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Influence of resistance and aerobic exercise on hunger, circulating levels of acylated ghrelin, and peptide YY in healthy males

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Abstract

Resistance (muscle strengthening) exercise is a key component of exercise recommendations for weight control, yet very little is known about the effects of resistance exercise on appetite. We investigated the effects of resistance and aerobic exercise on hunger and circulating levels of the gut hormones acylated ghrelin and peptide YY (PYY). Eleven healthy male students: age 21.1 +/- 0.3 yr, body mass index 23.1 +/- 0.4 kg/m(2), maximum oxygen uptake 62.1 +/- 1.8 ml.kg(-1).min(-1) (means +/- SE) undertook three, 8-h trials, 1) resistance exercise: a 90-min free weight lifting session followed by a 6.5-h rest period, 2) aerobic exercise: a 60-min run followed by a 7-h rest period, 3) control: an 8-h rest, in a randomized crossover design. Meals were provided 2 and 5 h into each trial. Hunger ratings and plasma concentrations of acylated ghrelin and PYY were measured throughout. Two-way ANOVA revealed significant (P < 0.05) interaction effects for hunger, acylated ghrelin, and PYY, indicating suppressed hunger and acylated ghrelin during aerobic and resistance exercise and increased PYY during aerobic exercise. A significant trial effect was observed for PYY, indicating higher concentrations on the aerobic exercise trial than the other trials (8 h area under the curve: control 1,411 +/- 110, resistance 1,381 +/- 97, aerobic 1,750 +/- 170 pg/ml 8 h). These findings suggest ghrelin and PYY may regulate appetite during and after exercise, but further research is required to establish whether exercise-induced changes in ghrelin and PYY influence subsequent food intake.
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The influence of resistance and aerobic exercise on hunger, circulating levels of acylated ghrelin
and peptide YY in healthy males
David R Broom1, Rachel L Batterham2, James A King1 and David J Stensel1
1 Loughborough University, UK
2 University College London, UK
Running head
Exercise, hunger, ghrelin and PYY
Corresponding author:
Dr David Stensel
School of Sport and Exercise Sciences
Loughborough University
Leicestershire
LE11 3TU
UK
Phone: +44 (0)1509 226344
Fax: +44 (0)1509 226301
E-mail: D.J.Stensel@lboro.ac.uk
David R Broom was supported by a Loughborough University faculty studentship
Rachel L Batterham is an MRC Clinician Scientist
Articles in PresS. Am J Physiol Regul Integr Comp Physiol (November 5, 2008). doi:10.1152/ajpregu.90706.2008
Copyright © 2008 by the American Physiological Society.
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ABSTRACT
Resistance (muscle strengthening) exercise is a key component of exercise recommendations for
weight control yet very little is known about the effects of resistance exercise on appetite. We
investigated the effects of resistance and aerobic exercise on hunger and circulating levels of the gut
hormones acylated ghrelin and peptide YY (PYY). Eleven healthy male students: age 21.1 ± 0.3 y,
body mass index 23.1 ± 0.4 kg/m2, maximum oxygen uptake 62.1 ± 1.8 mL/kg/min (mean ± SEM)
undertook three, 8-h trials, 1) resistance exercise: a 90 min free weight lifting session followed by a
6.5 h rest period, 2) aerobic exercise: a 60 min run followed by a 7 h rest period, 3) control: an 8 h
rest, in a randomised crossover design. Meals were provided 2 and 5 h into each trial. Hunger ratings
and plasma concentrations of acylated ghrelin and PYY were measured throughout. Two-way
ANOVA revealed significant (P<0.05) interaction effects for hunger, acylated ghrelin and PYY
indicating suppressed hunger and acylated ghrelin during aerobic and resistance exercise and
increased PYY during aerobic exercise. A significant trial effect was observed for PYY indicating
higher concentrations on the aerobic exercise trial than the other trials (8 h area under the curve:
control 1411 ± 110, resistance 1381 ± 97, aerobic 1750 ± 170 pg/mL 8 h). These findings suggest
ghrelin and PYY may regulate appetite during and after exercise but further research is required to
establish whether exercise induced changes in ghrelin and PYY influence subsequent food intake.
Key words
Acylated ghrelin, appetite, exercise, hunger, peptide YY
3
INTRODUCTION
Body weight is regulated by a balance between
food intake and energy expenditure (19).
Exercise is an effective method of increasing
energy expenditure (2) and it may,
paradoxically, lead to a short term hunger
suppression (6, 7, 24, 28, 29). This relationship
between exercise and hunger has led
investigators to study the role of gut hormones
in mediating exercise-induced hunger changes.
The majority of studies have focused on aerobic
(cardiovascular) exercise (31) with only three
studies examining the effects of resistance
(muscle strengthening) exercise and these have
reported contradictory effects (21, 33, 47).
Resistance exercise is a key component of
exercise recommendations for weight control (2)
and public health (23, 42) thus it is important to
clarify the effects of resistance exercise on
hunger and gut hormones.
The effect of acute exercise bouts on total
plasma ghrelin concentrations are controversial
with studies reporting no changes either during
or post-exercise (10, 15, 26, 27, 32, 39, 43, 45,
47), as well as increases (14, 17, 25, 44) and
decreases (21, 33, 48, 50). Acylation of ghrelin
is thought to be essential for appetite regulation
because only the acylated form of the hormone
can cross the blood-brain barrier (41). Thus,
measurements of total ghrelin may mask
important changes in acylated ghrelin.
Currently, little is known about the influence of
exercise on acylated ghrelin. Recently, we have
shown that plasma acylated ghrelin is
suppressed during vigorous treadmill running
(9) while another recent study has reported
increases in acylated ghrelin after five
consecutive days of aerobic exercise (1 h per
day) (36).
Less is known regarding the response of other
gut hormones to exercise. Several studies have
demonstrated increases in fasting and
postprandial levels of the satiety hormone
pancreatic polypeptide (PP) after aerobic
exercise (38) but there is a paucity of data on
peptide YY (PYY). There are two main
circulating forms of PYY; PYY1-36 and PYY3-36
(11) both have been shown to reduce food intake
when administered peripherally (13) however,
PYY3-36 is more potent than PYY1-36. Only one
study has investigated the response of PYY to
an acute bout of exercise (39). In this study
subjects consumed a standardised breakfast and
one hour later cycled for 60 min at 65% of their
maximal heart rate. Plasma PYY concentrations
were elevated during but not after exercise while
the satiety hormones glucagon-like peptide-1
(GLP-1) and PP were elevated during and for a
short while (up to 60 min) after exercise.
Another recent study (12) has demonstrated an
increased GLP-1 response to feeding after five
consecutive days of aerobic exercise (1 h/day).
Collectively, these findings suggest that hunger
is inhibited during and for a short while after
aerobic exercise.
Several limitations are apparent in the research
literature regarding exercise and gut hormones.
Most studies have measured gut hormone
responses in the fasted state and for relatively
short periods. Few studies have assessed post-
exercise gut hormone responses to feeding over
a prolonged period or attempted to relate these
responses to changes in hunger. Moreover, no
studies have examined acylated ghrelin and
PYY responses to resistance exercise. This
requires attention since ghrelin plays an
important role in meal initiation (1) and PYY
infusion, at normal postprandial concentrations,
suppresses hunger in humans (3). Thus, we
sought to investigate the acute effects of
resistance and aerobic exercise on hunger,
acylated ghrelin and total PYY in healthy male
fasted subjects. In addition, we evaluated the
effects of resistance exercise and aerobic
exercise on meal-stimulated changes in hunger,
acylated ghrelin and total PYY at two time
points (2 h and 5 h post-exercise) to gain
insights into the longer term effects of exercise
on these parameters.
MATERIALS AND METHODS
Subjects
Loughborough University’s Ethics Advisory
Committee approved the study. Eleven healthy
physically active, Caucasian males aged 19 to
23 yrs gave their written informed consent to
participate. Subjects were non-smokers, not
taking any medication, weight-stable for three
months prior to the study and had no food
allergies. The physical characteristics of the
subjects were: age 21.1 ± 0.3 yrs, body mass
index (BMI) 23.1 ± 0.4 kg/m2, waist
4
circumference 78.5 ± 1.1 cm, maximum oxygen
uptake 62.1 ± 1.8 mL/kg/min (4.6 ± 0.1 L/min).
Preliminary tests
Orientation session. Subjects attended the
laboratory for an initial session during which
anthropometric data were collected and they
were familiarised with treadmill running and
weight lifting. After this session subjects
returned to the laboratory on two further
occasions to complete weight lifting tests and on
one further occasion to complete two treadmill
running tests.
Weight lifting tests. A 12-repetition maximum
test was completed for each of the 10 resistance
exercises employed in the study. The order in
which each exercise was performed was: squat,
dumbbell lateral raise, bench press, upright row,
lunges, bicep curl, barbell pullover, seated
shoulder press, triceps extension and bent over
row. On a separate visit subjects undertook a 90
min familiarisation session where they
completed a full weight lifting session: three sets
of 12 repetitions of 10 different weight lifting
exercises at 80% of 12 repetition max.
Treadmill running tests. Subjects completed a
16-min submaximal treadmill running test and a
maximum oxygen uptake test on a motorised
treadmill as described previously (9). These tests
were performed on the same day with a 30 min
rest between tests. Expired air samples were
collected into Douglas bags during these tests
for the determination of oxygen consumption
and carbon dioxide production (9). The results
of the two tests were used together to determine
the running speed required to elicit 70% of
maximum oxygen uptake.
Main trials
One week after completing the preliminary
exercise tests subjects undertook a
counterbalanced randomised three-way
crossover study with an interval of 7 days
between each study day. The three trials were:
resistance exercise (weight lifting), aerobic
exercise (treadmill running) and control. For two
days before the first main trial participants
recorded their weighed food intake using a food
record diary. The same food intake was
consumed for the two days prior to subsequent
trials. Participants were also asked to refrain
from vigorous exercise and ingesting caffeine or
alcohol 24 h prior to the main trials. On trial
days participants arrived at the laboratory
between 08:00 and 09:00 having fasted for 10 h.
Water was permitted ad libitum during this time.
Resistance exercise trial. At the start of this trial
subjects completed a free weight session for 90
min performing three sets of 12 repetitions of 10
different weight lifting exercises at 80% of 12
repetition max. Participants were given 3 min to
complete each set. On completion of the 12
repetitions, participants rested for the remainder
of the 3 min. Exercises were completed in the
order described for the preliminary tests. All sets
for one exercise were completed before moving
onto the next exercise. An expired air sample
was taken for 3 min during the third set for each
exercise. After the session, participants rested
for 6.5 h. The short duration intermittent nature
of weight lifting invalidates the assumptions of
indirect calorimetry and therefore energy
expenditure during weight lifting was estimated
as 5.047 kcal (21.1 kJ) per litre of oxygen
consumed (40). This reflects the assumption that
energy was derived from carbohydrate rather
than fat and assumes no protein oxidation during
exercise. This assumption may not be entirely
valid but was used to provide an approximation.
Aerobic exercise trial. At the start of this trial
participants ran on the treadmill for 60 min at a
speed predicted to elicit 70% of maximum
oxygen uptake. One minute expired air samples
were collected into Douglas bags at 14-15, 29-
30, 44-45 and 59-60 min during the run. Oxygen
consumption and carbon dioxide production
were determined from expired air samples as
described previously (9). Energy expenditure
was predicted from oxygen consumption and
carbon dioxide production values using indirect
calorimetry (20). Ratings of perceived exertion
were recorded during each expired air collection
using the Borg scale (8). After the run,
participants rested for 7 h.
Control trial. For the control trial participants
rested for the entire duration of the trial.
Test meals
Participants were fed a test meal 2 h and 5 h into
each trial (approximately 11:00 and 14:00
respectively). Meals consisted of white bread,
butter, mayonnaise, Cheddar cheese, potato
5
crisps, whole milk and milk shake powder. The
macronutrient content of the meals was 33%
carbohydrate, 11% protein and 56% fat. The
energy content was 3230 kJ for a 70 kg person.
The amount of food consumed was adjusted for
each participant based on their bodyweight and
kept constant throughout all three trials.
Participants were encouraged to consume the
meal within 15 min and kept to the same start
and finish times on all trials. Water was
available ad libitum during trials.
Ratings of perceived hunger
Ratings of perceived hunger were assessed by
means of a validated visual scale which ranged
from 0 “not hungry” to 15 “very hungry” (10).
Hunger measurements were recorded at
baseline, 0.5, 0.75 and 1 h and every 30 min
thereafter for the duration of each trial.
Blood sampling
In each main trial venous blood samples were
collected into pre-cooled 9 mL EDTA
monovettes (Sarstedt, Leicester, U.K.) at 0, 0.75,
1.5, 2, 2.5, 3, 4, 5, 5.5, 6, 7 and 8 h. In the
control trial and the aerobic exercise trial all
samples were collected using a cannula
(Venflon, Becton Dickinson, Helsinborg,
Sweden) which was inserted into an antecubital
vein. In the weight lifting trial the first two
blood samples (0 and 0.75 h) were collected by
venepuncture and the remaining samples were
collected using a cannula inserted into an
antecubital vein. All blood samples were
collected whilst subjects lay in a semi-supine
position with the exception of the 0.75 h sample
during the running trial, this sample was
collected while subjects straddled the treadmill.
The EDTA monovettes were spun at 1681 g
(4000 revs/min) for 10 min in a refrigerated
centrifuge (Burkard, Hertfordshire, U.K.) at 4oC.
The plasma supernatant was then aliquoted into
Eppendorf tubes. These were stored at -80oC for
analysis of total PYY, glucose and insulin at a
later date.
Separate venous blood samples were drawn into
4.9 mL monovettes at 0, 0.75, 1.5, 2, 2.5, 5, 5.5
and 8 h for the determination of plasma acylated
ghrelin concentration. These monovettes
contained EDTA and p-hydroxymercuribenzoic
acid to prevent the degradation of acylated
ghrelin by protease. The monovettes were spun
at 1287 g (3500 revs/min) for 10 min in a
refrigerated centrifuge at 4oC. The supernatants
were then aliquoted into storage tubes and 100
μL of 1 M hydrochloric acid was added per mL
of plasma. Samples were then spun at 1287 g
(3500 revs/min) for 5 min in a refrigerated
centrifuge at 4oC before being transferred into
Eppendorf tubes and stored at -80oC for analysis
later.
At each acylated ghrelin blood sampling point,
duplicate 20 µL blood samples were collected
into micropipettes for the measurement of
haemoglobin concentration and triplicate blood
samples were collected into heparinised micro
haematocrit tubes for the determination of
haematocrit. Haemoglobin and haematocrit
values were used to assess plasma volume
changes (16).
Blood biochemistry
To eliminate inter-assay variation, samples from
each participant were analyzed in the same run.
Plasma acylated ghrelin concentrations were
determined by enzyme linked immunoassay
(ELISA) (SPI BIO, Montigny le Bretonneux,
France). The within batch coefficient of
variation (CV) was 4.8%. Total PYY was
measured by ELISA (Diagnostic System
Laboratories, Texas, USA). The within batch
CV was 1.2%. Plasma insulin concentrations
were determined by ELISA (Mercodia, Uppsala,
Sweden). The within batch CV was 3.3%.
Plasma glucose concentrations were determined
by enzymatic, colorimetric methods (Randox
Laboratories Ltd., County Antrim, UK) with the
aid of an automated centrifugal analyzer (Cobas
Mira Plus; Roche, Basel, Switzerland). The
within batch CV was 3.3%.
Statistical Analysis
Data were analyzed using the Statistical Package
for Social Sciences (SPSS) software version
14.0 for Windows (SPSS Inc, Chicago, IL,
USA). Area under the curve (AUC) values were
calculated using the trapezoidal rule. One-way
ANOVA and Bonferroni post-hoc tests were
used to assess differences between fasting and
AUC values across trials. Two-way ANOVA
was used to examine differences between trials
over time. Where significant interactions were
found, between trial differences at each time
6
point were examined using one-way ANOVA
and Bonferroni post-hoc tests. The Pearson
product moment correlation coefficient was used
to examine relationships between variables.
Statistical significance was accepted at the 5%
level. Plasma volume changes did not differ
significantly between trials and the unadjusted
values are reported. Results are given as mean ±
SEM.
RESULTS
Exercise responses
The total weight lifted during the 90 min
resistance exercise session was 10,568 ± 621 kg.
The gross energy expenditure from resistance
exercise was estimated to be 1473 ± 114 kJ. The
mean percentage of maximum oxygen uptake
elicited during aerobic exercise was 69 ± 2%
and the mean respiratory exchange ratio (RER)
was 0.92 ± 0.01. Average heart rate during
running was 167 ± 3 beats/min and the median
rating of perceived exertion (RPE) was 15 i.e.
‘hard’ (range 13-17). Gross energy expenditure
during aerobic exercise was 3832 ± 97 kJ with
27 ± 4% of energy provided from fat and 73 ±
4% of energy provided from carbohydrate. For
comparison gross energy expenditure during the
first hour of the control trial was 363 ± 24 kJ,
the mean RER value during this time was 0.84 ±
0.03 with 47 ± 11% of energy provided from fat
and 53 ± 4% of energy provided from
carbohydrate. Energy expenditure during
running was higher than energy expenditure in
resistance exercise which in turn was higher
than energy expenditure during an equivalent
(90 min) period of rest during the control trial
(P<0.0005 for each).
Hunger
Figure 1 displays the delta (difference from
baseline) scores for hunger on the three trials
(top panel) and the raw scores for hunger
(bottom panel). Fasting hunger did not differ
significantly between trials. There was an effect
of trial (P < 0.037), an effect of time (P < 0.001)
and a trial × time interaction (P < 0.001) for
hunger indicating that responses differed over
time between trials.
On the control trial hunger increased prior to the
first test meal. In response to consuming the first
test meal (t = 2 h) hunger scores fell and
returned to baseline just prior to the second test
meal (t = 5 h). Post-second meal hunger scores
decreased and remained suppressed until the end
of the study period (t = 8 h).
Hunger scores were reduced by resistance
exercise and this reduction became significant at
the 0.75 h time point compared with the control
trial (top panel on Figure 1). After exercise
hunger scores increased but remained
suppressed compared with the control trial in the
pre-meal interval. However, after consumption
of the test meal no further differences between
the resistance and control trials were apparent.
Hunger scores were reduced by aerobic exercise
from the first time point assessed during
exercise (t = 0.5 h) throughout the exercise
period. After exercise hunger scores increased in
the pre-meal interval but remained significantly
suppressed compared with the control trial until
initiation of the first test meal (t = 2 h). After
consumption of the first test meal there were no
differences between control and aerobic exercise
trials.
Aerobic exercise resulted in a greater
suppression of hunger than resistance exercise at
0.75 h and 1 h. Calculation of the AUC for
hunger for the pre-prandial period (0 to 2 h)
revealed that aerobic exercise significantly
reduced hunger in comparison with the control
trial (Table 1). No significant trial differences
were observed when AUC values for the entire
study period were assessed.
INSERT FIGURE 1 NEAR HERE
INSERT TABLE 1 NEAR HERE
Plasma acylated ghrelin and total PYY
Fasting acylated ghrelin concentrations did not
differ significantly between trials. There was an
effect of time (P<0.001) and a trial × time
interaction (P = 0.035) for acylated ghrelin
indicating that compared with the control trial,
values were suppressed at 0.75 h and 1.5 h in the
resistance exercise trial and at 0.75 h in the
aerobic exercise trial (Figure 2). Pre-prandial (0
to 2 h) AUC values were significantly lower
during the resistance exercise trial than the
control trial (Table 1).
7
Fasting PYY concentrations did not differ
significantly between trials. There was a main
effect of trial (P = 0.002), a main effect of time
(P<0.0005) and a trial × time interaction (P =
0.029) for PYY indicating higher values on the
aerobic exercise trial than both the control (P =
0.020) and resistance exercise trials (P = 0.017)
(Figure 2). These findings were confirmed when
analysing AUC values (Table 1). There were no
significant differences between the control and
resistance exercise trials.
INSERT FIGURE 2 NEAR HERE
Glucose and insulin
Fasting plasma glucose concentrations did not
differ significantly between trials. There was a
main effect of trial, a main effect of time and a
trial × time interaction (all P < 0.0005) for
glucose indicating higher values on the aerobic
exercise trial than both the control trial (P =
0.025) and the resistance exercise trial (P =
0.003) (Figure 3, bottom panel). These findings
were confirmed by analysis of the AUC values
for glucose (Table 1).
Fasting plasma insulin concentrations did not
differ significantly between trials. There was a
main effect of time (P<0.0005) but no
significant trial or interaction effects (Figure 3,
top panel). Pre-prandial (0 to 2 h) AUC values
were higher on the resistance exercise trial than
the control trial. There were no other significant
differences when comparing insulin AUC values
(Table 1).
INSERT FIGURE 3 NEAR HERE
Correlations
Baseline plasma acylated ghrelin and PYY
concentrations were not significantly correlated
with BMI, waist circumference, maximum
oxygen uptake, fasting hunger, fasting glucose
concentration or fasting insulin concentration.
Acylated ghrelin and PYY concentrations at
other time points were not consistently
correlated with each other or with corresponding
hunger, glucose and insulin values.
DISCUSSION
This study demonstrates that: 1) hunger is
suppressed during and for a short while after
resistance and aerobic exercise, 2) acylated
ghrelin is suppressed during resistance and
aerobic exercise, 3) PYY is increased during and
after aerobic exercise. In particular the
suppression of hunger and acylated ghrelin
during resistance exercise and the increase in
PYY for a prolonged period after aerobic
exercise are novel findings.
The finding that hunger is suppressed during and
immediately after vigorous treadmill running is
consistent with previous studies indicating that
strenuous (around 60% of maximum oxygen
uptake and above) aerobic exercise transiently
suppresses appetite (6, 9, 29, 39). The hunger
response to resistance exercise has not
previously been examined and the present
findings suggest a similar although slightly
attenuated response in comparison with vigorous
running. One possible explanation for this
attenuation is the lower energy expenditure
during resistance exercise. Another possibility is
that the attenuated responses are due to the
intermittent nature of resistance exercise and the
lower gut disturbance compared with running.
The current study confirms our previous
findings that treadmill running suppresses
acylated ghrelin and extends them by
demonstrating acylated ghrelin suppression
during resistance exercise. It is perhaps
surprising that acylated ghrelin concentrations
were not elevated towards the end of the
exercise trials since energy intake was not
increased in these trials to compensate for the
energy expended during exercise. These data are
consistent with the recent finding that post-
exercise ghrelin responses may be independent
of energy balance (22) and lend support to
previous research indicating that acute exercise
does not increase energy intake in the short term
i.e. one to two days after exercise (6, 7, 24, 28,
29). It would be of interest to examine acylated
ghrelin concentrations the day after exercise to
assess whether values are elevated in response to
a short term negative energy balance.
Only one previous study has examined the PYY
response to exercise (39). This study observed
elevations in PYY during a one-hour cycling
bout. These elevations were not maintained
post-exercise. In the present study PYY
concentrations were increased significantly
during treadmill running. Moreover, after
cessation of exercise total plasma PYY
8
concentrations remained elevated prior to
consuming the first meal and following meal
ingestion. By the end of the observation period,
however, PYY concentrations did not differ
among the three trials. Although PYY was not
elevated post-exercise in the study of Martins
and colleagues (39) they did observe a transient
elevation in GLP-1 after exercise. Another
recent study (12) has demonstrated an increased
GLP-1 response to feeding after five
consecutive days of aerobic exercise (1 h/day).
Collectively these findings suggest that aerobic
exercise exerts a transient, hormone mediated,
inhibition of appetite.
The lack of change in PYY in response to
weight lifting is perplexing in light of the
change in acylated ghrelin with weight lifting. It
is possible that the energy expenditure induced
by weight lifting was insufficient to evoke a
change in PYY. Alternatively, the lack of gut
upheaval and/or a lower perception of stress
during weight lifting in comparison with hard
continuous running may be an explanation. A
limitation of the present study was that total
PYY was measured rather than PYY3-36. The
majority of studies examining circulating PYY
have reported total PYY levels using assays
which detect both the PYY1-36 and PYY3-36 (5,
34, 35, 37, 38). Currently there is only one assay
which is specific for PYY3-36 form and this
requires the addition dipeptidyl peptidase IV
(DPPIV) inhibitor to the blood. As we did not
add DPPIV inhibitor we are unable to measure
PYY3-36. However, we and others have
previously shown that PYY3-36 is the
predominant form both in the fed and fasted
states and in lean and obese subjects (4, 30).
Moreover, we have shown a high positive
correlation (r = 0.98, P < 0.001) between total
PYY and PYY3-36 (49). Whilst future studies
need to be undertaken with DPPIV inhibitor
added to enable the assessment of PYY3-36
available evidence suggests that total PYY
measurements reflect changes in PYY3-36.
Glucose and insulin were measured in the
present study because they may interact with
ghrelin and PYY. The glucose elevation
observed during aerobic exercise might explain
the suppression of acylated ghrelin (46) but
glucose was not elevated when ghrelin was
suppressed in resistance exercise. In the
resistance exercise trial, an elevation in pre-
prandial insulin coincided with a decline in pre-
prandial ghrelin supporting a regulatory role for
insulin (18). Further research is required to
determine the true significance of these findings.
PERSPECTIVES AND SIGNIFICANCE
Previous studies have shown that aerobic
exercise can cause a transient suppression of
appetite that lasts from several hours to two or
more days. The mechanism for this effect is
unknown and the effects of resistance exercise
on appetite are uncertain. The present findings
confirm a transient (1 to 2 h) suppression of
appetite during and after aerobic and resistance
exercise. The findings suggest that ghrelin may
mediate this suppression for both forms of
exercise. There was an elevation in PYY during
and after aerobic exercise and this may possibly
contribute to appetite suppression. Further
research is required to determine how long
exercise induced changes in gut hormones
persist and whether the changes have any effect
on energy intake. A better understanding of the
role of exercise in appetite regulation may lead
to a more effective prescription of exercise for
weight control.
ACKNOWLEDGEMENTS
We thank Mr David Lord, Miss Charlotte
Mathers, Miss Nicola Whitehead and Miss Julia
Zakrzewski for help with the data collection,
and all of the volunteers for their participation in
this study. DRB supervised the data collection
and performed the biochemistry. RLB gave
advice and assistance with the measurement of
peptide YY. JK assisted DRB with data
collection and biochemistry. DJS conceived the
study, performed the venous cannulations and
took the lead in writing the manuscript. All
authors contributed to the writing of the
manuscript. None of the authors had any
conflicts of interest regarding any aspect of this
research.
DISCLOSURE
David Broom’s current affiliation is Sheffield
Hallam University.
9
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13
Table 1: Area under the curve values for hunger, plasma acylated ghrelin, total PYY, glucose and
insulin (mean ± SEM). Findings were analysed using one-way analysis of variance and Bonferroni
post-host tests.
Pre-prandial
0 to 2 h
Postprandial
2 to 5 h
Postprandial
5 to 8 h
Total
0 to 8 h
Hunger
(units 2 h)
(units 3 h)
(units 3 h)
(units 8 h)
Control 19 ± 2 19 ± 3 13 ± 2 51 ± 6
Resistance 12 ± 2 16 ± 2 12 ± 2 40 ± 5
Aerobic 9 ± 1a 16 ± 3 14 ± 3 39 ± 6
Ghrelin
(pg/mL 2 h)
(pg/mL 3 h)
(pg/mL 3 h)
(pg/mL 8 h)
Control 228 ± 62 304 ± 95 279 ± 101 811 ± 257
Resistance 169 ± 55 a 258 ± 67 269 ± 75 696 ± 196
Aerobic 188 ± 68 287 ± 102 261 ± 101 736 ± 270
PYY
(pg/mL 2 h)
(pg/mL 3 h)
(pg/mL 3 h)
(pg/mL 8 h)
Control 229 ± 29 459 ± 44 724 ± 55 1411 ± 110
Resistance 232 ± 43 498 ± 35 651 ± 47 1381 ± 97
Aerobic 324 ± 54 a 663 ± 79 a 763 ± 59 1750 ± 170 ab
Glucose
(mmol/L 2 h)
(mmol/L 3 h)
(mmol/L 3 h)
(mmol/L 8 h)
Control 9.9 ± 0.2 15.5 ± 0.3 15.1 ± 0.4 40.5 ± 0.7
Resistance 9.7 ± 0.2 11.9 ± 0.5 14.9 ± 0.5 38.8 ± 1.1
Aerobic 10.5 ± 0.4
b
16.5 ± 0.4
ab 16.1 ± 0.4 43.1 ± 0.9
ab
Insulin
(pmol/L 2 h)
(pmol/L 3 h)
(pmol/L 3 h)
(pmol/L 8 h)
Control 39 ± 5 272 ± 36 258 ± 21 568 ± 45
Resistance 58 ± 7
a 288 ± 26 220 ± 49 565 ± 60
Aerobic 46 ± 5 289 ± 25 237 ± 23 572 ± 46
Notes: Aerobic exercise was performed for the first hour of the pre-prandial period (0-1 h); resistance
exercise was performed for the first 90 minutes of the pre-prandial period (0-1.5 h); the units are area
under the curve values over 2 hours, 3 hours, 3 hours and 8 hours respectively for columns 1 to 4.
a Different from control P<0.05
b Different from resistance P<0.05
14
LEGENDS FOR FIGURES
FIGURE 1
Delta (i.e. change from baseline) hunger scores (top panel) and absolute hunger scores (bottom panel)
during the three trials (mean ± SEM, n = 11). Lightly shaded rectangle indicates the treadmill run,
open rectangle indicates weight lifting, black rectangles indicate consumption of the test meals.
a Control different from aerobic exercise P<0.05, b control different from resistance exercise P<0.05,
c aerobic exercise different from resistance exercise P<0.05. Error bars are omitted from some trials
for clarity.
FIGURE 2
Plasma concentrations of acylated ghrelin (top panel) and total PYY (bottom panel) during the three
trials (mean ± SEM, n = 11). Lightly shaded rectangle indicates the treadmill run, open rectangle
indicates weight lifting, black rectangles indicate consumption of the test meals. a Control different
from aerobic exercise P<0.05, b control different from resistance exercise P<0.05, c aerobic exercise
different from resistance exercise P<0.05. Error bars are omitted from some of trials for clarity.
FIGURE 3
Plasma concentrations of insulin (top panel) and glucose (bottom panel) during the three trials (mean
± SEM, n = 11). Lightly shaded rectangle indicates the treadmill run, open rectangle indicates weight
lifting, black rectangles indicate consumption of the test meals. a Aerobic exercise different from
control P<0.05, b Aerobic exercise different from resistance exercise P<0.05. Error bars are omitted
from some trials for clarity.
Figure 1
0
2
4
6
8
10
12
14
012345678
Time (Hours)
Hunger (0 Not Hungry - 15 Very Hungry)
a
a
aa
,
b
cc
-6
-4
-2
0
2
4
6
Hunger (delta score)
Control
Resistance exercise
Aerobic exercise
a
a,b
a,b
b
b
Figure 2
0
40
80
120
160
Plasma acylated ghrelin (pg/mL)
Control
Resistance exercise
Aerobic exercise
a,b
b
0
80
160
240
320
012345678
Time (Hours)
Plasma total PYY (pg/mL)
a,c
a
c
c
Figure 3
0
30
60
90
120
150
180
Plasma insulin (pmol/L)
Control
Resistance exercise
Aerobic exercise
0.0
1.0
2.0
3.0
4.0
5.0
6.0
7.0
012345678
Time (Hours)
Plasma glucose (mmol/L)
a,b
ba,b
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8 ‫ﭘﭙﺘﯿﺪ‬ ‫ﺑﺮ‬ ‫ﻣﻘﺎوﻣﺘﯽ‬ ‫ﺗﻤﺮﯾﻦ‬ ‫ﻫﻔﺘﻪ‬ YY ‫ﻓﻌﺎل‬ ‫ﻏﯿﺮ‬ ‫ﭼﺎق‬ ‫زﻧﺎن‬ ‫در‬ ‫اﺳﺪ‬ ‫ﻣﺤﻤﺪرﺿﺎ‬ 1 * ‫آﻫﻮر‬ ‫ﻋﻠﯽ‬ ، 2 ‫ﻧﺠﻔﯽ‬ ‫ﻣﻬﻨﺎز‬ ، 3 ‫اﺳﻤﺎﻋﯿﻠﯽ‬ ‫ﻧﺎﻫﯿﺪ‬ ، 4 1 ‫ﻧﻮر‬ ‫ﭘﯿﺎم‬ ‫داﻧﺸﮕﺎه‬ ‫اﺳﺘﺎدﯾﺎر‬. 2 ‫ﻧﻮر‬ ‫ﭘﯿﺎم‬ ‫داﻧﺸﮕﺎه‬ ‫ﺑﺪﻧﯽ‬ ‫ﺗﺮﺑﯿﺖ‬ ‫ارﺷﺪ‬ ‫ﮐﺎرﺷﻨﺎس‬. 3 ‫ﻧﻮر‬ ‫ﭘﯿﺎم‬ ‫داﻧﺸﮕﺎه‬ ‫ﺑﺪﻧﯽ‬ ‫ﺗﺮﺑﯿﺖ‬ ‫ارﺷﺪ‬ ‫ﮐﺎرﺷﻨﺎس‬. 4 ‫ﻧﻮر‬ ‫ﭘﯿﺎم‬ ‫داﻧﺸﮕﺎه‬ ‫ﺑﺪﻧﯽ‬ ‫ﺗﺮﺑﯿﺖ‬ ‫ارﺷﺪ‬ ‫ﮐﺎرﺷﻨﺎس‬. ‫ﻣﻘﺎﻟﻪ:‬ ‫درﯾﺎﻓﺖ‬ ‫ﺗﺎرﯾﺦ‬ 20 / 12 / 92 ‫ﺗﺎرﯾ‬ ‫ﻣﻘﺎﻟﻪ:‬ ‫ﭘﺬﯾﺮش‬ ‫ﺦ‬ 26 / 8 / 93 ‫ﭼﮑﯿﺪه‬ ‫ﭘﭙﺘﯿﺪ‬ YY ‫دارد‬ ‫اﺳﺎﺳﯽ‬ ‫ﻧﻘﺶ‬ ‫ﻏﺬا‬ ‫درﯾﺎﻓﺖ‬ ‫ﺗﻨﻈﯿﻢ‬ ‫در‬ ‫ﮐﻪ‬ ‫اﺳﺖ‬ ‫اي‬ ‫روده‬ ‫ﭘﭙﺘﯿﺪ‬ ،. ‫ﭘﭙﺘﯿﺪ‬ ‫ﺗﻐﯿﯿﺮات‬ ‫ﺣﺎل‬ ‫اﯾﻦ‬ ‫ﺑﺎ‬ YY ‫ﺗﻤﺮﯾﻨـﺎت‬ ‫ﺑﺎ‬ ‫ﺳﺎزﮔﺎري‬ ‫از‬ ‫ﭘﺲ‬ ‫ﭘﻼﺳـﻤﺎﯾ‬ ‫ﺳـﻄﻮح‬ ‫ﺑـﺮ‬ ‫ﻣﻘـﺎوﻣﺘﯽ‬ ‫ﺗﻤـﺮﯾﻦ‬ ‫ﻫﻔﺘـﻪ‬ ‫ﻫﺸﺖ‬ ‫اﺛﺮ‬ ‫ﺑﺮرﺳﯽ‬ ‫ﭘﮋوﻫﺶ‬ ‫اﯾﻦ‬ ‫از‬ ‫ﻫﺪف‬ ‫اﺳﺖ.‬ ‫ﻧﮕﺮﻓﺘﻪ‬ ‫ﻗﺮار‬ ‫ﺑﺮرﺳﯽ‬ ‫ﻣﻮرد‬ ‫ﮐﻨﻮن‬ ‫ﺗﺎ‬ ‫ﻣﻘﺎوﻣﺘﯽ‬ ‫ﯽ‬ ‫ﭘﭙﺘﯿﺪ‬ YY ‫راﺳﺘﺎ‬ ‫اﯾﻦ‬ ‫در‬ ‫ﺑﻮد.‬ ‫ﻓﻌﺎل‬ ‫ﻏﯿﺮ‬ ‫ﭼﺎق‬ ‫زﻧﺎن‬ ‫در‬ ‫ﻧﺎﺷﺘﺎﯾﯽ‬ 24) ‫ﺳﻦ‬ ‫ﻣﯿﺎﻧﮕﯿﻦ‬ ‫ﺑﺎ‬ ‫ﭼﺎق‬ ‫زن‬ ‫ﻧﻔﺮ‬ 24 / 2 ± 08 / 33 ‫ﺑﯿﻤـﺎري‬ ‫ﺳـﺎﺑﻘﻪ‬ ‫ﮐﻪ‬ ‫ﺳﺎل(‬ ‫ﺗﺠﺮﺑﯽ‬ ‫ﮔﺮوه‬ ‫دو‬ ‫در‬ ‫ﺗﺼﺎدﻓﯽ‬ ‫ﻃﻮر‬ ‫ﺑﻪ‬ ‫ﻧﺪاﺷﺘﻨﺪ،‬ ‫ﺧﺎﺻﯽ‬ n=13) (‫ﮐﻨﺘﺮل‬ ‫و‬ n=11) ‫وزن،‬ ‫ﻗـﺪ،‬ ‫ﻣﺜـﻞ‬ ‫ﮔـﺮوه‬ ‫دو‬ ‫اوﻟﯿـﻪ‬ ‫اﻃﻼﻋـﺎت‬ ‫ﮔﺮﻓﺘﻨﺪ.‬ ‫ﻗﺮار‬ (‫ﺗﻮد‬ ‫ﺷﺎﺧﺺ‬ ‫و‬ ‫ﭼﺮﺑﯽ‬ ‫درﺻﺪ‬ ‫و‬ ‫وزﻧـﻪ‬ ‫ﺑﺎ‬ ‫اي‬ ‫داﯾﺮه‬ ‫ﺻﻮرت‬ ‫ﺑﻪ‬ ‫ﺗﻤﺮﯾﻨﯽ‬ ‫ﺑﺮﻧﺎﻣﻪ‬ ‫ﺑﺎ‬ ‫ﺗﺠﺮﺑﯽ‬ ‫ﮔﺮوه‬ ‫ﺳﭙﺲ‬ ‫ﺷﺪ.‬ ‫ﮔﯿﺮي‬ ‫اﻧﺪازه‬ ‫ﻣﺨﺼﻮص‬ ‫وﺳﺎﯾﻞ‬ ‫ﺑﺎ‬ ‫ﺑﺪن‬ ‫ه‬ ‫ﻣﺪت‬ ‫ﺑﻪ‬ ‫ﺑﺎر‬ ‫اﺿﺎﻓﻪ‬ ‫اﺻﻞ‬ ‫رﻋﺎﯾﺖ‬ ‫ﺑﺎ‬ ‫و‬ ‫اﺻﻠﯽ‬ ‫ﻋﻀﻼت‬ ‫ﺑﮑﺎرﮔﯿﺮي‬ ‫ﺑﺎ‬ 8 ‫ﻫﻔﺘﻪ‬ ‫ﻫﺮ‬ ‫و‬ ‫ﻫﻔﺘﻪ‬ 3 ‫ﺣﺎﻟـﺖ‬ ‫در‬ ‫ﮔﯿﺮي‬ ‫ﺧﻮن‬ ‫ﻣﺮﺣﻠﻪ‬ ‫دو‬ ‫ﻧﻤﻮد.‬ ‫ﺗﻤﺮﯾﻦ‬ ‫ﺟﻠﺴﻪ‬ 12 ‫و‬ ‫ﺗﻤﺮﯾﻦ‬ ‫ﺷﺮوع‬ ‫از‬ ‫ﻗﺒﻞ‬ ‫ﻧﺎﺷﺘﺎﯾﯽ،‬ ‫ﺳﺎﻋﺖ‬ 48 ‫ﺳﺎﻋ‬) ‫ﮔﺮﻓﺖ‬ ‫اﻧﺠﺎم‬ ‫اﻓﺮاد‬ ‫ﺗﻤﺎﻣﯽ‬ ‫از‬ ‫ﺗﻤﺮﯾﻦ‬ ‫ﺟﻠﺴﻪ‬ ‫آﺧﺮﯾﻦ‬ ‫از‬ ‫ﭘﺲ‬ ‫ﺖ‬ 2 ‫دﺳﺖ‬ ‫ﺳﺎﻋﺪ‬ ‫از‬ ‫ﺳﯽ‬ ‫ﺳﯽ‬ ‫ﻫﻮرﻣـﻮن‬ ‫ﺳـﻄﻮح‬ ‫دار‬ ‫ﻣﻌﻨـﯽ‬ ‫ﺗﻐﯿﯿـﺮ‬ ‫ﺑﺎﻋـﺚ‬ ‫ﻣﻘـﺎوﻣﺘﯽ‬ ‫ﺗﻤﺮﯾﻦ‬ ‫ﮐﻪ‬ ‫ﺑﻮد‬ ‫ﻣﻮﺿﻮع‬ ‫اﯾﻦ‬ ‫ﺑﯿﺎﻧﮕﺮ‬ ‫ﭘﮋوﻫﺶ‬ ‫اﯾﻦ‬ ‫از‬ ‫آﻣﺪه‬ ‫ﺑﺪﺳﺖ‬ ‫ﻧﺘﺎﯾﺞ‬ ‫ﭼﭗ(.‬ ‫ﭘﭙﺘﯿـﺪ‬ YY ‫ﮔﺮدﯾﺪه‬ ‫ﻫﻮرﻣﻮن‬ ‫اﯾﻦ‬ ‫ﻧﺎﺷﺘﺎﯾﯽ‬ ‫ﺳﻄﺢ‬ ‫ﮐﺎﻫﺶ‬ ‫ﺑﺎﻋﺚ‬ ‫و‬ ‫ﮐﻨﺘﺮل‬ ‫ﮔﺮوه‬ ‫ﺑﻪ‬ ‫ﻧﺴﺒﺖ‬ ‫ﺗﺠﺮﺑﯽ‬ ‫ﮔﺮوه‬ ‫اﺳﺖ‬ (p=0/001) ، ‫ﻻ‬ ‫اﺣﺘﻤـﺎ‬ ‫ﻣﻮﺿـﻮع‬ ‫اﯾـﻦ‬ ‫ﮐـﻪ‬. ‫ﺑﺎﺷﺪ‬ ‫ﻣﯽ‬ ‫ﺗﻤﺮﯾﻨﺎت‬ ‫ﻃﯽ‬ ‫رﻓﺘﻪ‬ ‫دﺳﺖ‬ ‫از‬ ‫اﻧﺮژي‬ ‫ﺟﺒﺮان‬ ‫ﻋﻠﺖ‬ ‫ﺑﻪ‬ ‫ﻏﺬا‬ ‫درﯾﺎﻓﺖ‬ ‫ﺑﻪ‬ ‫ﺑﯿﺸﺘﺮ‬ ‫ﺗﻤﺎﯾﻞ‬ ‫و‬ ‫اﺷﺘﻬﺎ‬ ‫اﻓﺰاﯾﺶ‬ ‫ﺑﯿﺎﻧﮕﺮ‬ ‫ﺧﻮد‬ ‫واژه‬ ‫ﮐﻠﯿﺪ‬ ‫ﻫﺎ:‬ ‫ﻣﻘﺎوﻣﺘﯽ،‬ ‫ﺗﻤﺮﯾﻦ‬ PYY3-36 ‫ﻓﻌﺎل‬ ‫ﻏﯿﺮ‬ ‫ﭼﺎق‬ ‫زﻧﺎن‬ ‫ﻏﺬا،‬ ‫ﺗﻨﻈﯿﻢ‬ ، The effect of eight weeks resistance training in response to PYY hormone in nonathletic fat women Abstract PYY is an intestinal peptid that has a basic role in control of receiving food. However, changes of PYY after adaptaion to resistance training has not been examined. The purpose of this research is examining of the effect of eight weeks resistance training on PYY levels of the plasma in nonathletic fat women in the fast conditions. For this purpose, 24 fat women with average age (33/08±2/24 year) that had not antecedent in a specific sickness accidentally divided into experimental group (n=13) and control group (n=11). The amount of weight, eight, percent of fat and body mass index (BMI) as primary data were measured by specific instruments. Then, experimental group did circle training with weight and by using main muscles and regarding excess load principle for eight weeks and 3 sessions of a week. Two procedures of blooding was done, one was done in the morning while all subjects had not eaten anything for 12 hours and the other one was done 48 hours after the last session of training (2cc from left forearm). The results show that resistance training significantly changesPYY levels of experimental group (p=0/001) in compare to control group and decreased level of this hormone in the fast conditions. This shows increased appetite and desire to eat to compensate the amount of energy that is used during the training.
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Despite the irrefutable benefits of achieving the UK Chief Medical Officers physical activity guidelines, including the prevention and treatment of non-communicable diseases for people with obesity, misrepresentation of physical activity and exercise in mainstream media has become a public health problem. This poor representation of physical activity and exercise is damaging and could contribute to uncertainty regarding the role of energy expenditure in weight management. When healthcare professionals fail to promote physical activity and exercise in the populations that need it, the impact of this misinformation can be very damaging. This chapter addresses physical activity, exercise, and weight management issues for people with obesity. By firstly challenging misconceptions that exercise makes you hungrier and eat more at the next meal and thereafter presenting evidence that physical activity can contribute to weight loss but more importantly weight loss maintenance and the prevention of weight regain. Finally, examples of key considerations when trying to increase physical activity and exercise in people with obesity are provided.KeywordsPhysical activityExerciseEnergy expenditureObesity
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Obesity is one of the major pandemics of the 21st century. Due to its multifactorial etiology, its treatment requires several actions, including dietary intervention and physical exercise. Excessive fat accumulation leads to several health problems involving alteration in the gut-microbiota-brain axis. This axis is characterized by multiple biological systems generating a network that allows bidirectional communication between intestinal bacteria and brain. This mutual communication maintains the homeostasis of the gastrointestinal, central nervous and microbial systems of animals. Moreover, this axis involves inflammatory, neural, and endocrine mechanisms, contributes to obesity pathogenesis. The axis also acts in appetite and satiety control and synthesizing hormones that participate in gastrointestinal functions. Exercise is a nonpharmacologic agent commonly used to prevent and treat obesity and other chronic degenerative diseases. Besides increasing energy expenditure, exercise induces the synthesis and liberation of several muscle-derived myokines and neuroendocrine peptides such as neuropeptide Y, peptide YY, ghrelin, and leptin, which act directly on the gut-microbiota-brain axis. Thus, exercise may serve as a rebalancing agent of the gut-microbiota-brain axis under the stimulus of chronic low-grade inflammation induced by obesity. So far, there is little evidence of modification of the gut-brain axis as a whole, and this narrative review aims to address the molecular pathways through which exercise may act in the context of disorders of the gut-brain axis due to obesity.
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Human studies and assays Test meals were prepared using conventional pasta (Sainsbury, London UK) or high- protein pasta (Atkins, Shelton, CT, USA) with a tomato based sauce. Additional protein, carbohydrate and fat supplements were added (Maxipro, UK, Maxijuel and Calogen, SHS International, Merseyside, UK) to the tomato sauce and dessert. Blood was collected into EDTA tubes containing 5000 kallikrein inhibitor units of aprotonin (Bayer, Newbury, Berks, U.K.) per ml. Plasma samples were separated immediately by centrifugation at 4°C. For subsequent PYY (total and PYY3-36) and active GLP-1 DPPIV inhibitor (Linco Research Inc., St Louis, MO, USA) was added to plasma samples to give a final concentration of 100 µM. Samples for analysis of active ghrelin had 100 µl of 1M HCL added per ml of plasma. ELISA kits were used to quantify desacyl-ghrelin, active-ghrelin,
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The ability to maintain adequate nutrient intake is critical for survival. Complex interrelated neuronal circuits have developed in the mammalian brain to regulate many aspects of feeding behaviour, from food-seeking to meal termination. The hypothalamus and brainstem are thought to be the principal homeostatic brain areas responsible for regulating body weight1, 2. However, in the current ‘obesogenic’ human environment food intake is largely determined by non-homeostatic factors including cognition, emotion and reward, which are primarily processed in corticolimbic and higher cortical brain regions3. Although the pleasure of eating is modulated by satiety and food deprivation increases the reward value of food, there is currently no adequate neurobiological account of this interaction between homeostatic and higher centres in the regulation of food intake in humans1, 4, 5. Here we show, using functional magnetic resonance imaging, that peptide YY3–36 (PYY), a physiological gut-derived satiety signal, modulates neural activity within both corticolimbic and higher-cortical areas as well as homeostatic brain regions. Under conditions of high plasma PYY concentrations, mimicking the fed state, changes in neural activity within the caudolateral orbital frontal cortex predict feeding behaviour independently of meal-related sensory experiences. In contrast, in conditions of low levels of PYY, hypothalamic activation predicts food intake. Thus, the presence of a postprandial satiety factor switches food intake regulation from a homeostatic to a hedonic, corticolimbic area. Our studies give insights into the neural networks in humans that respond to a specific satiety signal to regulate food intake. An increased understanding of how such homeostatic and higher brain functions are integrated may pave the way for the development of new treatment strategies for obesity.
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