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Original Studies |
Lipid Research Center, Laval University Medical Research Center (P.M., D.P., S.L., J.P.D.); Diabetes Research Unit, CHUL Medical Research Center (A.N.), and Physical Activity Sciences Laboratory (P.M., M.B., D.P., A.T.), Laval University, Ste-Foy, Quebec, Canada
Address all correspondence and requests for reprints to: Pascale Mauriège, Ph.D., Lipid Research Center, Laval University Medical Research Center, CHUL, 2705 boulevard Laurier, Ste-Foy, Quebec, Canada G1V 4G2.
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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2-adrenergic agonist)
assessed in sc adipocytes were similar among men with low
vs. high levels of visceral AT. However, the
ß-adrenoceptor sensitivity was increased in sc abdominal adipose
cells of individuals with a high visceral AT accumulation compared to
those with a low intraabdominal fat deposition. Positive relationships
were also found between the lipolytic sensitivity of sc abdominal
adipocytes and plasma insulin concentrations measured in the fasting
state and after an oral glucose load. These results suggest that
variation in the degree of visceral adiposity in men does not seem to
be associated with differences in regional adipose cell maximal
lipolytic capacity once fat cell size is taken into account. However,
the greater ß-adrenoceptor lipolytic sensitivity of sc abdominal
adipocytes could be considered a significant correlate of the increased
insulinemia observed among men characterized by high levels of visceral
AT. |
Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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2-adrenoceptor component (12, 13, 14, 15, 16, 17). The greater
portal free fatty acid (FFA) release by visceral adipose cells may lead
to reduced hepatic insulin extraction and hyperinsulinemia, as well as
to an enhanced production of triglyceride and apolipoprotein
B-rich lipoproteins, which are features of an insulin-resistant state
(1, 3, 18). However, it is also possible that the relationship observed
between visceral AT deposition and metabolic complications may not
exclusively result from an increased FFA flux from visceral adipocytes
into the portal vein, but could also be partly attributed to an
enhanced lipolytic response of sc fat cells. Indeed, sc abdominal
adipose cell lipolysis has been shown to be positively related to
plasma triglyceride and insulin levels in premenopausal women (19).
Basal and stimulated lipolysis, when expressed per cell number, have
also been associated with high plasma FFA levels, suggesting that these
metabolic alterations were simply the result of an enlarged adipose
tissue mass (20). When its activity was adjusted for the concomitant
variation in cell surface area, adipose tissue lipolysis was no longer
a strong predictor of an altered metabolic risk profile (20). However,
to the best of our knowledge, no study has attempted to identify
primary alterations in sc adipose tissue lipolysis in visceral obesity
once the concomitant variation in adipose cell size is taken into
account. Indeed, prior experiments that have been conducted on subjects
with low vs. high levels of visceral AT have compared the
lipolytic activities of sc adipocytes that differed in size among
groups (8, 9, 17, 21, 22, 23, 24, 25). Therefore, the aim of the present investigation was to examine whether regional differences in sc adipose tissue lipolysis may be considered one mechanism by which an increased amount of visceral AT is related to an altered metabolic risk profile in 18 pairs of moderately overweight men matched for a similar sc abdominal fat cell weight but characterized by low vs. high levels of visceral AT.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Thirty-six healthy, moderately overweight, male volunteers, aged 36 ± 3 yr (mean ± SD; range, 30–42 yr), were recruited through the media and gave their written informed consent to participate in this study, which was approved by the Laval University Medical ethics committee. Eighteen pairs of subjects individually matched both for similar levels of sc abdominal adipose tissue area (within 5 cm2) measured by computed tomography (CT) and for sc abdominal fat cell weight (within 0.02 µg lipid/cell), but displaying marked differences in visceral adipose tissue accumulation determined by CT, were compared for potential differences in sc adipocyte lipolysis. All participants were subjected to a physical examination by a physician, which included medical history. Subjects with cardiovascular disease, diabetes, or other endocrine disorders or those taking medication that could have potentially influenced lipid metabolism were excluded. All men were sedentary, nonsmokers, moderate alcohol consumers, and had stable body weights at the time of the study, i.e. no subject had been involved in a weight loss program or on a diet for the last 6 months.
Total body fatness and regional fat distribution
Body density was determined by the underwater weighing technique (26), and the percent body fat was derived from body density (27). Pulmonary residual volume was measured using the helium dilution method (28). Fat mass was calculated as total body weight minus fat-free mass. Waist girth was measured according to the procedures recommended at the Airlie Conference (29).
CT was performed with a Siemens Somatom DRH scanner (Erlangen, West Germany), as previously described (30). Subjects were examined in the supine position. CT scans were performed at the abdominal (between L4 and L5 vertebrae) and at the femoral (middistance between the knee joint and the iliac crest) levels, with a radiograph of the skeleton as a reference to establish the position of the scan to the nearest millimeter. The total AT area was calculated by delineating the abdomen with a graph pen and then computing the AT surface using an attenuation range of -190 to -30 HU. The visceral abdominal AT area was measured by drawing a line within the muscle wall surrounding the abdominal cavity. The abdominal sc AT area was calculated by subtracting the visceral AT area from the total abdominal AT area.
AT biopsy procedure and adipocyte lipolysis
After an overnight fast, men were subjected to biopsies of sc fat, one performed in the periumbilical region (abdominal site) and the other at the midthigh level (femoral site). A small cutaneous incision (1 cm) was made at both sites, and about 200 mg sc adipose tissue were surgically removed from the two fat depots. Adipocytes were isolated according to the method of Rodbell (31) in a Krebs-Ringer bicarbonate buffer (pH 7.4) containing 4% BSA (KRBA) and 5 mmol/L glucose plus 1 mg/mL collagenase, as previously described (14, 25, 26). Digestion took place in a shaking water bath under an air-gas phase of 95% O2 and 5% CO2, for 40 min at 37 C. The suspension was then filtered, and the cellular filtrate obtained was rinsed three times with 5 mL KRBA. Isolated adipocytes were finally resuspended in KRBA to obtain a final concentration of approximately 500 cells/50 µL.
Extracellular glycerol release was used as the indicator of adipocyte lipolysis. One hundred-microliter aliquots of the continuously stirred cell suspension were placed in 1.5-mL conical tubes. Two of these tubes were used for cell counting and sizing; two others containing 20 µL KRB were immediately placed on ice and provided an evaluation of the initial concentration of glycerol in the medium. Ascorbic acid (0.1 mmol/L) was included in the incubation medium to prevent catecholamine degradation. Agents for lipolysis stimulation or inhibition were added just before the beginning of the assay in 20-µL portions to obtain the desired final concentration. After a 2-h incubation at 37 C in a shaking water bath under an air-gas phase of 95% O2 and 5% CO2, 100 µL HCl (1 N) were added to all tubes to stop the reaction, then 100 µL NaOH (1 N) were added to neutralize the medium. All tubes were stoppered and stored at -20 C until glycerol determination, and the NADH concentration was measured by bioluminescence with a luciferase solution, using an 125I LKB Wallac luminometer (Gaithersburg, MD) (13, 24, 25). For each concentration of stimulator or inhibitor, the amount of glycerol was taken as the average of the concentrations assessed in two incubated tubes. Glycerol measurement by bioluminescence is very sensitive and especially well adapted when only small amounts of adipose tissue are available (24, 25). Fat cell diameters were determined using a Leitz microscope equipped with a graduated ocular (Rockleigh, NJ). The mean fat cell diameter was assessed from the measurement of 500 cells, and the density of triolein was used to transform adipose cell volume into fat cell weight (24).
The lipolytic activity of the isolated fat cells was assessed in the
presence of epinephrine (EPI), which is a mixed agonist
(2/ß) with a higher affinity for
2-adrenoceptor sites (12), clonidine
(2-agonist) (12, 24), and isoproterenol (nonselective
ß-agonist). When antilipolytic effects were investigated
(i.e. for EPI and clonidine), the incubation buffer was
supplemented with 5 µg/mL adenosine deaminase (ADA) to remove
adenosine released in the incubation medium by the isolated fat cells;
this procedure allows for more accurate investigations of
2-mediated antilipolytic effects (12, 24). Some
experiments were also conducted with postadrenoceptor agents, which
were tested at maximum effective concentration: forskolin (direct
activator of adenylate cyclase), theophylline (mainly inhibitor of
phosphodiesterase), and dibutyryl cAMP (stimulator of the protein
kinase hormone-sensitive lipase complex) (13, 25). Finally, due to the
limited amount of fat that could be obtained from biopsies, additional
assays using selective ß1-adrenoceptor (dobutamine) and
ß2-adrenoceptor (procaterol) agonists (13, 32) were only
performed on eight pairs of matched men. Glycerol release was expressed
per cell surface area to compensate for regional and individual
differences in fat cell size. In cases where complete dose-response
curves were obtained (i.e. for the 2- and
ß-adrenoceptor agonists), they were compared for both sensitivity and
responsiveness. The ß-adrenergic sensitivity was considered the
ß-agonist concentration giving half-maximal stimulation of lipolysis
(EC50), whereas the 2-adrenergic sensitivity
was calculated as the dose of clonidine that produced half-maximal
inhibition of lipolysis (IC50). Both were evaluated by
logarithmic conversion of each dose-response curve. The higher was the
EC50 of the ß-agonist or the IC50 of
clonidine; the lower was the ß- or 2-adrenergic
sensitivity, respectively. Responsiveness was expressed as the
difference between basal glycerol release and the lipolytic rate at the
maximum effective concentration of the agents tested (10-5
mol/L various ß-agonists or forskolin; 10-3 mol/L
dibutyryl cAMP or theophylline). Maximal inhibition of lipolysis noted
at 10-7 mol/L EPI or 10-5 mol/L clonidine was
calculated as the following ratio: (ADA - EPI or
clonidine/ADA - basal), where ADA represents ADA-stimulated
lipolysis.
Oral glucose tolerance test (OGTT)
A 75-g OGTT was performed in the morning after an overnight fast. Blood samples were collected in tubes containing ethylenediamine tetraacetate and Trasylol (Miles Pharmaceutics, Rexdale, Canada) through a venous catheter from an antecubital vein at -15, 0, 15, 30, 45, 60, 90, 120, 150, and 180 min. Plasma glucose was measured enzymatically (33), whereas the plasma insulin concentration was determined by RIA with polyethylene glycol separation (34). Plasma FFA levels were determined at -15, 0, 60, 120, and 180 min using a colorimetric method (35). The total glucose, insulin, and FFA areas under the curve during OGTT were calculated with the trapezoid method.
Drugs and chemicals
Collagenase, BSA, ADA, and enzymes for glycerol assays were obtained from Boehringer Mannheim (Montréal, Canada). Ascorbic acid, theophylline, forskolin, dibutyryl cAMP, clonidine hydrochloride, (-)isoproterenol bitartrate, and (-)EPI bitartrate were purchased from Sigma Chemical Co. (St. Louis, MO). Procaterol (OPC 2009; 5-(1-hydroxy-2-isopropylaminobutyl)-8-hydroxycarbostyril hydrochloride hemihydrate) was a generous gift from Otsuka Pharmaceuticals (Tokushima, Japan), whereas dobutamine hydrochloride (Dobutrex) was obtained from Eli Lilly & Co. (Indianapolis, IN). All other chemicals and organic solvents were of the highest purity grade commercially available. The same batches of hormones, pharmacological agents, collagenase, and albumin were used in all experiments.
Statistical methods
The normality of distribution of each variable was tested, and whenever necessary, log-transformed data were used in statistical analyses. Two subgroups of 18 men characterized by a low or a high visceral AT accumulation were individually matched for similar sc abdominal AT area determined by CT and fat cell size and were compared. Differences between groups were tested for significance with Student’s unpaired t test or the 2 (fat distribution type) x 2 (site) ANOVA. Associations between two variables were quantified using the Pearson product-moment correlation coefficient. All statistical analyses were performed using Super ANOVA and StatView software programs (SPSS, Evanston, IL) adapted for MacIntosh computers (Apple Computer, Cupertino, CA).
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The physical characteristics of our sample of moderately
overweight men with either low or high levels of visceral AT are
presented in Table 1
. As expected from
the matching procedure, neither the body mass index nor the percent
body fat differed among subjects with either a low or a high visceral
AT accumulation. Obviously, the two subgroups were quite different for
visceral AT (P < 0.05) but showed similar sc abdominal
AT areas. On the other hand, no regional variation was found in sc
adipose cell size in both groups (Table 1). As shown in Table 2, subjects with high visceral AT areas
displayed higher fasting plasma insulin levels and insulin responses to
an OGTT than matched men characterized by low levels of visceral AT
(P < 0.05).
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Basal lipolytic rate, ADA-stimulated lipolysis, and lipolytic
response to postadrenoceptor agents. When expressed per cell
number, basal lipolysis was not significantly different between both
adipose regions and groups. There was also no regional variation or any
difference between matched men with low vs high levels of visceral fat
when lipolysis was stimulated with maximal concentrations of either
dibutyryl cAMP (10-3 mol/L), forskolin (10-5
mol/L), or theophylline (10-3 mol/L). On the other hand,
when the incubation buffer was supplemented with ADA at 5 µg/mL,
basal lipolysis was increased by about 2–2.3 times in all cell types.
Glycerol release in the presence of this enzyme was similar in both
adipose depots and groups (Table 3).
Similar results were obtained when lipolysis was expressed per U cell
surface area (not shown).
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2 and ß) adrenergic
properties on lipolysis, initiated a similar biphasic responsiveness in
sc abdominal and femoral adipocytes from both groups (Fig. 1). The catecholamine initiated a
biphasic response profile in all adipose cells; an inhibition of
lipolysis was observed at the lowest concentrations (from
10-9–10-7 mol/L), and this effect was
completely reversed at higher doses (from
10-6–10-5 mol/L), at which the
hormone exerted a lipolytic action. Both the maximal lipolytic response
(at 10-5 mol/L) as well as the maximal antilipolytic
effect (at 10-7 mol/L) of the hormone assessed in sc
abdominal or femoral adipocytes did not vary among individuals
characterized by low or high levels of visceral AT. However, the only
group difference was found at 10-6 mol/L EPI (a
concentration at which the ß-adrenoceptor component is expressed),
which promoted a greater lipolysis in sc abdominal adipose cells of men
displaying a high visceral AT accumulation compared to individuals with
a low visceral AT deposition (P < 0.05). On the other
hand, the catecholamine response profile in femoral adipocytes was
similar in both groups. The maximal hormonal lipolytic response was
also lower in femoral than in sc abdominal adipose cells regardless of
the subjects’ level of visceral AT (P < 0.05).
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2- and ß-adrenergic
effects. As EPI responsiveness results from both
2- and ß-adrenoceptor stimulation, selective
adrenergic agonists were used to discriminate between these two
antagonistic effects.
To study the influence of the 2-adrenoceptor component,
the effect of the 2-agonist clonidine was tested on
ADA-stimulated lipolysis (Fig. 2).
Neither the maximal antilipolysis (at 10-5 mol/L) nor the
2-adrenergic sensitivity, estimated as the half-maximal
antilipolysis induced by clonidine (which clustered at 10 nmol/L), was
significantly different among adipose depots or between the two matched
groups.
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). Maximal stimulation of lipolysis
induced by isoproterenol (at 10-5 mol/L) did not
strikingly differ among adipose regions or between the two matched
groups. However, the concentration of agonist required for
half-maximal lipolysis was significantly lower in sc abdominal
adipose cells from individuals with high levels of visceral AT compared
to that in subjects with low visceral AT accumulation
(P < 0.01), suggesting a greater ß-adrenergic
sensitivity in visceral obese men. In contrast, no difference between
groups was observed in the sensitivity of femoral adipose cells to the
ß-agonist. Moreover, abdominal adipocytes showed a higher
ß-adrenoceptor sensitivity than femoral adipose cells among men with
high levels of visceral AT exclusively (P < 0.01;
Table 4).
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). However, the shift
to the left of the dose-response curve for procaterol in sc abdominal
adipocytes of visceral obese men (Fig. 4)
was consistent with an increased ß2-adrenergic
sensitivity in the adipose cells of visceral obese men (Table 4)
compared to that in individuals with low amounts of intraabdominal fat.
Abdominal adipocytes of visceral obese men were also more sensitive to
ß2-adrenoceptor stimulation than femoral adipose cells,
although no regional variation in the ß2-adrenergic
sensitivity was observed in individuals characterized by low visceral
AT deposition (Table 4). In contrast, the ß1-adrenergic
sensitivity of adipocytes from both regions did not differ among men
with low or high levels of visceral AT (Table 4).
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Plasma insulin levels measured in the fasting state and after the OGTT
were negatively associated with the concentration of ß-agonist,
(EC50; isoproterenol) required for half-maximal lipolysis
assessed in sc abdominal adipocytes (-0.48 < r < -0.50;
P < 0.005; Fig. 5).
These associations remained significant after adjustment for visceral
AT (-0.36 < r < -0.41; P < 0.05),
although they were of lower magnitude than those previously shown.
Similarly, fasting plasma insulin concentrations or insulin responses
after the OGTT displayed negative relationships with the dose of
ß2-agonist (EC50; procaterol) that promoted
half-maximal lipolysis in sc abdominal adipose cells from a subsample
of 16 individuals (-0.42 < r < -0.45; P
< 0.05; not shown). However, plasma insulin levels showed no
significant association with the ß1-adrenergic
sensitivity estimated by the EC50 (dobutamine) assessed in
sc abdominal adipocytes from the latter subgroup of men (-0.10 <
r < -0.15). No consistent relationship was also observed between
subjects’ insulin levels and femoral adipose cell ß-adrenergic
sensitivity (-0.16 < r < -0.20). Neither the maximal
lipolytic response to ß-agonists, the maximal antilipolysis promoted
by epinephrine or clonidine, nor the 2-adrenoceptor
sensitivity in adipose cells showed a significant correlation with
plasma insulin levels (not shown).
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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To the best of our knowledge, this study documents for the first time that visceral obese men display higher epinephrine-induced lipolysis (at 10-6 mol/L) combined with increased lipolytic effects of both isoproterenol and procaterol (noted at 10-8 mol/L), which suggests an enhanced ß-adrenergic receptor (more particularly ß2) component in sc abdominal adipocytes compared to individuals with low levels of visceral AT. However, the lack of difference in the ß1-adrenergic receptor component of adipose cells between the two subgroups is concordant with the idea that the ß2-adrenergic receptor subtype is the major component regulating lipolysis in sc adipocytes assessed in both in vitro and in vivo conditions (32, 36, 37). Our results combined with previous observations (36) reemphasize the fact that individual variation in average ß-AR sensitivity could be largely attributed to differences in ß2- rather than ß1-adrenergic receptors. Furthermore, the higher in vitro ß-adrenergic receptor sensitivity of sc abdominal adipose cells that we observed in visceral obese men may be of physiological relevance, as this variable was found to be a significant correlate of the in vivo lipolytic sensitivity to catecholamines (36).
As only a low proportion of ß-adrenergic receptors needs to be occupied to obtain a maximal effect in human fat cells (5), changes in sensitivity may reflect alterations in hormone action that are located at or near the receptor level (17), whereas alterations in responsiveness are usually linked to changes in hormone action at further intracellular steps in the pathway of the signal. Therefore, the greater ß-adrenergic receptor sensitivity observed in men characterized by high levels of visceral AT could be directly related to a higher number of ß-adrenergic receptors (38), although a better coupling of these receptors to stimulatory GTP-sensitive (Gs) proteins is a possibility that cannot be excluded. The lack of difference between the two matched groups in the maximal lipolytic rates promoted by the ß-agonists or postadrenoceptor agents thus suggests an unaltered hormone responsiveness in visceral obesity when there is proper control for variation in adipose cell size. The finding that the adipose cell lipolytic capacity did not vary among men with low vs. high levels of visceral AT also reemphasizes the fact that the difference in the regulation of adipose cell lipolysis observed between the two matched groups is located at the adrenoceptor level and may be due to alterations in ß-adrenergic receptor (and more particularly ß2) density and/or affinity, but not in adrenergic lipolytic responsiveness. The associations that we have found between insulinemia and the ß-adrenergic receptor (or ß2) sensitivity of sc abdominal fat cells suggest that individuals who were hyperinsulinemic also displayed the lowest EC50 (isoproterenol) or (procaterol) values (i.e. the highest ß- or ß2-adrenergic receptor lipolytic sensitivity) in these cells. Such a relationship between the ß-adrenergic receptor (and to a lesser extent ß2) lipolytic sensitivity of sc abdominal adipose cells and plasma insulin levels is independent from variation in adipose cell size and may suggest a potential role for abdominal adipose tissue lipolysis in the development of hyperinsulinemia in visceral obese men (10, 19, 21, 22, 23, 24).
Finally, whether 1) a high visceral AT deposition results in a greater lipolytic capacity of sc abdominal adipocytes; 2) elevations in sc adipose cell lipolysis may lead to an accumulation of intraabdominal fat; or 3) a third factor, such as an altered neuroendocrine profile, could lead to both an increase in sc adipose cell lipolysis and intraabdominal fat mass, is unclear. We believe that it is unlikely that enhanced sc fat cell lipolysis causes intraabdominal fat deposition, because visceral adipocytes are more lipolytic than sc abdominal adipose cells (8, 9, 10, 11, 12, 13, 14, 17). Although direct evidence is still lacking, it is possible that the association between sc abdominal fat cell lipolysis and intraabdominal fat area instead reflects an alteration in sc adipose cell metabolism resulting from a peculiar neuroendocrine profile in visceral obese patients. Indeed, visceral obesity and its related metabolic complications are associated with alterations in circulating sex steroid hormone levels, and abdominal obese subjects have been suggested to be characterized by an activation of the hypothalamic-pituitary-adrenal axis leading to elevated cortisol secretion and reduced gonadal androgen levels (1, 3, 7, 38). It thus appears possible that glucocorticoids that show permissive effects on catecholamine-induced lipid mobilization may be involved in the abdominal obesity syndrome (1, 3, 7, 38). In this regard, an oral glucocorticoid treatment has been shown to enhance the ß2-adrenergic receptor lipolytic sensitivity and density of sc abdominal adipocytes without affecting the ß1-adrenergic receptor subtype (39), a finding concordant with our observations.
Conclusion
Taken together, these results show that visceral obesity in men does not seem to influence the maximal lipolytic capacity of sc abdominal or femoral adipocytes once the concomitant variation in adipose cell size is taken into account. However, among men characterized by high levels of visceral adipose tissue, a greater ß-adrenergic (and more particularly ß2) lipolytic sensitivity of sc abdominal adipocytes may further exacerbate an impaired insulin action, which seems to be of importance in the etiology of the insulin resistance syndrome of visceral obesity.
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Acknowledgments |
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Footnotes |
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Received June 25, 1998.
Revised November 2, 1998.
Accepted November 11, 1998.
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References |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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2-adrenoceptor binding sites in human fat cells from
various deposits: functional consequences. Eur J Clin Invest. 17:156–165.[Medline]
2A-Adrenergic regulation of cyclic AMP accumulation and
lipolysis in human omental and subcutaneous adipocytes. Int J Obesity. 20:185–189.
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| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
) vs. high (n = 18; 
) levels of
visceral AT. Values are the mean ± SE. Glycerol
release was expressed as the difference between stimulated (with EPI)
and basal (i.e. in the presence of 5 µg/mL ADA)
values. Negative values reflect inhibition of lipolysis. Significant
differences between groups are indicated (*, P <
0.05). a and b, Regional variation in adipose cell hormonal
responsiveness from both groups of men (P <
0.05).
