetite is more difficult to
demonstrate in human subjects than in animals. This may be due
to the confounding factors that influence feeding behaviors in
humans and/or sensory acuity, which might be less pronounced in
humans than in other animals. As a first attempt to test the valid-
ity of a calcium appetite in humans, obese individuals with very
low calcium intake participated in a weight loss program with or
without calcium plus vitamin D supplementation. The mean weight
loss over 15 weeks was 5.8 and 1.4 kg in supplemented and placebo
controls, respectively (Major et al. 2009). The use of a buffet-type
meal to measure ad libitum energy intake before and after the
study revealed that most of the between-group difference in en-
ergy balance was explained by variations in energy/lipid intake.
More recently, Jones et al. (2013) showed that the supplementa-
tion of calcium in obese low-calcium consumers significantly in-
creased the plasma concentration of the anorexigenic hormone
PYY.
Other micronutrients might exert inhibitory influences on ap-
petite. Obese women on a weight loss program displayed favor-
able changes in their appetite sensations when receiving a
multivitamin supplement compared with their placebo controls
(Major et al. 2008). As discussed by these investigators, the appetite-
related effects of multivitamin supplementation might be related
to the role of some vitamins and minerals in the synthesis of
975
peptides and neurotransmitters that control food intake. Further-
more, beyond a possible calcium-specific appetite control effect, it
is realistic to hypothesize that the intake of other micronutrients
could be controlled to permit the maintenance of essential func-
tions of body homeostasis.
Globally, these observations suggest that changes in appetite
and food intake can reflect a strategy to maintain homeostasis
under conditions of suboptimal micronutrient intake. For obese
individuals with an inadequate micronutrient intake, vitamin
and/or mineral supplementation may thus facilitate appetite con-
trol and compliance with a targeted energy deficit.
Non-nutrients and bioactive food constituents
Some food ingredients cannot be considered nutrients because
they are not essential to body homeostasis, but they nevertheless
have the potential to influence appetite control. They can act
peripherally, for example in the stomach or the gut, where they
affect fullness or transit responses. This is the case with fibres,
which promote satiety at a reduced energy intake level, particu-
larly in the context of weight loss programs. In this category of
non-nutrients, glucomannan fibres seem to have the best potency
to affect energy balance, presumably because of their ability to
bind water and thus promote satiety, inducing a decrease in en-
ergy intake that results in a substantial weight loss over time
(Drapeau and Tremblay 2000).
Non-nutrient food constituents also include ingredients that
produce centrally mediated effects on energy intake and expen-
diture that resemble psychoactive drug effects. Caffeine can pro-
duce a substantial decrease in energy intake when administered
as a preload in a pre-breakfast decaffeinated coffee beverage
(Tremblay et al. 1988). When combined with catechins, caffeine
significantly increases energy expenditure while also increasing
ambulatory blood pressure (Bérubé-Parent et al. 2005).
Capsaicin is another non-nutrient food constituent that has
been shown to reduce post-intake appetite sensations and subse-
quent energy intake (Yoshioka et al. 1999). The measurement of
heart rate variability revealed an association between an increase
in SNS activity and the satiating effects induced by capsaicin
(Yoshioka et al. 1999). In a more recent study, preprandial intake
of capsaicin, whether in capsules or diluted in tomato juice, in-
creased satiety and reduced energy intake (Westerterp-Plantenga
et al. 2005). When tested in combination with caffeine, capsaicin
produced the same effects as when used alone to influence energy
intake (Yoshioka et al. 2001). Capsaicin and green tea decrease
hunger and increase satiety to a greater extent during negative
than during positive energy balance (Reinbach et al. 2009). This is
consistent with the observation that following the completion of
a 4-week, very low-energy diet, post-weight-loss fat oxidation was
better sustained during a 3-month observation period with capsaicin
supplementation compared with a placebo condition (Lejeune et al.
2003).
Gut microbiota and satiety
Beyond their direct digestive effects, macro- and micronutri-
ents can have an indirect but powerful influence on satiety via
their action on the gut microbiota. In animal models, a high-fat
diet induces alterations in the composition of the gut microbiota
that favor the development of obesity (Neyrinck et al. 2011). Alter-
ations in the gut microbiota are also observed when the diet varies
in its content of many micronutrients and elements. Prebiotics, a
class of nondigestible/fermentable CHO likely to increase bifido-
bacteria, decrease food intake in different animal models of obe-
sity. For example, a 3-week treatment on a standard diet enriched
with the prebiotic oligofructose (OFS), which is rapidly and exten-
sively fermented in the proximal part of the colon, induced a
decrease in energy intake, leading to a significant decrease in
epidydimal fat, in parallel with an increase in the anorexigenic
Published by NRC Research Press
 976
peptides PYY and GLP-1 and a decrease in the orexigenic hormone
ghrelin (Cani et al. 2004).
Recently, experimental evidence has been obtained in human
subjects of consistent links between nutrient intake, the gut mi-
Appl. Physiol. Nutr. Metab. Downloaded from www.nrcresearchpress.com by DIRECTORATE OF COLDWATER FISHERIES RES on 09/27/15
crobiota, and satiety. Evening meals rich in dietary fibres contain-
ing nondigestible/fermentable CHO, such as whole-grain barley
kernel, reduce appetite on the following day (Johansson et al.
2013) in parallel with an increase in the satiety peptide GLP-1 and
a decrease in fasting serum free fatty acids. These effects are hy-
pothesized to be mediated by gut microbial fermentation of the
indigestible CHO. Consistent with this hypothesis, a fructan pre-
biotic treatment over 2 weeks increased breath-hydrogen excre-
tion (a marker of gut microbiota fermentation) 3-fold, lowered
hunger ratings, and increased anorexigenic gut peptide concen-
trations (GLP-1 and PYY) (Cani et al. 2009). Administration of OFS
supplements to men and women increased satiety sensations fol-
lowing breakfast and dinner and reduced overall energy intake
(Cani et al. 2006). In a 12-week randomized study, overweight
adults received either 21 g of OFS per day or a maltodextrin pla-
cebo (Parnell and Reimer 2009). A decrease in self-reported energy
intake coincided with a reduction in ghrelin and an increase in
PYY in the prebiotic group. Accordingly, over the course of the
intervention, the OFS group lost weight, whereas control subjects
gained weight. Some evidence exists that prebiotic effects on gut
peptide release and appetite might be dose-dependent. In a cross-
over study carried out in adults receiving a supplement of either
10 or 16 g of OFS versus placebo for 13 days, a significant effect of
OFS on energy intake and gut PYY and GLP-1 responses appeared
only with the 16-g dose (Verhoef et al. 2011).
For personal use only.
Our own experience reinforces the idea of a potential role of
probiotic bacteria on gut microbiota and energy intake. Specifically,
obese women receiving a supplement of Lactobacillus rhamnosus dur-
ing weight loss exhibited a decrease in Lachnospiraceae, an im-
portant subclass of Firmicutes (Sanchez et al. 2014). This change
was related to a better capacity to adhere to a reduced-energy diet
and achieve significant body weight and fat losses. In a recent
study, probiotic intake resulted in lower energy intake without
subjective changes in appetite sensations in humans (Bjerg et al.
2014).
At this time, the links between the gut microbiota and satiety
remain controversial. The field is young and it is premature to
provide recommendations or advice based on the existing evi-
dence, particularly in human subjects.
Satiety and potential benefits for consumers
The short-term effects of nutrients on satiety are well docu-
mented. At least in the context of one meal or one day, satiety can
be influenced significantly by modifying the nutrient content of
foods or beverages. For example, the appetite-reducing effects of
an innovative low-fat yogurt enriched with protein (8 g/serving)
and fibre (2.6–2.9 g/serving) were assessed using a preload para-
digm under laboratory conditions (Lluch et al. 2010). The test yo-
gurt reduced appetite ratings for 2 h after consumption and
decreased energy intake at the next ad libitum lunch. Poortlviet
et al. (2007) demonstrated that calorie for calorie, a meal course
focusing on optimal nutrient composition acutely promoted a
substantial decrease in daily energy intake without compromis-
ing satiety and palatability (Table 1).
Less is known, however, about how satiety manipulations
might affect intake over the long term and, critically, how the
modulation of satiety via nutritional or other factors might affect
body weight changes. Would it be possible to use the satiating
power of existing foods, or to engineer novel foods to optimize
their satiating efficiency, to enhance satiety over the long term
and facilitate body weight control (Blundell 2010)? Many func-
tional foods have been developed to maximize satiety effects
(Hetherington et al. 2013). Such foods include dairy products (yo-
Appl. Physiol. Nutr. Metab. Vol. 40, 2015
Table 1. Impact of a satiating meal course (chicken stir-fry) and a
control food (fettucine carbonara) on energy intake.
Mean energy intake (kJ) Chicken Fettucine Difference
Energy content of the standardized 2090 2090 0
meal course
Ad libitum energy intake for the rest 2362 3106 744
of the meal (dessert)
Energy intake for the rest of the day 4932 5961 1029
Note: Adapted from Poortvliet et al. (2007).
gurts), cereals, ready-to-eat meals, and even snack foods (choco-
late bars). Satiety claims may suggest a reduction in hunger or an
increase in the duration of satiety following consumption. Such
claims raise a number of issues. First, it is important to assess the
consumer’s understanding of satiety claims, or even satiety itself.
Second, the long-term benefits that can be reasonably expected
from the use of these products must be ascertained.
In a focus group study, British consumers described fullness as
having physical (perception of gastric signals arising from the
presence of food) and psychological (satisfaction, lack of desire to
eat) aspects (Murray and Vickers 2009). These notions reflect an
awareness of some important features of the Satiety Cascade, al-
though the participants in the study did not spontaneously use
the term “satiety”. Consequently, it is likely that consumers could
correctly understand enhanced satiety claims that have to do with
post-meal fullness and absence of hunger. A concern has been
expressed in the literature about the potential misinterpretation
of satiety claims as slimming claims (Booth and Nouwen 2010).
Indeed, changes in experienced satiety do not necessarily trans-
late into decreased intake and weight loss. Satiety enhancement is
one influence that could favor weight loss, but it should not be
equated with it. A study of consumers’ understanding (Bilman
et al. 2012) showed sensible expectations in most people, who
understand that such products can only play a part in weight
management and that personal efforts are required. However, the
same study also revealed that restrained eaters appear more in-
clined to over-interpret satiety claims than peers with lower levels
of dietary restraint, suggesting a particular vulnerability in cer-
tain groups of consumers.
Enhanced satiety can also have potential indirect benefits such
as improved hunger management, reduced opportunistic eating
in dieters, reduced hunger dysphoria, and improved compliance
with goal-directed behaviors, for example the dietary aspects of a
weight loss program (Hetherington et al. 2013). Indeed, it has been
confirmed that higher ratings of appetite are associated with
lower weight loss in dieters (Drapeau et al. 2007) and higher levels
of perceived hunger predict a poor outcome of weight loss inter-
ventions (Womble et al. 2001) and weight loss maintenance (Pasman
et al. 1999).
Enhanced satiety should endure over time and not be counter-
acted by energy compensation. In a recent note about the substan-
tiation of satiety claims, the European Food Safety Authority
(EFSA 2012) stated that evidence for a sustained effect on appetite
ratings with continuous consumption of the food (to exclude ad-
aptation) should be provided. The long-term maintenance of sati-
ety effects is a clear condition for satiety-related weight effects.
However, the maintenance of a satiety effect should be inter-
preted with caution following weight loss in obese individuals.
Indeed, substantial weight loss favors numerous metabolic changes
such as mild hypoglycemia (Tremblay et al. 1999), a decrease in
leptinemia and SNS activity (Rosenbaum et al. 2010), an increase
in hunger (Doucet et al. 2000), and a greater than predicted de-
crease in energy expenditure (Doucet et al. 2001; Leibel et al. 1995).
Under these conditions, it is clear that the decreased satiety pro-
file of weight-reduced obese individuals may be strong enough to
counteract the chronic satiating effect of a functional food. This
does not imply that the satiety effect of the functional food is not
Published by NRC Research Press
 Tremblay and Bellisle
Fig. 2. Weight loss maintenance over 26 weeks under 5 diet conditions.
At the end of follow-up, a diet with higher protein content and lower
glycemic index significantly improved weight loss maintenance
compared with diets with lower protein content or higher glycemic
Appl. Physiol. Nutr. Metab. Downloaded from www.nrcresearchpress.com by DIRECTORATE OF COLDWATER FISHERIES RES on 09/27/15
index. The number of participants in each diet condition at each time
point is indicated below the figure. LP, low protein; HP, high protein;
LGI, low glycemic index; HGI, high glycemic index. (From Larsen et al.
2010, reproduced with permission of N. Engl. J. Med., vol. 363, p. 2109,
© 2010 Massachusetts Medical Society.)
For personal use only.
present anymore; rather, it means that this effect is masked by the
metabolic vulnerability of the post-obese individual. To overcome
this difficulty, Gilbert et al. (2009) developed regression equations
to predict changes in appetite following weight loss. Based on
these equations, even if an absolute satiety effect is no longer
significant after a substantial weight loss, a score of satiety higher
than the predicted score indicates a maintained satiating effect.
There is presently no convincing direct evidence supporting the
notion that diet-induced satiety enhancement per se can produce
significant weight loss. In contrast, there is evidence that enhanc-
ing satiety by selecting appropriate foods (foods high in fibre, high
in protein, and/or with functional ingredients that promote sati-
ety) can assist in the maintenance of body weight loss over the
long term. The multicentric DIOGENES project was carried out in
773 overweight adults from 8 European countries. After an initial
diet-induced body weight loss, the participants were randomized
to 1 of 5 ad libitum diets, of which 4 were either high or low in
protein and GI, according to a 2 × 2 factorial design. The 5th diet
was a control standard diet. The completion rate of the 26-week
weight maintenance program and the actual maintenance of the
weight loss were highest in the high-protein, low-GI condition
(Larsen et al. 2010). Figure 2 presents the changes in body weight
over the 26 weeks in the 5 conditions. These results show how a
combination of increased protein content and decreased GI, two
factors known to enhance satiety, had a significant cumulative
impact on one of the most difficult problems in obesity treatment:
maintaining the weight loss following a reducing diet. In addi-
tion, this study confirms the long-term benefits of enhanced sati-
ety effects, even in a post-weight-loss situation.
977
Conclusions
The scientific study of satiety and its determinants is of great
importance both for the basic understanding of the mechanisms
of appetite and for applied purposes, particularly in the context of
the global epidemic of obesity. Beyond the well-established immediate
effects, the direct and indirect (e.g., via gut microbiota) satiety
effects of nutrients should now be investigated over sufficiently
long periods of time to determine under what conditions a
nutrient-induced enhancement of satiety can affect health or
body weight control. Weight loss, the maintenance of a previous
weight loss, and the prevention of weight gain are all legitimate
but very ambitious targets. Clearly, nutrient composition is one
among many factors that affect satiety, and satiety is but one of
the numerous influences that determine energy intake and body
weight. One important challenge for researchers is to establish
how the nutrient-induced modulation of satiety can contribute to
a multidimensional strategy that can ultimately facilitate body
weight control.
Conflict of interest statement
There is no conflict of interest related to the content of this
paper.
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