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Québec Heart Institute (M.C., N.A., I.L., J.-P.D.), Laval Hospital Research Center, Ste-Foy, Québec, Canada G1V 4G5; Department of Food Sciences and Nutrition (M.C., N.A.); Division of Kinesiology (P.M., A.T., J.-P.D.), Department of Social and Preventive Medicine; and Institute on Nutraceuticals and Functional Foods (A.T.), Laval University, Ste-Foy, Québec, Canada G1K 7P4; and Lipid Research Center (J.B.), CHUL Research Center, Ste-Foy, Québec, Canada G1V 4G2
Address all correspondence and requests for reprints to: Jean-Pierre Després, Ph.D., FAHA, Québec Heart Institute, Laval Hospital Research Center, 2725, chemin Ste-Foy, Pavilion Marguerite-D’Youville, 4th Floor, Ste-Foy, Québec, Canada G1V 4G5. E-mail: jean-pierre.despres{at}crhl.ulaval.ca.
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDISCUSSIONReferences |
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r –0.32; P < 0.04), multiple regression analyses revealed that visceral AT accumulation was the only independent predictor of adiponectin levels, with 10% of its variance explained by visceral AT (P < 0.0001). Comparison of obese men with similar body mass index values (
30 kg/m2) but who markedly differed in their level of visceral AT (< vs. 130 cm2; n = 15) revealed significant differences in adiponectin levels (7.0 ± 3.0 vs. 11.1 ± 4.9 µg/ml; P < 0.02 for men with high vs. low visceral AT, respectively). Finally, when men were stratified into tertiles of visceral AT and further classified on the basis of the 50th percentile of adiponectin levels ( vs. >8.8 µg/ml), a 3 x 2 ANOVA revealed an independent contribution of adiponectin on the variation of high-density lipoprotein cholesterol levels (P < 0.002) and of the glucose area (P < 0.02). These results support the notion that adiponectin concentration is influenced to a greater extent by visceral than sc obesity. Furthermore, adiponectin predicts glucose tolerance and plasma high-density lipoprotein cholesterol levels in a manner that is partly independent from the contribution of visceral adiposity. |
Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDISCUSSIONReferences |
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In this regard, the size of the visceral AT depot is an important correlate of plasma adiponectin levels that may potentially be the link between visceral obesity and some of its related metabolic abnormalities, which contribute to the development of insulin resistance, type 2 diabetes, and coronary heart disease (13, 14). However, whether adiponectin levels explain some of the individual differences in metabolic risk variables for type 2 diabetes and cardiovascular disease after control for the concomitant variation in the level of visceral AT remains unclear. Therefore, the purpose of the present study was to explore the associations between adiponectin levels and adiposity and body fat distribution indices assessed by computed tomography (visceral and sc AT) and to evaluate the independent contribution of adiponectinemia to the variation in metabolic risk variables beyond the effect of visceral AT.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDISCUSSIONReferences |
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The study sample included 190 men (mean age ± SD, 43.5 ± 8.5 yr) who were recruited from the Québec City metropolitan area by solicitation through the media. Participants were selected on purpose to cover a wide range of body mass index (BMI) values (18.7–39.1 kg/m2). All subjects were healthy, nonsmoking volunteers and were not under treatment for coronary heart disease, diabetes, dyslipidemias, or endocrine disorders. All participants gave their written consent to participate in the study, which was approved by the Medical Ethics Committee of Laval University.
Anthropometric measurements and computed tomography
Height, body weight (15), and waist circumference (16) were measured following standardized procedures. Body density was measured by the hydrostatic weighing technique (17). The mean of six measurements was used to calculate percent body fat from body density using the equation of Siri (18). Fat mass was obtained by multiplying body weight by percent body fat. Measurement of abdominal AT areas was performed by computed tomography with a Siemens Somatom DHR scanner (Siemens, Erlanger, Germany) as previously described (19). Briefly, the subjects were examined in the supine position with both arms stretched above the head. The scan was performed at the abdominal level (L4 and L5 vertebrae) using an abdominal scout radiograph to standardize the position of the scan to the nearest millimeter. Total AT area was calculated by delineating the abdominal scan with a graph pen and then by computing the total abdominal AT area with an attenuation range of –190 to –30 Houndsfield units (19). The abdominal visceral 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.
Plasma lipoprotein and lipid variables
Blood samples were collected in the morning from an antecubital vein into vacutainer tubes containing EDTA (Miles Pharmaceuticals, Rexdale, Ontario, Canada) after a 12-h overnight fast for the measurement of plasma lipid and lipoprotein levels. Cholesterol and triglyceride levels were determined in plasma and lipoprotein fractions on Technicon RA-500 (Bayer, Tarrytown, NY), and enzymatic reagents were obtained from Randox (Crumlin, UK). Plasma very low-density lipoproteins (density > 1.006 g/ml) were isolated by ultracentrifugation (20). The high-density lipoprotein (HDL) fraction was obtained after precipitation of low-density lipoprotein in the infranatant (density > 1.006 g/ml) with heparin and MnCl2 (21). The cholesterol and triglyceride concentrations of the infranatant were measured before and after the precipitation step.
Oral glucose tolerance test (OGTT)
A 75-g OGTT was performed in the morning after an overnight fast. Blood samples were collected in EDTA-containing tubes through a venous catheter placed in an antecubital vein at –15, 0, 15, 30, 45, 60, 90, 120, 150, and 180 min for the determination of plasma glucose and insulin concentrations. Plasma glucose was measured enzymatically (22), whereas plasma insulin was measured by RIA with polyethylene glycol separation (23). The total glucose and insulin areas under the curve during the OGTT were determined with the trapezoid method.
Determination of adiponectin concentrations
Fasting plasma adiponectin concentrations were determined by an ELISA (B-Bridge International, Inc., San Jose, CA) on whole plasma kept at –80 C before use. The intra- and interassay coefficients of variation were 3.3 and 7.4%, respectively.
Statistical analyses
Data are presented as means ± SE. Linear relationships among variables were computed by Pearson’s correlation coefficients. A multiple linear regression analysis was performed to evaluate the independent contribution of adiposity variables to the variance in adiponectin concentrations. Subjects were individually matched for BMI (30 kg/m2) but with high vs. low levels of visceral AT (< vs. 130 cm2; n = 15) and compared with a subgroup of nonobese men (BMI < 25 kg/m2). The threshold value of visceral AT of 130 cm2 had been previously reported to be associated with a significant deterioration of metabolic variables predictive of type 2 diabetes and cardiovascular disease (24). A one-way ANOVA was used to compare the group of lean men with the two subgroups of obese men. Moreover, to verify the potentially additional effect of adiponectin levels to the variance in metabolic risk variables beyond visceral AT accumulation, subjects were stratified into tertiles of visceral AT and further classified on the basis of the 50th percentile of adiponectin levels ( vs. >8.8 µg/ml). Differences between groups were tested using ANOVA followed by Duncan’s multiple range test. Contributions of adiponectin (low vs. high according to the 50th percentile) and visceral AT (tertiles) and their interaction term (adiponectin * visceral AT) on metabolic risk variables were tested by ANOVA. All statistical analyses were performed with the SAS statistical system (SAS Institute, Cary, NC).
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDISCUSSIONReferences |
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. Overall, subjects covered a wide range of age, BMI, and body fat distribution variables. Figure 1 illustrates relationships between selected variables of adiposity and adiponectin concentrations in the overall sample. Plasma adiponectin levels were negatively correlated with BMI (r = –0.18, P < 0.02), sc AT (r = –0.14, P < 0.04), visceral AT (r = –0.32, P < 0.0001), and total AT (r = –0.24, P < 0.0009). Moreover, Fig. 2 depicts relationships between lipoprotein and lipid variables and adiponectin concentrations. Despite the absence of correlation with low-density lipoprotein cholesterol (r = –0.05, P = not significant), plasma adiponectin levels were negatively correlated with triglyceride concentrations (r = –0.26, P < 0.0004) and positively correlated with HDL cholesterol levels (r = 0.33, P < 0.0001). Negative associations between area under the curve of plasma glucose (r = –0.23, P < 0.001) or fasting insulin (r = –0.25, P < 0.0005) levels measured during a 75-g oral glucose load and adiponectin concentrations were also observed. Although all adiposity and AT distribution indices were negatively correlated with plasma adiponectin levels, multiple regression analyses revealed that visceral AT accumulation was the only independent predictor of adiponectin levels. For instance, approximately 10% of the variance in adiponectin concentrations was explained by visceral AT in a model including waist girth, fat mass, BMI, and visceral AT (P < 0.0001).
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30 kg/m2) were individually matched for similar BMI values (n = 15) but with high vs. low levels of visceral AT (< vs. 130 cm2; average visceral AT areas of 227.3 vs. 103.4 cm2 for men with high vs. low visceral AT, respectively; P < 0.0001) and then compared with nonobese subjects (with both BMI < 25 kg/m2 and visceral AT < 130 cm2, n = 39; Fig. 3). Comparison of these two subgroups of obese patients revealed significant differences in adiponectin levels. Indeed, this procedure revealed that viscerally obese men were characterized by the lowest adiponectin concentrations (7.0 ± 3.0 µg/ml) compared with obese men with low visceral AT accumulation (11.1 ± 4.9 µg/ml) or nonobese men (11.9 ± 6.8 µg/ml). Furthermore, no difference was observed between obese men with low visceral AT and nonobese subjects.
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vs. >8.8 µg/ml). Figure 4 shows that, although visceral AT contributed to the variation in HDL cholesterol and the glucose area, adiponectin levels also had a statistically significant and independent impact on the variation of these metabolic variables. However, the interaction term between adiponectin concentrations and visceral AT regarding their impact in these metabolic risk variables was not significant.
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DISCUSSION |
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TopAbstractIntroductionSubjects and MethodsResultsDISCUSSIONReferences |
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Results of the present study also support the notion that variations in adiponectin levels are influenced by visceral AT to a greater extent than sc obesity. In our study, although adiponectin concentrations correlated with BMI, fat mass, sc AT, and total AT, the strongest relationship was observed with visceral AT. Moreover, results of the multiple regression analysis revealed that, among all adiposity variables studied, visceral AT accumulation was the only independent predictor of adiponectin levels. Indeed, our study has shown that visceral AT could explain 10% of the variation in adiponectin concentrations. Accordingly, a study by Yatagai et al. (13), which investigated the contribution of regional adiposity to adiponectinemia, showed that visceral fat area but not sc fat area measured by computed tomography was independently related to adiponectinemia. To further document this issue, the comparison of obese men with similar BMI but who substantially differed in their level of visceral AT revealed marked differences in adiponectin levels, with viscerally obese men (130 cm2) being characterized by lower adiponectin concentrations than obese men with low levels of visceral AT (<130 cm2). Other study groups have previously reported that visceral AT accumulation was closely associated with substantial alterations in indices of plasma glucose-insulin homeostasis and with variables of the plasma lipoprotein and lipid profile (28, 29). The present study supports the notion that the cluster of high-risk metabolic complications associated with visceral obesity is also associated with low plasma adiponectin concentrations. Thus, considering the significant relationships between adiponectin concentrations, hyperinsulinemia, and visceral AT, hypoadiponectinemia might be responsible, at least in part, for the link between insulin resistance and visceral fat accumulation. Our results indicate that a low adiponectin concentration represents another metabolic complication observed in the presence of visceral obesity among individuals characterized by the features of the metabolic syndrome.
In this regard, we were interested in quantifying the specific contribution of adiponectin concentrations to the variance in metabolic risk variables beyond visceral AT. Our results revealed independent contributions of adiponectin concentrations to the variance in HDL cholesterol levels and in the glucose area after a 75-g OGTT. Thus, in our study, adiponectin levels were independently predictive of some metabolic complications beyond the contribution of visceral adiposity. Cnop et al. (14) have reported a strong positive correlation between adiponectin and HDL cholesterol independently from visceral AT, explaining 37% of the variance in HDL cholesterol. Our results are also concordant with a previous study that has shown a strong correlation between plasma adiponectin levels and HDL cholesterol independently of age, gender, BMI, and fasting insulin concentration (30). In that study, adiponectin appeared to predict HDL cholesterol levels in patients with type 2 diabetes, independently of common metabolic risk factors (30). Thus, it is possible that adiponectin, like HDL cholesterol, could eventually be considered as an independent protective cardiovascular risk factor (30). Such a strong correlation between adiponectin and HDL cholesterol levels may possibly be explained by the activation of peroxisome proliferator-activated receptor-
, which influences the expression of genes encoding for proteins involved in HDL metabolism (31). For instance, adiponectin has been reported to increase peroxisome proliferator-activated receptor- ligand activities both in skeletal muscle and liver (32, 33), leading to an increased synthesis of HDL cholesterol.
Moreover, the independent contribution of adiponectin concentrations to the variance in glucose tolerance also supports the role of adiponectin levels in the regulation of plasma glucose and insulin homeostasis. In this regard, it has been previously reported that plasma adiponectin levels were negatively associated with fasting plasma insulin and glucose concentrations (34). These results are concordant with the concept that adiponectin may have an insulin-sensitizing effect. For instance, numerous studies have reported an association between circulating adiponectin concentrations and various metabolic parameters regulating insulin sensitivity (9, 10, 35). Recent studies have also shown a relationship between high plasma adiponectin levels and an increased insulin sensitivity independent of BMI, percent body fat, and waist to hip ratio (36). Furthermore, increased concentrations of adiponectin were found to be strongly and independently associated with reduced risk of incident type 2 diabetes in apparently healthy individuals (37). Studies in mouse have shown that administration of recombinant adiponectin improved hyperglycemia and hyperinsulinemia in a lipoatrophic mouse model (38) and that it had a glucose-lowering effect (39). In fact, an increase in circulating adiponectin levels was shown to inhibit both the expression of hepatic gluconeogenic enzymes and the rate of endogenous glucose production, which could explain the improvement in insulin sensitivity (40). Furthermore, the molecular mechanism by which adiponectin may affect insulin action has been suggested to involve a molecule playing a role in fatty acid oxidation and glucose uptake in the muscle; this molecule is the 5'-AMP-activated protein kinase (41). For instance, high adiponectin levels induce the expression of 5'-AMP-activated protein kinase, which increases glucose uptake and fatty acid oxidation in muscle, leading to improved insulin sensitivity (41). Taken together, these results suggest that adiponectin is a regulator of insulin sensitivity through the reduction of ectopic fat deposition. Finally, in accordance with the notion that adiponectin is secreted by visceral AT (26) and that it is under feedback inhibition in obesity, a high visceral fat accumulation will lead to decreased adiponectin concentrations and then to an increased susceptibility to a whole cluster of metabolic complications, increasing the risk of type 2 diabetes, atherosclerosis, and cardiovascular disease. Although it is still unclear whether the hypoadiponectinemia that is observed in type 2 diabetic patients is attributed to visceral fat accumulation or to some other genetic factors, there is compelling evidence that adiponectin plays a role in the regulation of insulin action and that it may protect against the impairment of insulin action and of glucose homeostasis. Thus, adiponectin may play a significant role in the pathogenesis of type 2 diabetes, and it may eventually be used as an index of risk for the development of this metabolic disease (37).
In conclusion, results of the present study indicate that adiponectin concentrations are more closely related to visceral AT than total adiposity. Furthermore, adiponectin predicts glucose tolerance and HDL cholesterol levels beyond the contribution of visceral adiposity. These findings support the notion that adiponectinemia could play a role in the development of a dysmetabolic state and could, therefore, be involved in the relationship between visceral obesity and the development of type 2 diabetes and cardiovascular disease. Additional studies will be required to understand the molecular mechanisms behind these associations.
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Footnotes |
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First Published Online December 14, 2004
Abbreviations: AT, Adipose tissue; BMI, body mass index; HDL, high-density lipoprotein; OGTT, oral glucose tolerance test.
Received August 30, 2004.
Accepted December 1, 2004.
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References |
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TopAbstractIntroductionSubjects and MethodsResultsDISCUSSIONReferences |
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: direct role in obesity-linked insulin resistance. Science 259:87–91 activation and high-density lipoprotein metabolism. Am J Cardiol 88:24N–29N
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