TEMPERATURE

2017, VOL. 4, NO. 2, 166–175

https://doi.org/10.1080/23328940.2017.1294235

RESEARCH PAPER

Leptin, adiponectin, and ghrelin responses to endurance exercise in different

ambient conditions
Terence L. Laursena, Roksana B. Zaka, Robert J. Shutea, Matthew W. S. Heeschb, Nicholas E. Dinana,
Matthew P. Bubaka, D. Taylor La Sallea, and Dustin R. Slivkaa
a
School of Health, Physical Education, and Recreation, Exercise Physiology Laboratory, University of Nebraska-Omaha, Omaha, NE, USA;
b
Kinesiology Department, Washburn University, Topeka, KS, USA

ABSTRACT ARTICLE HISTORY

Excessive positive energy balance is a major factor leading to obesity. The ability to alter the Received 18 November 2016
appetite-regulating hormones leptin, adiponectin, and ghrelin may help decrease excessive energy Revised 7 February 2017
intake. Exercise and exposure to extreme temperatures can independently affect these appetite- Accepted 7 February 2017
regulating hormones. PURPOSE: To determine the effect of exercising in different environmental KEYWORDS
conditions on the circulating concentrations of leptin, adiponectin, and ghrelin. METHODS: Eleven adipokines; appetite; cold;
recreationally-trained male participants completed 3 separate 1 h cycling bouts at 60% Wmax in hot, exercise; hormones; hot;
cold, and room temperature conditions (33 C, 7 C, 20 C), followed by a 3 h recovery at room temperature
temperature. Blood was drawn pre-exercise, post-exercise, and 3 h post-exercise. Hematocrit and
hemoglobin were measured to account for change in plasma volume. RESULTS: Leptin
concentrations were lower at post and 3 h post-exercise compared with pre-exercise, with and
without correction for plasma volume shifts, regardless of temperature (p < 0.05). Adiponectin was
higher post-exercise compared with pre-exercise (p D 0.021) but not 3 h post-exercise (p D 0.084)
without correction for plasma volume shifts. However, adiponectin concentrations were not
different at any time point when plasma volume shifts were accounted for (p > 0.05). Total ghrelin
and acylated ghrelin concentrations were not affected at post and 3 h post-exercise compared with
pre-exercise, with and without correcting for plasma volume shifts, regardless of ambient
temperature (p > 0.05). No differences in leptin, adiponectin, or ghrelin were found between trials
(p > 0.05). CONCLUSION: Temperature does not affect the circulating concentrations of appetite-
regulating hormones during an acute bout of endurance exercise.

Introduction
Environmental temperature has a large impact on fat
mass and metabolic homeostasis. Indigenous popula-
tions that live in polar climates have elevated basal
metabolic rates and decreased fat mass,1-3 whereas
populations from tropical climates have decreased
basal metabolic rates and increased fat mass.4,5 Thus,
there appears to be an effect of temperature on energy
balance. However, the relationship between environ-
mental temperature and the circulating concentration
of appetite-regulating hormones is less clear. Exercise
has been shown to be an effective method for altering
the appetite-regulating hormones leptin, adiponectin,
and ghrelin.6-14 Exercise in a hot environment, com-
pared with a room temperature environment appears
to attenuate appetite.15,16 However, exercise in a cold
environment may stimulate appetite.17
Adipose tissue plays an important role in the effect
that different environmental temperatures have on
appetite.18 Adipose tissue can act as an endocrine
organ, instead of solely as an energy storage
depot.19-22 Adipokines are secreted by adipose tissue
and are involved in homeostatic and appetite-regulat-
ing signaling in the body. Specifically, leptin23 and adi-
ponectin24 are adipokines that play a major role in
energy homeostasis and appetite regulation.25 Leptin
signals the hypothalamus that energy requirements
are being met and that no more food intake is
required.26 Adiponectin also acts at the hypothalamus
but works to stimulate food intake.27 Ghrelin is

CONTACT Dustin R. Slivka dslivka@unomaha.edu School of Health, Physical Education, and Recreation, University of Nebraska-Omah, 6001 Dodge
Street, HPER #207R, Omaha, NE 68182, USA.
© 2017 Taylor & Francis

produced and released from the fundus of the stom-
ach.28 Unlike leptin, ghrelin is an orexigenic or an
appetite-stimulating hormone.29 Acylation of ghrelin
is essential for appetite regulation.30 The ability to
alter these hormones could lead to a better control of
appetite and potentially used in treating conditions
commonly associated with increased levels of fat mass
such as obesity, metabolic syndrome, and type 2 dia-
betes. Increasing leptin concentrations and decreasing
adiponectin and ghrelin may lead to a decreased appe-
tite. This change in hormone concentration could lead
to a reduction in caloric intake and thus a more nega-
tive energy balance resulting in a subsequent reduc-
tion in fat mass.
Exercise is a well-known therapy to combat the
conditions of obesity, metabolic syndrome, and diabe-
tes.31 Circulating concentrations of leptin generally
decrease,6-8,13,14 whereas adiponectin generally
increases in response to an exercise bout.9-12 It has
been demonstrated that an acute exercise bout sup-
presses plasma levels of acylated ghrelin,30 but has no
effect on total ghrelin.32 Thus, exercise induces an
increased appetite in an attempt to replace energy
reserves. However, there is contradicting evidence that
claims exercise has no effect on these hormones.6,7,33-
35
The exact response of these hormones appears to be
influenced by intensity, mode, and duration of exer-
cise and may help explain the variability of response
in these previous studies.
The ambient temperature may further alter adipo-
kine response related to appetite. Research investigat-
ing the relationship between environmental
temperature and the cytokines responsible for appetite
regulation is limited to few human trials. These
research studies show no change in circulating hor-
mone levels. Current study investigates the influence
of temperature in conjunction with endurance exer-
cise on circulating hormone levels. To our knowledge,
this is the first study attempting to investigate this
relationship in a human model. Previously, results in
human trials demonstrated conflicting results.15,16,36
However, in a mouse model, heat exposure generally
increased leptin and adiponectin concentration while
cold exposure decreased leptin and adiponectin con-
centration.37-40
Temperature and exercise both appear to indepen-
dently affect leptin, adiponectin, and ghrelin. The
potential impact of exercising in different environ-
mental temperatures on appetite-regulating hormones
TEMPERATURE 167
is unknown. If there is an effect, however, it may lead
to the development of temperature-optimized exercise
protocols to control appetite. These temperature-opti-
mized protocols could be implemented in the preven-
tion and treatment of chronic conditions associated
with excessive positive energy balance. Thus, the pur-
pose of the current study is to determine the effects of
exercise in hot, cold, and room temperature environ-
mental conditions on circulating levels of leptin, adi-
ponectin, and ghrelin in humans.
Materials and methods
Subjects
This study recruited 11 recreationally-trained male
subjects (age 25 § 4, height 178 § 5 cm, weight 79.4
§ 13.5 kg, body fat 14.7 § 3.6%, VO2peak 54.6 §
12.0 ml¢ kg¡1¢ min¡1, power at VO2peak 277 § 41 W).
Recreationally-trained was defined as engaging in
physical activity at least 1-2 times per week. Due to
hormonal differences in men and women, exclusively
male subjects were recruited for the study. Participants
were between the ages of 19 and 45 and capable of
cycling consistently for one hour. Participants were
considered “low risk” according to ACSM risk stratifi-
cation. All participants were to understand and sign
an Institutional Review Board approved informed
consent form before participating in this study.
Preliminary testing
The initial testing session included an exercise proto-
col to determine maximal aerobic capacity and collec-
tion of participant descriptive data. Specifically, height
(Seca North America, Chino, CA), weight (Befour,
Saukville, WI), body composition and VO2peak were
assessed. Body composition was assessed using a
hydrostatic weighing technique that uses a custom
load cell based system (Exertech, Dresbach, MN).
Body density was converted to percent body fat using
the Siri equation.41 To determine VO2peak participants
performed a graded exercise test using an electroni-
cally braked cycle ergometer (Velotron, RacerMate
Inc., Seattle WA). The test began at 95 W and work-
load was increased by 35 W every 3 min. Participants
cycled until volitional fatigue and the highest VO2
obtained was recorded as the VO2peak. The maximum
workload was measured by adding the highest com-
pleted stage (in watts) to the proportion of the last
168 T. L. LAURSEN ET AL.
stage multiplied by the 35 W per stage increment.
During the experimental trials participants cycled at
60% of this maximum calculated workload.
Experimental protocol
Each participant completed 3 separate trials that were
no less than 4 and no more than 7 d apart. Average
monthly temperature for the testing period (April–
May) was 56.8 F. Participants tested were natives of
the area, therefore not recently exposed to prolonged
periods of hot or cold climates.
For each trial, the subject cycled in one of the
experimental environmental conditions chosen by a
randomized, counterbalanced, repeated measures
design. The 3 trials consisted of a hot (33 C, 60%
humidity), cold (7 C, 60% humidity), or room tem-
perature (20 C, 60% humidity) environment. Partici-
pants came into the laboratory following a 12 h
overnight fast and having not engaged in exercise
within the previous 24 h. A 24 h food consumption
log was maintained by the participant and replicated
as closely as possible between trials. As subjects ini-
tially entered the laboratory, urine specific gravity was
tested to ensure consistent hydration between trials
(Pocket Refractometer, ATAGO Tokyo, Japan). Prior
to exercise, a resting blood draw (»6 mL) was taken
from the antecubital vein of the arm. During the
experimental portion of the trial, participants cycled
at 60% of the peak aerobic power that was previously
determined. The cycling bout was one hour in a tem-
perature and humidity controlled environmental
chamber (Darwin Chamber Company, St. Louis,
MO). During the exercise bout, subjects were also
required to ingest 500 mL of water. Immediately post-
exercise, subjects were removed from the chamber,
had blood drawn, and began a 3 h recovery period
lying in a supine position quietly at room temperature
(»22 C). Participants were not allowed to eat during
Figure 1. Schematic representation of the protocol. RPE: rating of
perceived exertion, EV: environmental conditions, CT: core tem-
perature, ST: skin temperature.
the recovery. At the end of the 3 h recovery period
another blood draw was taken (Fig. 1).
Measurements
Core temperature, skin temperature, and heart rate
Immediately upon arrival for the experimental trials
(»45 min before exercise), subjects ingested a Jonah
Core Body Temperature Capsule (JCBC, Hidalgo Lim-
ited, Cambridge, UK). After capsule ingestion, subjects
drank 125 mL of water and ate a fiber bar (Fiber One
bar, 140 kcal, 4 g fat, 29 g carbohydrates, 2 g protein)
to facilitate movement of the capsule out of the stom-
ach and into the small intestine. The capsule transmit-
ted core temperature data and heart rate to an EQ02
LifeMonitor Sensor Electronics Module vest (SEM,
Hidalgo Limited, Cambridge, UK) that was worn
throughout the exercise and recovery.
Blood draws and plasma levels
Blood draws were taken before exercise, immediately
post-exercise, and 3 h post-exercise from the antecubi-
tal vein of the arm. Approximately 6 mL of blood was
drawn into an Ethylenediaminetetraacetic acid
(EDTA) coated vacutainer, (Greiner Bio-One, Mon-
roe, NC) and whole blood was immediately tested for
hematocrit (ZIPOcrit, LW Scientific, Lawrenceville,
GA) and hemoglobin (HemoCue Cypress, CA) for the
calculation of plasma volume shifts that occurred
throughout each trial.42 The whole blood was then
centrifuged at 10,000 X g for 15 min to separate
plasma for later analysis. The plasma was aliquoted
and stored at ¡80 C.
Circulating leptin, adiponectin, and ghrelin
Circulating plasma levels of the hormones of interest
were quantified by enzyme-linked immunosorbent assays
(ELISA). Protocols for each specific hormone were com-
pleted according to manufacturer’s instructions. Prepack-
aged ELISA kits from Invitrogen (Life Technologies
Corporation, Frederick, MD) were used to measure leptin
and adiponectin. Prepackaged ELISA kits from Sigma-
Aldrich (St. Louis, MO) were used to measure total ghre-
lin and kits from LifeSpan BioSciences Inc. (Seattle, WA)
were used for acylated ghrelin. Plasma samples were
diluted 1:100 for leptin, 1:2000 for adiponectin. No dilu-
tions were used for ghrelin.

Statistical analysis
Environmental temperature, core and skin temperature,
heart rate, VO2, and plasma content of each of the hor-
mones of interest were analyzed with a repeated measures
2-way ANOVA (time x trial). If F-ratio values were found
to be significant, a Fisher’s protected LSD (least signifi-
cant difference) post hoc was performed to evaluate
where significance occurred. A probability of type I error
of less than 5% was considered significant (p < 0.05). All
statistical data were analyzed using the Statistical Package
for Social Sciences software (SPSS 23.0; Chicago, IL).
Data are reported as mean § SE (standard error).
Results
Core and skin temperature
Core temperature was higher in the hot condition than
the cold and room temperature conditions at 50, 55, and
60 min (p < 0.05; Fig. 2). During recovery, core tempera-
ture was higher in the hot condition (37.4 § 0.3 C) com-
pared with the cold (37.1 § 0.3 C, p D 0.001), and room
temperature conditions (37.1 § 0.2 C, p D 0.038),
regardless of time. Skin temperature was highest in the
hot condition and lower in the cold condition, compared
with the room temperature condition by minute 5 of
exercise and persisted to be different throughout the exer-
cise bout (p < 0.001; Fig. 3). During the recovery period,
there were no differences in skin temperature between
the 3 conditions (hot: 34.2 § 1.0 C, cold: 33.6 § 1.1 C,
room temperature: 34.4 § 0.8 C; p D 0.101).
Oxygen consumption
During exercise, both absolute and relative oxygen
consumption were higher in the hot condition (3.0 §
Figure 2. Core temperature during exercise. p < 0.05 from
room temperature and cold conditions. Data are mean § SE. RT:
room temperature.
TEMPERATURE 169
Figure 3. Skin temperature during exercise. p <0.05 between all
conditions. Data are mean § SE. RT: room temperature.
0.5 L¢ min¡1, 38.5 § 6.6 mL ¢ kg¡1 ¢ min¡1) and lower
in the cold condition (2.7 § 0.4 L¢ min¡1, 34.5 §
5.4 mL ¢ kg¡1 ¢ min¡1), compared with room tempera-
ture (2.8 § 0.4 L¢ min¡1, 35.7 § 5.3 mL ¢ kg¡1 ¢
min¡1; p < 0.05). During recovery there were no dif-
ferences in absolute (hot: 0.35 § 0.05 L¢ min¡1, cold:
0.33 § 0.05 L¢ min¡1, room temperature: 0.34 §
0.05 L¢ min¡1; p D 0.237), or relative oxygen con-
sumption (hot: 4.5 § 0.4 mL ¢ kg¡1 ¢ min¡1, cold: 4.3
§ 0.4 mL ¢ kg¡1 ¢ min¡1, room temperature: 4.3 §
0.5 mL ¢ kg¡1 ¢ min¡1; p D 0.236).
Heart rate
During exercise, heart rate in the hot condition (165 §
10 bpm) was higher than in the cold (152 § 8 bpm)
and room temperature condition (154 § 11 bpm; p <
0.001), but no difference was observed between cold
and room temperature (p D 0.318) conditions. During
recovery, there were no differences in heart rate, but
there was a trend toward higher heart rate in the hot
condition (82 § 11 bpm) compared with cold (75 §
12 bpm) and room temperature (76 § 10 bpm; p D
0.067) conditions.
Plasma leptin concentrations
Hematocrit and hemoglobin levels were significantly
lower in the hot condition, compared with cold and
room temperature conditions (p < 0.05).
There were no differences in leptin concentrations
between any of the temperature conditions when concen-
trations were not corrected for plasma volume shifts (p D
0.458; Fig. 4A), or when concentrations were corrected
for plasma volume shifts (p D 0.465; Fig. 4B). However,
leptin concentrations were lower at post-exercise and 3 h
post-exercise when compared with pre-exercise
170 T. L. LAURSEN ET AL.
Figure 4. (A) Leptin concentration not correcting for plasma vol-
ume shifts. (B) Leptin concentration corrected for plasma volume
shifts. p < 0.05 from pre-exercise (main effect of time). Data are
mean § SE.
regardless of temperature and with and without correct-
ing for plasma volume shifts (p < 0.05, Fig. 4).
Plasma adiponectin concentrations
There were no differences in adiponectin concentrations
between any of the temperature conditions without cor-
recting concentration for plasma volume shifts (p D
0.752; Fig. 5A), or when concentrations were corrected
Figure 5. (A) Adiponectin concentration not corrected for plasma
volume shifts. (B) Adiponectin concentration corrected for plasma
volume shifts. p < 0.05 from pre-exercise (main effect of time).
Data are mean § SE.
for plasma shifts (p D 0.691; Fig. 5B). Adiponectin
plasma concentrations were higher post- exercise when
compared with pre-exercise when concentrations were
not corrected for plasma volume shifts (p D 0.021;
Fig. 5A). There were no differences between the pre-exer-
cise and 3 h post-exercise adiponectin concentrations
when uncorrected for plasma volume shifts (p D 0.395;
Fig. 5B). When adiponectin concentration was corrected
for plasma volume shifts, no differences between any of
the time points were observed (p D 0.790; Fig. 5B).
Plasma ghrelin concentrations
There were no differences in acylated and nonacylated
ghrelin concentrations between any of the temperature
conditions without correcting concentration for plasma
volume shifts (p D 0.917 and p D 0.963; Figs. 6A and
7A), or when concentrations were corrected for plasma
shifts (p D 0.939 and 0.792; Figs. 6B and 7B).
Discussion
This study proposed that exercising in different envi-
ronmental temperatures would alter circulating con-
centrations of appetite-regulating hormones. Based on
previous research, it was hypothesized that in a hot
environment both leptin and adiponectin would
increase compared with a room temperature condi-
tion. It was also hypothesized that in a cold
Figure 6. (A) Total ghrelin concentration not corrected for plasma
volume shifts. (B) Total ghrelin concentration corrected for
plasma volume shifts. Data are mean § SE.

Figure 7. (A) Acylated ghrelin concentration not corrected for
plasma volume shifts. (B) Acylated ghrelin concentration cor-
rected for plasma volume shifts. Data are mean § SE.
environment both leptin and adiponectin would
decrease compared with a room temperature environ-
ment. However, contrary to the hypothesis, the results
of this study did not demonstrate temperature related
effects on these hormones. Exercise independent of
temperature did stimulate a decrease in leptin and a
potential increase in adiponectin, but had no effect on
circulating levels of total and acylated ghrelin. This
hormonal profile would suggest an increase in appetite
after exercise.
Research that has linked changes in leptin and adi-
ponectin concentration to different temperature expo-
sures has used mice and cell line models. Mice
subjected to 8 C for 12 h had decreases in leptin con-
centrations.39 Additionally, mouse preadipocytes
exposed to 39 C and 41 C produced incremental
increases in leptin when compared with cells exposed
to 37 C.43 Similar to leptin in a mouse model, mice
that were exposed to chronic heat stress showed ele-
vated adiponectin concentrations,38 whereas, during a
24 h exposure to 4 C adiponectin levels were
decreased.37 It is difficult to interpret the effect on
appetite when an appetite-reducing hormone (leptin)
and an appetite-stimulating hormone (adiponectin)
are increased or decreased together. However, in the
case of temperature, leptin appears to play a more
dominant role since exercise in the heat suppresses
appetite,15,16,36 while exercise in the cold increases
TEMPERATURE 171
appetite15,16 relative to a room temperature exercise
condition. Based on this previous data showing an
effect of temperature on hormones and appetite, we
were surprised not to see any effect of temperature on
leptin and adiponectin using our human exercise
model. Furthermore, current findings may be attrib-
uted to less influence of temperature on thermoregula-
tory responses in humans, compared with rodents.
Specifically, high body surface area-to-mass ratio and
differences in metabolism and thermal tolerance of
rats may explain changes in hormone responses com-
pared with those observed in humans.44,45
Lack of differences in hormone concentrations
between temperatures in the current study may be
due to the relatively short exposure times incorpo-
rated into the current design. In non-human mod-
els exposures were 8 to 24 times longer37,38 and
more intense,37-39,43 than in the current study. Pro-
longed extreme temperature exposure may cause a
greater difference in core body temperature com-
pared with the moderate, short-lived effects
observed here. A greater change in core body tem-
perature may be required to induce the changes in
hormone concentration that have been observed in
non-human models. Ethical limitations using a
human model may preclude this effect to be
observed and thus may not have practical
implications.
The current study did not directly measure appe-
tite, and thus we cannot be certain that the lack of hor-
monal differences between exercise in different
temperatures does not affect appetite. Indeed, previous
research studies have shown a change in subjective
appetite without a corresponding change in appetite-
regulating hormones.15,16,36 Further mechanistic work
is needed to determine the sensitivity of hormonal
concentration to predict appetite, as factors such as
receptor number and receptor sensitivity may also be
important.
Leptin and adiponectin are secreted from adipose
tissue, and therefore leptin and adiponectin concen-
trations are elevated in obese individuals due to the
increased adipose tissue mass. Much of the previous
research examining appetite-regulating hormones has
focused on overweight or obese populations.7,8,46 The
present study used recreationally active, relatively fit,
and healthy male participants. These individuals were
not having the hormonal imbalances, and/or receptor
sensitivity issues associated with excess adipose
172 T. L. LAURSEN ET AL.
tissue.47,48 This population may be able to better regu-
late homeostasis when adding the additional stress of
extreme temperatures and exercise.48,49 During the
hot trial heart rate and oxygen consumption were
higher than the other trials. This physiologically more
challenging trial likely placed additional stress on the
participants. It appears that the current participants
were able to adapt to this slight elevation in stress and
relative intensity, whereas a less trained population
may not be able to withstand these stresses without
augmenting appetite-regulating hormones. Thus, it is
possible that less trained individuals may show a dif-
ferent hormonal response to exercise in hot or
cold environmental conditions than the current
participants.
Results from the current study are in agreement
with previous research that demonstrates decreases in
leptin concentrations,7,8,13,14,50 and increases in adipo-
nectin concentrations with exercise.9-12 Previous liter-
ature has reported that exercise bouts shorter than
60 min may not alter leptin concentration.6 However,
the current study using a 60 min cycling bout did
result in decreased leptin levels. Not only are changes
in leptin concentrations dependent on duration,
but also depends upon intensity and exercise
mode.13,35,51-54 Thus, it appears that a 60 min bout of
cycling at 60% of maximal workload associated with
VO2max is sufficient to alter leptin and adiponectin
concentrations in a recreationally trained healthy pop-
ulation. Furthermore, it has been demonstrated that
swimming stimulates appetite and acylated ghrelin
concentrations and lowers energy balance when com-
pared with no exercise control.55
Blood plasma volume lost during exercise by way of
sweating and respiration should be accounted for when
analyzing concentrations of circulating hormones. The
loss of plasma will increase hormone concentration
without a change in absolute hormone level. The cur-
rent study analyzed the concentrations of leptin and
adiponectin with and without considering changes due
to plasma volume shifts.42 Leptin was decreased post
exercise when changes in plasma volume were not con-
sidered and when changes in plasma volume were con-
sidered. When adiponectin concentrations were
uncorrected for plasma volume shifts, adiponectin
increased post-exercise. Whereas, correcting for the
plasma volume shifts resulted in no changes in adipo-
nectin or ghrelin concentrations. It is uncertain
whether an increased concentration of adiponectin due
to a reduction in plasma volume is sufficient to cause a
physiologic change or if an increase in total adiponec-
tin is needed. No clear standard has been established
on the need to correct for plasma volume shifts as there
are many cases in which these shifts are ignored, calcu-
lated but not corrected for, or calculated and corrected
for.56 Thus, the current study reports both corrected
and uncorrected concentrations so that future research
may consider the impact of correcting leptin and adi-
ponectin concentrations for shifts in plasma volume.
In conclusion, these results indicate that in healthy,
recreationally-trained human participants, environ-
mental temperature has no effect on the circulating
concentrations of leptin, adiponectin or ghrelin imme-
diately post-exercise or 3 h post-exercise. Furthermore,
the current protocol seems to be of adequate duration,
intensity, and mode to cause a decrease in leptin and
increase of adiponectin concentrations. Further
research is needed to determine the impact that tem-
perature and exercise have on energy intake in the face
of a change in leptin and adiponectin concentrations.
Future studies investigating the effects of combined
effects of exercise and temperature in clinical popula-
tions are warranted. Additionally, chronic exposure to
temperature and exercise is needed to determine the
therapeutic use of such interventions to treat and pre-
vent conditions associated with high-energy intake.
Abbreviations
ANOVA analysis of variance
VO2peak peak oxygen consumption
Wmax Wattage max
Disclosure of potential conflicts of interest
No potential conflicts of interest were disclosed.
Funding
This publication was made possible by grants from the Univer-
sity Committee on Research and Creative Activity (UCRCA)
and the National Institute for General Medical Science
(NIGMS) (5P20GM103427), a component of the National
Institutes of Health (NIH). The contents of this paper are the
sole responsibility of the authors and do not necessarily repre-
sent the official views of NIGMS or NIH.
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