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2-adrenergic receptors
impairs exercise-induced lipolysis in SCAT of obese
subjects
1 Department of Sport Medicine, Third Faculty of Medicine, Charles University, 10000 Praha, Czech Republic; 2 Department of the Adaptation to Exercise, Purpan Hospital, Toulouse; 4 Department of Physiology, Claude Bernard University, 69373 Lyon; 5 Department of Medical and Clinical Pharmacology, Faculty of Medicine, 31073 Toulouse; and 3 Institut National de la Santé et de la Recherche Médicale Unité 317 Rangueil Hospital, Paul Sabatier University, 31403 Toulouse, France
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
SUBJECTS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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With the
use of the microdialysis method, exercise-induced lipolysis was
investigated in subcutaneous adipose tissue (SCAT) in obese subjects
and compared with lean ones, and the effect of blockade of
2-adrenergic receptors (ARs) on lipolysis during exercise was explored. Changes in extracellular glycerol concentrations and blood flow were measured in SCAT in a control microdialysis probe
at rest and during 60-min exercise bouts (50% of heart rate reserve)
and in a probe supplemented with the 2-AR antagonist phentolamine. At rest and during exercise, plasma norepinephrine and
epinephrine concentrations were not different in obese compared with
lean men. In the basal state, plasma and extracellular glycerol concentrations were higher, whereas blood flow was lower in SCAT of
obese subjects. During exercise, the increase of plasma glycerol was
higher in obese subjects (115 ± 35 vs. 65 ± 21 µmol/l).
Oppositely, the exercise-induced increase in extracellular glycerol
concentrations in SCAT was five- to sixfold lower in obese than in lean
subjects (50 ± 14 vs. 318 ± 53 µmol/l). The
exercise-induced increase in extracellular glycerol concentration was
not significantly modified by phentolamine infusion in lean subjects
but was strongly enhanced in the obese subjects and reached the
concentrations found in lean sujects (297 ± 46 µmol/l). These
findings demonstrate that the physiological stimulation of SCAT
adipocyte 2-ARs during exercice-induced sympathetic
nervous system activation contributes to the blunted lipolysis noted in
obese men.
microdialysis; catecholamines; blood flow; phentolamine; glycerol; lipid mobilization
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
SUBJECTS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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HUMAN
ADIPOCYTES EXPRESS SIGNIFICANT levels of 
1-,
2-, and 2-adrenergic receptors (ARs) that
couple positively (1- and 2-ARs) and
negatively (2-AR) to adenylyl cyclase (24).
The relative contributions of - and 2-ARs to the fine
tuning of the lipolytic response has been demonstrated by functional in vitro assays in isolated human fat cells. Moreover, binding studies with selective ligands have been used to determine the affinity patterns of the various fat cell AR subtypes for catecholamines (21, 22, 24, 30).
In vitro studies in isolated human fat cells have shown that the
activation of 2-ARs by epinephrine and norepinephrine
impairs the -adrenergic component of catecholamine-induced lipolysis. In human fat cells, where 2-AR outnumber
-AR, the preferential recruitment of the 2-AR at the
lowest catecholamine concentrations inhibits lipolysis
(30). The strongest 2-adrenergic effect has
been observed in the adipocytes from subcutaneous adipose tissue (SCAT)
from both men and women. The antilipolytic action of catecholamines,
particularly that of epinephrine, which exhibits a higher affinity to
2-AR (22), is particularly expressed in subcutaneous adipocytes from obese subjects (29). Whatever
the number of converging in vitro results suggesting an important role
for fat cell 2-ARs in the control of lipolysis in obese subjects, convincing demonstrations of their involvement in
physiological situations are still lacking. In the search for relevant
physiological protocols, exercise was selected as a prerequisite to
activate the sympathetic nervous system (SNS). Exercise-increased SNS
activity is responsible for exercise-promoted lipid mobilization in
normal subjects. Catecholamines are of major importance for the
regulation of lipid mobilization in human adipose tissue during
exercise (8, 9, 19) and for the
increase of nonesterified fatty acid (NEFA) supply to the working
muscle (8, 16). Microdialysis is a method
particularly suitable to study the in vivo lipolytic responses of
adipose tissue to pharmacological or endogenous stimulation (2-4, 12, 20,
28, 33). In a recent study using
microdialysis, it was demonstrated that 2-ARs are
involved in the regulation of lipolysis during an acute bout of
exercise (33). Taking into account that the adipocytes of
SCAT express the highest known 2-AR-mediated
antilipolytic component in vitro in obese men (29), it is
of interest to study the extent of the catecholamine-induced 2-AR activation in adipose tissue in obese subjects
during exercise compared with nonobese counterparts.
The aim of the present study was to reveal the incidence of
physiological activation of fat cell 2-ARs in SCAT and
to delineate the importance of 2-AR-mediated pathways in
the adipose tissue of obese subjects. With the use of in situ
microdialysis, the changes in lipolysis and local blood flow were
studied in SCAT of obese subjects during exercise (60 min, 50% of
their heart rate reserve) and the effect of the blockade of
2-ARs on these changes was explored. The results were
compared with those of lean subjects.
The present study demonstrates that exercise-induced lipolysis in SCAT
is impaired in obese subjects and that the physiological stimulation of
adipocyte 2-ARs during exercise contributes to this
impairment. The blunting of lipid mobilization was suppressed by local
administration of an 2-AR antagonist.
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SUBJECTS AND METHODS |
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TOP
ABSTRACT
INTRODUCTION
SUBJECTS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects. Seven lean untrained men (mean age 22.9 ± 0.8 yr) and seven obese men (24.9 ± 2.8 yr) participated in the study. The mean body weight and body mass index (BMI) of the lean subjects were 73.6 ± 3.5 kg (range 70-81.5 kg) and 23.2 ± 1.2 kg/m2 (range 21.2-25.2 kg/m2), respectively. The mean body weight and BMI of the obese subjects were 96.9 ± 3.4 kg (range 89-110 kg) and 31.4 ± 1.4 kg/m2 (range 29-38 kg/m2), respectively. All were drug free, and their weights had remained stable for at least 3 mo before the beginning of the study. All subjects had given their written informed consent before the experiments began. The studies were performed according to the Declaration of Helsinki and approved by the Ethical Committee of Third Faculty of Medicine (Prague, Czech Republic).
Experimental protocol.
The subjects were investigated at 0800 after an overnight fast and were
placed in a semirecumbent position. Microdialysis probes (Carnegie
Medecin, Stockholm, Sweden) of 20 × 0.5 mm and 20,000-molecular
wt cut-off were inserted percutaneously after epidermal
anesthesia (200 µl of 1% lidocaine, Roger-Bellon, Neuilly-s-Seine, France) into the abdominal SCAT at a distance of 10 cm immediately to
the right of the umbilicus. Two probes, separated by at least 10 cm,
were connected to a microinjection pump (Harvard apparatus, Les Ulis,
France). One probe was perfused with Ringer solution (in
mmol/l: 139 sodium, 2.7 potassium, 0.9 calcium, and 140.5 chloride) and
the second with Ringer plus 0.1 mmol/l phentolamine (-AR
antagonist). This nonselective
1-/2-antagonist, having an efficient
2-AR antagonist action in human fat cells in vitro, was
the only agent allowed by the ethical committee for use in microdialysis assays in humans. The two perfusate solutions were supplemented with ethanol (1.7 g/l). Ethanol was added to the perfusate
to estimate changes occurring in the local blood flow of SCAT, as
previously described (11-13). After a 30-min
equilibration period, a 30-min fraction of dialysate was then collected
at a flow rate of 0.5 µl/min. Then, the perfusion was set at 2.5 µl/min for the remaining experimental period. A calibration procedure using various perfusion rates for determination of interstitial glycerol concentration in SCAT has already been reported by our group
(3, 4). A simplified, but relevant
and less time-consuming method was selected in this study. The
estimated extracellular glycerol concentrations were calculated by
plotting (after log transformation) the concentration of glycerol in
the dialysate measured at 0.5 and 2.5 µl/min against the perfusion
rates. The values of extracellular glycerol concentrations found in the
present study fit with previous determinations performed in lean and
obese subjects (17, 18).
80°C until analysis.
Drugs and analytical methods. Phentolamine methanesulfonate (Regitine) was obtained from Ciba-Geigy (Reuil-Malmaison, France). Glycerol in dialysate (10 µl) and in plasma (20 µl) was analyzed with an ultrasensitive radiometric method (7); the intra-assay and interassay variabilities were 5.0% and 9.2%, respectively. Ethanol in dialysate and perfusate (5 µl) was determined with an enzymatic method (6); the intra-assay and interassay variabilities were 3.0% and 4.5%, respectively. Plasma glucose was determined with a glucose-oxidase technique (Biotrol kit, Merck-Clevenot, Nogent-s-Marne, France) and NEFA by an enzymatic procedure (Wako kit, Unipath, Dardilly, France). Plasma insulin concentrations were measured using RIA kits from Sanofi Diagnostics Pasteur (Marnes la Coquette, France). Plasma epinephrine and norepinephrine were assayed in 1-ml aliquots of plasma by high-pressure liquid chromatography using electrochemical (amperometric) detection (10). The detection limit was 20 pg/sample. Day-to-day variability was 4% and within-run variability 3%.
Statististical analysis. All the values are means ± SE. The responses to exercise were analyzed using a paired t-test and ANOVA when appropriate. During exercise, plasma and extracellular response curves were calculated as the total integrated changes over baseline values [area under the curves (AUC)] using the trapezoidal method; P < 0.05 was considered statistically significant.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
SUBJECTS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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General observations.
The power developed by the subjects was regularly adjusted to maintain
the heart rate constant over the exercise bout. Similar power was
developed by obese and lean subjects during exercise (Table
1).
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Extracellular glycerol concentration in SCAT at rest and during exercise. At rest, the baseline extracellular glycerol concentrations in SCAT were higher in obese (275 ± 38 µmol/l) than in lean subjects (194 ± 39 µmol/l) in the control probes. Adipose tissue glycerol levels at rest were two to three times higher than those in venous plasma in both groups of subjects. No modifications in basal extracellular glycerol concentration were observed in the probes containing phentolamine (280 ± 35 and 238 ± 30 µmol/l in SCAT of obese and lean, respectively) compared with the control probes.
During exercise, the extracellular glycerol concentration increased in the control probe in both groups of subjects, the increase being significant from the 15th min of exercise (Fig. 1). The exercise-induced increase of glycerol was 19% of the baseline value in obese subjects and was markedly lower compared with lean men (172% of baseline). Absolute values of exercise-induced increment were 52 ± 14 vs. 318 ± 53 µmol/l after 60 min of exercise in obese and lean subjects, respectively. The calculated average AUC for glycerol increase over 60 min of exercise was significantly lower in obese than in lean subjects (2,345 ± 342 vs. 9,430 ± 1,301 µmol · l
1 · 60 min1, P < 0.006).
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1 · 60 min1;
P < 0.01). It is noteworthy that the exercise-induced
increase in the phentolamine probe in the obese group reached that
observed in the control probe in lean subjects. In individual cases,
the rise of glycerol during exercise in the phentolamine probe was about four- to sixfold higher when compared with the control one. In
lean subjects, the exercise-induced rise in extracellular glycerol was
enhanced in the probe perfused with phentolamine, but the corresponding
AUC for glycerol response (14,632 ± 5,885 vs. 9,430 ± 1,301 µmol · l1 · 60 min1) was
far from being statistically different compared with the control probe
(P < 0.2).
SCAT blood flow.
Adipose tissue blood flow was assessed by ethanol outflow-to-inflow
ratios [ethanol concentration measured in the dialysate divided by the
ethanol concentration measured in the perfusate × 100 (%)] from
the two probes, and the results are reported in Fig.
2. In rest conditions and during
exercise, the ethanol outflow-to-inflow ratio was higher in obese than
in lean subjects (P < 0.05). In both groups, no
significant variations of the ethanol outflow-to-inflow ratio were
observed during the exercise bout either in the control probe or in the
probe with phentolamine (Fig. 2).
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Plasma NEFA and glycerol levels.
During the baseline period, plasma NEFA and glycerol
concentrations were higher in obese subjects (Table
2). In both groups, plasma NEFA
concentrations did not significantly change throughout the exercise
period. The plasma glycerol level increased 30 min after the beginning
of exercise in both groups and peaked at the 60th min of exercise.
During recovery, it decreased to values not different from those found
in basal conditions. The average exercise-induced increment was
115 ± 35 and 65 ± 21 µmol/l in obese and lean subjects,
respectively (Table 2). The calculated AUC for the plasma glycerol
response was higher in obese than in lean subjects (4,792 ± 875 vs. 2,084 ± 697 µmol · l1 · 60 min1, P < 0.01).
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Plasma catecholamine concentrations.
At rest, plasma norepinephrine and epinephrine concentrations were
similar in the two groups. Plasma norepinephrine concentration increased significantly at the 30th min of exercise; the increase during subsequent 30 min of exercise was not significant. The plasma
epinephrine concentration rose at the 30th min of exercise and
continued to increase (P < 0.01) until the end of
exercise. During recovery, 60 min after the end of exercise, both
catecholamines decreased to values not different from the baseline
(Table 2). The AUC calculated for the exercise-induced
increases in norepinephrine (35,005 ± 4,464 vs. 33,005 ± 4,283 pg · ml1 · 60 min1
in lean and obese, respectively) and epinephrine plasma levels (2,335 ± 493 vs. 3,639 ± 1,868 pg · ml1 · 60 min1 in lean and obese,
respectively) showed no significant differences between the two groups
of subjects.
Plasma glucose and insulin concentrations. During the baseline period, the plasma concentration of glucose was similar in both groups, whereas the plasma insulin level was higher in obese subjects (Table 2). No significant variations of plasma glucose level were observed in either group during the exercise bout. A significant decrease in plasma insulin concentration was observed at the end of the exercise period in obese and lean subjects. The AUC calculated for glucose and insulin variations in the plasma during the exercise bouts did not show significant differences between the two groups.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
SUBJECTS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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The present study demonstrates that the exercise-induced lipolysis
is impaired in SCAT in obese subjects and that the physiological activation of 2-ARs during exercise (60 min, 50% of the
heart rate reserve of the subjects) contributes to the blunted
lipolysis. The involvement of 2-ARs in the suppression
of lipolysis was demonstrated by the enhancement of exercise-induced
lipolysis produced by local perfusion of the
2-AR-antagonist phentolamine. The action of
catecholamines on lipolysis is determined by the differential
stimulation of lipolysis-promoting -ARs and antilipolytic 2-ARs (1, 23, 29,
30). In in vivo physiological conditions, epinephrine
secretion is typically elevated during exercise. It was demonstrated in
our previous study (33) that the increased activation of
2-ARs by epinephrine during a bout of moderate exercise
produces an antilipolytic effect, i.e., the antilipolytic 2-ARs are involved in the control of exercise-induced
lipolysis. The aim of this study was to investigate in situ, using
microdialysis, the lipolytic response to exercise in SCAT in obese
subjects and its hormonal regulation. Namely, we hypothesized that the
previously demonstrated involvement of the antilipolytic
2-ARs could be enhanced in exercising obese men.
In agreement with previous human studies, the basal extracellular glycerol concentrations in SCAT as well as basal plasma glycerol and NEFA were higher in obese than in lean fasting subjects, suggesting that basal spontaneous SCAT glycerol production is increased in obesity (4, 17, 31). The local blood flow, evaluated with the ethanol escape method, was found to be lower in obese subjects (Fig. 2). Our data agree with a previous report that revealed a lower blood flow in SCAT of obese than lean subjects, as assessed by the 133Xe-clearance method (35).
During exercise, a higher increase in plasma glycerol was observed in
obese than in lean subjects. The epinephrine and norepinephrine responses to exercise were not different in both groups. The average plasma insulin level was higher in obese subjects, whereas the well-known exercise-induced reduction in plasma insulin concentration was similar in both groups. Consequently, the higher plasma glycerol levels observed during the time course of exercise in obese subjects could be related to the increased adipose tissue mass. Moreover, it is
not excluded that the increased plasma glycerol levels could be related
to the higher efficacy of catecholamines to induce lipid mobilization
in omental and visceral adipocytes, which are known for their strong
-adrenergic responsiveness and reduced 2-AR-mediated
responses (27, 30).
Unlike plasma responses, the exercise-induced increase in extracellular glycerol concentration was markedly lower (+19%) in obese than in lean subjects (+172%). This observation could reflect not solely the exercise-induced local lipolytic response of the adipocytes, but could be influenced by changes occurring in local blood flow in SCAT (11, 13). In this study, the adipose tissue blood flow did not show a significant variation during the exercise neither in lean nor in obese subjects as previously shown (14, 32, 33). Similarly, no exercise-induced variations were found in the probe with phentolamine. Consequently, the differences in exercise-induced changes in extracellular glycerol concentration between the two groups cannot be attributed to changes in the local adipose tissue blood flow.
The fact that the exercise-induced increase of extracellular glycerol
was potentiated by the local phentolamine perfusion in obese subjects
demonstrates that the reduced lipid mobilization in SCAT is, at least
partly, due to the stimulation of fat cell antilipolytic
2-ARs by exercise-released catecholamines. Phentolamine is also known for its 1-antagonist properties. However,
1-AR stimulation or blockade has never been shown to
alter lipolytic processes. In conditions of 2-AR
blockade, the inhibitory action mediated by 2-AR
stimulation was completely suppressed and the lipid-mobilizing activity
induced by exercise reached that observed in lean subjects. In lean
subjects, phentolamine also produced an enhancement of the lipolytic
response to exercise, but the effect was not significant, and in
absolute terms, it was much lower than in obese subjects.
Whatever the importance of the 2-AR in SCAT of obese
patients, we must keep in mind that -AR-mediated responses also
represent a major element in the control of lipolytic processes.
Exercise-induced lipid mobilization is suppressed by -adrenergic
blockade in lean subjects (2). However, no major
disturbances have been reported in vitro in fat cells from SCAT of lean
and obese subjects except in patients with a specific
2-AR gene polymorphism associated with altered adipocyte
2-AR function (26) or in obesity associated with other diseases such as diabetes or hyperlipidemia
(25). Any reduction of the -AR-mediated pathway would
tend to strengthen the counterregulatory action of the
2-AR-dependent pathway and worsen the lipid-mobilizing defect.
In summary, these in vivo results provide evidence, for the first time,
of the important contribution played by 2-ARs in the
physiological impairement of lipolysis in the adipose tissue of the
obese men. Such an observation reconciles a number of results obtained
in previously reported in vitro studies with physiological approaches
in men.
Perspectives
The present results stress on the great potential of exploring fat deposits from different anatomical locations using in situ microdialysis. The role of2-ARs must be explored in
other fat deposits, both in men and women, in which the adipocytes
express a high level of 2-ARs largely outnumbering those
of -ARs (30). Moreover, the lipolytic response to
exercise has been shown to be sex- and anatomical site-dependent
(2). These findings may have important physiopathological
implication in men developing large subcutaneous fat deposits and women
with excessive hip and femoral fat deposits. It is tempting to
speculate that adipocyte 2-ARs may have a major
contribution in the resistance of SCAT to fat loss during very
low-calorie diets (15) and during slimming programs
including physical activity in obese subjects (34). Administration of an 2-AR antagonist could represent a
possible strategy to facilitate mobilization of SCAT when obese
subjects are submitted to periods of exercise in dietary conditions
facilitating NEFA use (5). It has been reported that oral
yohimbine (2-AR antagonist) administration
potentiated lipolysis and exercise-induced energy expenditure
(36). The balance between fatty acid and carbohydrate use,
with and without 2-AR antagonist administration, merit
further studies in the exercising conditions.
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ACKNOWLEDGEMENTS |
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The authors express gratitude to M.-T. Canal and Z. Parizkova for contributions to the study.
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FOOTNOTES |
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This study was financially supported by the Charles University, Czech Republic Grant GAUK 199, the Commission of the European Communities specific RTD programme CT98-4141 (FATLINK: Dietary fat, body weight control, and links between obesity and cardiovascular disease), and the Fondation pour la Recherche Médicale.
Address for reprint requests and other correspondence: M. Berlan, Institut National de la Santé et de la Recherche Médicale U 317, Laboratoire de Pharmacologie Médicale et Clinique, Faculté de Médecine, 37 Allées Jules Guesde, 31073 Toulouse Cedex, France (E-mail: berlan{at}cict.fr).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Received 29 December 1999; accepted in final form 29 February 2000.
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TOP
ABSTRACT
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SUBJECTS AND METHODS
RESULTS
DISCUSSION
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) or was not (
) added to the
perfusion medium. Data are expressed as means ± SE.
* P < 0.05 compared with baseline value.
