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Experimental Studies |
INSERM U-317, Faculté de Médecine, Toulouse, France; Department of Sport Medicine (V.S.) and Obesity Unit, Fourth Internal Medicine Department, Charles University (M.K., V.H), Prague, Czech Republic
Address all correspondence and requests for reprints to: Dr. Michel Berlan, Laboratoire de Pharmacologie Médicale et Clinique, INSERM U-317, Faculté de Médecine, 37 allées Jules Guesde, 31073 Toulouse Cedex, France.
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Abstract |
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Therefore, the present study was conducted in vivo in obese subjects to investigate 1) changes in the ß-adrenergic lipolytic response in sc adipose tissue during a very low calorie diet (VLCD), 2) the involvement of ß3-AR-mediated lipolysis in these patients. The microdialysis method was used to assess the interstitial glycerol concentration as a lipolysis index and the change in nutritive blood flow in adipose tissue. The probes were infused with various pharmacological agents: isoprenaline (a nonselective ß-AR agonist), dobutamine (a selective ß1-AR agonist), terbutaline (a selective ß2-AR agonist), and CGP 12,177 (a ß1- and ß2-AR antagonist with ß3-AR agonist activity) (18). Our data show an increase in the in vivo lipolytic responses to isoprenaline and dobutamine during the hypocaloric diet. Furthermore, functional ß3-AR are present in the sc adipose tissue of obese patients; their activation is only weakly involved in the lipolytic process in this population and is not modified by the hypocaloric diet.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Twenty-four obese subjects (15 women and 9 men), from 37–60 yr old (mean ± SE, 52 ± 2 yr), were selected for this study. Their mean body weight was 118.3 ± 5.7 kg (range, 76–181 kg) and had been stable for at least 3 months before the beginning of the study. Their mean body mass index was 42.6 ± 2.2 kg/m2 (range, 32–62 kg/m2). Most of the patients exhibited various signs of the metabolic syndrome; 9 patients had mild type 2 diabetes mellitus (fasting plasma glucose <8.5 mmol/L before the diet; none received hypoglycemic drugs), 14 patients received antihypertensive drugs (either furosemide and/or verapamil or captopril, but none of them received ß-blockers), and 7 patients had coronary heart disease (treated with organic nitrates). This population of massively or severely obese people corresponds to the obese patients currently submitted to VLCD treatment in European countries.
All of the patients received a 382 Cal/day [1.6 megajoules (MJ)] liquid formula diet (Redita) for 28 days. The formula included 36 g protein, 50 g carbohydrate, 4 g fat, and the recommended daily allowance of vitamins and minerals. The subjects were in-patients throughout duration of the diet, and their usual medication was maintained. All subjects had given their informed consent before the study, and the investigation protocol was approved by the ethical committee of Prague University Hospital.
Experimental protocol
The subjects were investigated in the supine position at 0800 h after an overnight fast. A venous blood sample was drawn from an indwelling polyethylene catheter in the cubital vein before the dialysis experiment. Microdialysis probes (Carnegie Medecin, Stockholm, Sweden) of 20 x 0.5 mm and 20,000 mol wt cut-off were inserted percutaneously after epidermal anesthesia (200 µL 1% lidocaine, Roger-Bellon, France) into the abdominal sc adipose tissue at a distance of 100 mm immediately to the right of the umbilicus. The probes were connected to a microinjection pump (Harvard Apparatus, South Natick, MA) and perfused at 0.8 µL/min with a sterile Ringer’s solution (154 mmol/L sodium, 4 mmol/L potassium, 2.5 mmol/L calcium, and 160 mmol/L chloride) supplemented with ethanol (1.7 g/L). No outgoing dialysate was collected during the first 30 min after the implantation. Then, the in vivo recovery rate was evaluated for each probe using measurements of dialysate glycerol concentrations at various perfusion rates. This calibration procedure was previously described for the estimation of the extracellular amino acid concentration in brain (19) and was recently used for determination of the interstitial glycerol concentration in muscle and adipose tissue (20). Briefly, the probes were perfused at four successive rates (0.8, 1.5, 2.5, and 3.5 µL/min), separated by appropriate wash-out periods, and glycerol concentrations were determined in the dialysate for each perfusion rate. Dialysate was collected in tubes that were weighed before and after collection to check the actual flow rate through the microdialysis probes. Dialysate concentrations were plotted (after log transformation) against the perfusion rates. Linear regression analysis was used to calculate the glycerol concentration at zero flow, corresponding to the interstitial glycerol concentration. The ratio between dialysate glycerol concentration at 2.5 µL/min and calculated interstitial glycerol concentration represented the in vivo recovery rate of the probe. After this calibration period, the perfusion flow rate was maintained at 2.5 µL/min to evaluate the effects of the different pharmacological agents. Depending on the protocol, three or four 10-min fractions of the outgoing dialysate of each probe were collected to evaluate basal levels.
In eight obese patients (five women and three men), one probe was inserted and perfused with three concentrations of the nonselective ß-AR agonist isoprenaline (0.001, 0.1, and 10 µmol/L). Each dose was applied for 40 min (concentration-periods), and four successive 10-min fractions were collected during the different concentration-periods.
In a second group of 16 obese patients (10 women and 6 men), 3 probes were simultaneously inserted. The distance between adjoining probes was always at least 100 mm. After the basal period, the probes were perfused, within a 100-min period, with 100 µmol/L dobutamine (selective ß1-AR agonist), 100 µmol/L terbutaline (selective ß2-AR agonist), or 100 µmol/L CGP 12,177 (a nonselective ß1- and ß2-AR antagonist possessing ß3-AR agonist properties), and fractions were collected every 10 min.
In all experiments, the fractions were collected on ice. Glycerol analysis was performed in each fraction collected. The changes in nutritive blood flow were assessed using the ethanol outflow/inflow ratio measurement as previously described (21, 22). For practical reasons, ethanol levels were not determined in all collected fractions. In the first set of experiments, ethanol dialysate concentrations were measured in the last two fractions of each period (basal and concentration periods). In the second set of experiments, ethanol dialysate concentrations were measured in the 20–30 min fractions of the basal period, in the 70–80 min fractions, and in the last two fractions (120–130 min). In every case, the mean of the two fractions was considered.
The same protocol of investigation was performed before and on the 28th day of the hypocaloric diet.
Drugs and chemicals
CGP 12,177 was obtained from Ciba-Geigy (Basel, Switzerland). Isoprenaline hydrochloride, dobutamine hydrochloride, and terbutaline sulfate were obtained from Winthrop (Clichy, France), Lilly (Saint-Cloud, France), and Astra (Nanterre, France), respectively.
Analytical methods
Glycerol in dialysate (10 µL) and in plasma (20 µL) was analyzed with an ultrasensitive radiometric method (23); the intra- and interassay variabilities were 5.0% and 9.2%, respectively. Ethanol in dialysate and perfusate (5 µL) was determined with an enzymatic method (24); the intra- and interassay variabilities were 3.0% and 4.5%, respectively. Plasma glucose and nonesterified fatty acids were determined with a glucose oxidase technique (Biotrol, Paris, France) and an enzymatic procedure (Wako, Unipath, Dardilly, France), respectively. Plasma cortisol and insulin concentrations were measured using RIA kits from ICN Biomedicals (Orsay, France) and Institut Pasteur (Paris, France), respectively.
Statistical analysis
All values are the mean ± SE. Flow rate calibration data were analyzed by linear regression, tested for goodness of fit. Student’s paired t test and ANOVA with Bonferroni’s and Student-Newman-Keuls tests for post-hoc analysis were used for statistical comparisons as appropriate. P < 0.05 was considered statistically significant.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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. As expected, there was a marked weight loss
and a significant reduction in postabsorptive glucose and insulin
plasma levels. Plasma nonesterified fatty acids, glycerol, and cortisol
concentrations were not modified.
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). The mean ethanol inflow/outflow ratio in the same
fractions was significantly lower on day 28 (see Table 1).
The effects of increasing concentrations of isoprenaline on glycerol
concentrations are depicted in Fig. 1. Before and at the
end of the diet, the mean glycerol level during the basal period
(10–40 min) was used as the reference value to compare the changes in
each fraction during the test. Before the diet, interstitial glycerol
levels were not modified during the addition of 0.001 and 0.1 µmol/L
isoprenaline to the perfusate; the interstitial glycerol concentrations
increased significantly in the 130–160 min fractions
(P < 0.05 vs. reference value using
Student’s paired t test) with the addition of 10 µmol/L
isoprenaline. On the 28th day of the diet, the interstitial glycerol
concentrations increased in the 100–160 min fractions
(P < 0.05 vs. reference value),
i.e. during the addition of 0.1 and 10 µmol/L isoprenaline
(155% and 240% of the baseline value, respectively). The two curves
were statistically different (see Fig. 1).
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. Before the diet, the perfusion of isoprenaline
decreased the ethanol ratio at doses of 0.1 and 10 µmol/L compared to
the basal value (P < 0.05, using Student’s paired
t test), indicating a vasodilating effect. After 28 days of
the diet, the basal ethanol ratio was lower than that before the diet,
and a significant vasodilating effect was observed even at the lowest
concentration (0.001 µmol/L). The vasodilating effects of
isoprenaline were different before and at the end of the diet (see Fig. 2).
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The effects of the three ß-AR agonists on lipolysis before and after
28 days of the hypocaloric diet are depicted in Fig. 3.
The addition of each ß-AR agonist to the perfusate induced a
significant increase in the interstitial glycerol concentration
(lipolytic effect) before as well as after 28 days of the diet. This
effect occurred at slightly different times according to the
individuals. Before the diet, the lipolytic responses induced by the
ß-AR agonists were different. The terbutaline effect on glycerol
levels was higher than that of dobutamine or CGP 12,177. The lipolytic
responses induced with dobutamine and CGP 12,177 were also different.
After 28 days of the diet, the lipolytic responses induced by the
perfusion of dobutamine and terbutaline were not different, but were
significantly higher than that induced by CGP 12,177. The effect of
each agonist on glycerol levels was analyzed with ANOVA over the whole
time course, with the diet period as factor analysis. The diet induced
a significant increase in dobutamine-stimulated glycerol release
(F = 18.39; P < 0.001). The lipolytic effects of
terbutaline and CGP 12,177 were unchanged by the hypocaloric diet.
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. Dobutamine,
terbutaline, and CGP 12,177 decreased the ethanol ratio regardless of
the diet period (by one-way ANOVA with repeated measures,
P < 0.001). The vasodilating effects of the three
agonists were not different either before or after 28 days of the
hypocaloric diet.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The calculated interstitial levels of glycerol in the sc adipose
tissue, which were similar before and after 28 days of VLCD (
2- to
3-fold higher than those in plasma), are in agreement with the results
previously reported by Jansson et al. in obese patients
using a different calibration method (no net flux method) (25) and
close to those reported for lean subjects by us (17) and others
(25, 26, 27) and in the venous blood draining the sc abdominal adipose
tissue (28). However, 10-fold higher extracellular concentrations of
glycerol in the adipose tissue of nonobese subjects have been recently
reported (20). This large discrepancy with previous reports cannot be
explained otherwise than by the physical characteristics of the
microdialysis system used in this single study.
In vitro, isolated adipocytes spontaneously release more glycerol during hypocaloric diets (6, 8, 29). In the present investigation, fasting plasma and interstitial glycerol concentrations did not change during the hypocaloric diet. The ethanol ratio during the basal period was lower after the diet, which indicates an improvement in local nutritive blood flow and, therefore, an increase in glycerol drainage (22). This strongly suggests increased glycerol release from adipose cells, which could explain the steady interstitial levels in adipose tissue. The increased glycerol production reflects adaptation of the lipolytic process to the increased lipid substrate requirement (2).
Animal studies performed in vivo and in vitro have shown that fasting or energy restriction increases the lipolytic response to epinephrine (30, 31). In humans, conflicting results have been reported. The lipolytic response to isoprenaline is unmodified or diminished in isolated sc fat cells from obese subjects during fasting (6, 7) or after a 15-day 3.3 MJ/day diet (8). This is in contrast with in vivo studies in which increased responsiveness of adipose tissue to catecholamine infusion has been demonstrated after short term fasting (3, 9, 10). A very low calorie diet (2 MJ/day for 4 weeks) led to an increased lipolytic response to exercise in obese subjects (32). These discrepancies between in vivo and in vitro studies could reflect regional differences in adaptive mechanisms. The increased in vivo responsiveness to catecholamines, assessed through the rates of appearance in the circulation of nonesterified fatty acids and glycerol, could only concern the internal (visceral) adipose tissue, whereas the sensitivity of sc adipocytes, assessed by the in vitro studies, may be less modified. The in vitro artificial conditions used for the study of isolated fat cells can also contribute to these conflicting results, insofar as cells are deprived of their physiological hormonal environment (1, 33). The microdialysis of sc adipose tissue, which largely alleviates the technical problems introduced by the in vitro systems, allows the study of adipose cells in their actual milieu and provides an alternative method for investigation of in vivo lipolysis (34).
The glycerol increase initiated by isoprenaline infusion was markedly elevated during VLCD. These results strongly argue for an increase in the ß-adrenergic sensitivity of the sc adipocytes of obese subjects submitted to a hypocaloric diet.
The change in local blood flow, which influences the concentration of the interstitial metabolites, is an important variable in microdialysis studies (21). The isoprenaline-mediated lipolytic response was associated with vasodilating effects as previously described in lean subjects (35), and the vascular effects could be seen to be concentration dependent and enhanced during the diet. A significant effect on lipolysis appeared at the last step of isoprenaline infusion (10 µmol/L) before the diet and at the medium dose (0.01 µmol/L) after the diet. The default of the increase in interstitial glycerol concentration with the lower isoprenaline concentrations (0.1 µmol/L, before the diet, 0.001 µmol/L after the diet) could be linked to the simultaneous increase in blood flow. The vascular effect could partly mask the positive action of the drug on lipolysis, as an increment in glycerol drainage in the circulation could be simultaneously promoted. At higher concentrations, although blood flow and glycerol drainage were increased, the lipolytic effect was observed and the true effect of isoprenaline acting on both lipolysis and vascular tone could be underevaluated.
To study the relative involvement of ß1-, ß2-, and ß3-AR in the changes in lipolysis and nutritive blood flow during the diet, comparisons of dobutamine (selective ß1-agonist), terbutaline (selective ß2-agonist), and CGP 12,177 (selective ß3-agonist) effects were performed. CGP 12,177 was used because this drug, which is a nonselective antagonist of ß1- and ß2-AR, was reported to selectively stimulate ß3-AR at concentrations higher than those required for ß1/ß2-AR antagonism (12, 13).
The choice of the concentration of drugs used in this study needs some comment. In isolated human fat cells, the three ß-AR agonists have 50- to 90-fold lower affinity than isoprenaline, and their maximal lipolytic effect is obtained at 10 µmol/L (17). Thus, to compare the relative lipolytic and vascular effects of the three ß-agonists, a 10-fold higher concentration was used because the concentration leaving the probe has been roughly estimated to be 10–20% of that entering it (36). In addition, before the drugs reach the adipocytes and the vascular bed, an unknown further dilution can occur.
Before the diet, the selective stimulation of ß2-AR was greater than the stimulation of ß1-AR or ß3-AR. The changes in nutritive blood flow did not explain these differences in lipolytic responses. Using the microdialysis method and lower doses (10 µmol/L), Enocksson et al. (16) found a similar difference between terbutaline and dobutamine in lean subjects, whereas dobutamine and CGP 12,177 exerted similar effects. We have previously shown that dobutamine and terbutaline exhibited similar effects in lean healthy volunteers (17). Taken together, these results indicate that in vivo lipolysis is mainly dependent on ß1/ß2-AR stimulation in normal and in obese subjects.
ß3-AR stimulation promoted a minor increase in glycerol concentration in the interstitial space compared to the effects of isoprenaline or selective ß1- or ß2-AR agonists. Although the ß3-AR gene is present in the human genome (37), it seems to be poorly expressed in human fat cells (11, 38, 39, 40). The weak, but significant, increase in interstitial glycerol levels during CGP 12,177 infusion in our study strongly suggests that in vivo functional ß3-AR exist in sc adipose tissue of obese subjects, although their lipolytic action seems to be of minor importance. This is in agreement with recent reports of functional ß3-AR in lean subjects (16, 17). Moreover, Lönnqvist et al. reported a lower intrinsic activity of CGP 12,177 in sc adipocytes than in omental fat cells from normal weight subjects (11). Our results do not exclude a more substantial role for ß3-AR in the visceral fat from obese patients (15).
The vasodilating effect of CGP 12,177 is in agreement with our previous findings in lean subjects (17). The presence of ß3-AR in the smooth muscle cells from the gastrointestinal tract (41) suggests that ß3-AR could also be present in the vascular bed. This has been demonstrated in the blood vessels of adipose tissue (42) and skin (43) in the dog. As CGP 12,177 has never been shown to exert any ß1- or ß2-agonist effect, the vasodilation observed in the present study suggests the presence of ß3-AR in the vascular bed of sc adipose tissue in obese subjects. This point can be assessed only when a selective ß3-antagonist becomes available.
The lipolytic response to dobutamine increased at the end of the diet, whereas no modification was observed with terbutaline or CGP 12,177 infusion. Such a result suggests a specific enhancement of the ß1-AR mediated pathway through an increased receptor number and/or improved coupling with Gs and adenylyl cyclase (31). Although determinations were not made in the present study, the change in the ß1-AR response in the adipose tissue of our patients fits with the increased heart rate observed during exercise after reduction of energy intake in obese patients (32, 44) or after epinephrine infusion in lean subjects (10). The absence of modification of the terbutaline lipolytic response in our study is in agreement with the absence of modification of lymphocyte ß2-AR density in obese patients subjected to a VLCD (32). Until the present work, no data were available concerning changes in the ß3-AR response during hypocaloric diet in adipose tissue from obese patients.
Several mechanisms can be proposed to explain the increased ß-adrenergic sensitivity of adipose tissue after VLCD. This may result from an up-regulation of ß-AR and/or an increase in the efficiency of the coupling between ß-AR and adenylyl cyclase. Thyroid hormones and glucocorticoids are known to increase ß-AR activity. However, thyroid hormones are known to be decreased after a reduction of energy intake (45), and plasma cortisol levels were unmodified in our study, as previously reported (3).
The decrease in plasma insulin levels is usual during VLCD treatment (46, 47) and could be an important factor for the regulation of adrenergic responsiveness. In elderly men with the insulin resistance syndrome, multiple lipolysis defects have been reported (5); the most obvious defect was the resistance to the lipolytic action of catecholamines, located at a posttranscriptional level of ß-AR expression. In the present study, obese patients also displayed several features of the metabolic syndrome (glucose intolerance or noninsulin-dependent diabetes mellitus, hypertension, and CHD); they exhibited great weight loss and a marked reduction of plasma insulin levels after the 28-day VLCD. The improvement of lipolytic response to ß-AR stimulation could be related to the modification of the insulin status of the subjects. A modification of other steps of the lipolytic cascade (i.e. hormone-sensitive lipase, protein kinase A, and cAMP phosphodiesterase activities) cannot explain the specific improvement in the ß1-AR-mediated pathway.
Finally, the up-regulation of ß-AR could be a consequence of the reduction of sympathetic nervous system basal activity. The resting plasma norepinephrine concentration decreases during energy restriction in normal weight and obese subjects (32, 44, 48, 49, 50, 51) as a result of reductions in both the appearance and clearance rates of norepinephrine.
Our data do not allow differentiation between the effects of the hypocaloric diet and the effects of weight reduction. Nevertheless, it is possible that the increased ß-adrenergic response was a consequence of both. Reduced weight obese subjects with stable body weight exhibited decreased basal sympathetic activity and an increased lipolytic response to catecholamine infusion compared to obese or lean subjects (51). Increased lipolytic norepinephrine sensitivity of sc adipocytes was also reported in women with upper body obesity after weight reduction and refeeding an isocaloric diet (52). In these conditions, increased ß2-AR sensitivity without any change in ß2-AR number was observed (52). Although comparison is difficult (the diet, the characteristics of the patients, and the techniques of investigations were different), the increase in ß1-AR mediated lipolysis in our study could be linked more to hypocaloric diet than to weight reduction.
In conclusion, a hypocaloric diet promotes increased ß-adrenergic lipolysis in vivo in sc adipose tissue in obese patients. This change is associated with an improvement in the ß1-AR-mediated pathway. It remains to be established whether the present findings persist after weight loss and during a weight maintenance diet.
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Acknowledgments |
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Footnotes |
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Received March 11, 1996.
Revised September 4, 1996.
Accepted September 11, 1996.
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References |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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2-adrenoceptors in obese women: effect of exercise and caloric
restriction. Clin Sci. 78:81–87.[Medline]
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