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Obesity: Original Article |
Division of Endocrinology, Department of Internal and Specialistic Medicine, Garibaldi Hospital, University of Catania Medical School, 95123 Catania, Italy
Address all correspondence and requests for reprints to: Lucia Frittitta, M.D., Endocrinologia, Ospedale Garibaldi, Piazza S. M. di Gesù, 95123 Catania, Italy. E-mail: lfritti{at}unict.it.
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Abstract |
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Considering all subjects both together and subdivided into nonobese (n = 107) and obese (n = 135) groups, plasma adiponectin, but not plasma leptin, was significantly (P < 0.01) correlated with insulin sensitivity [homeostasis model assessment of insulin-resistance index (HOMAIR), insulin sensitivity index (ISI) at oral glucose tolerance test, and clamp in 115 of 242 individuals], high-density lipoprotein cholesterol, and triglycerides. These relationships were still significant (P < 0.01) after adjusting for age, gender, body mass index (BMI), and ISI. After WL (–16.8 ± 0.8%), plasma adiponectin increased, and plasma leptin decreased (P < 0.0001 for both). Their changes (
) were significantly correlated with -BMI (P < 0.05 for both). -Adiponectin, but not -leptin, significantly (P < 0.001) correlated with -high-density lipoprotein cholesterol and -triglycerides; these correlations were independent of age, gender, -BMI, and -ISI (P < 0.005). In conclusion, both cross-sectional and intervention studies indicate that plasma adiponectin level correlates with serum lipids independently of fat mass. The intervention study also suggests that adiponectin increase after WL is correlated with serum lipid improvement independently of insulin sensitivity changes.
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Adipose tissue, a major regulator of the metabolic adaptation to stored energy availability (5, 6, 7), exerts these functions through the secretion of different hormone-like peptides, named adipocytokines. Adipocytokines include leptin, adipsin, TNF-
, adiponectin, and resistin (8, 9, 10, 11, 12, 13, 14): their dysregulation is known to be involved in the etiology of insulin resistance (5, 6, 15).
Leptin affects energy homeostasis by inhibiting food intake and stimulating energy expenditure (8). Both leptin synthesis and circulating levels are increased in obese patients and are correlated with the fat mass in a chronic manner (16, 17); most obese patients are leptin resistant. Adiponectin is inversely correlated with leptin (18, 19); its plasma levels are significantly reduced in obese subjects (20), in insulin-resistant subjects, and in type 2 diabetic patients (21) and increased after weight reduction (22). Two independent case-control studies in healthy Caucasians (23) and in Pima Indians (24) indicate that low plasma adiponectin levels are associated with an increased risk of type 2 diabetes.
Adiponectin has antidiabetic and antiatherogenic properties (25, 26) that are believed to be related to its inverse relationship with body fat mass and insulin resistance. Whether these parameters are necessary mediators for the metabolic effects of adiponectin, however, is not clear. Evidence in the adiponectin knockout mouse (25) and in subjects with genetic backgrounds of diabetes (27) suggest that adiponectin’s biological effect may be independent of fat mass and insulin resistance.
To address this issue, we first studied the relationship between plasma adiponectin concentrations, insulin sensitivity, and serum lipid parameters in a large series of unrelated nondiabetic individuals who were either nonobese (n = 107) or obese (n = 135) to evaluate the influence of body fat mass. Second, we carried out an intervention study and evaluated both these parameters and adiponectin changes in a subgroup of 95 obese patients before and after weight loss (WL). In all subjects, plasma leptin was also measured both to have an independent marker of fat mass and to compare adiponectin behavior with that of another adipocytokine with a well-established relationship with insulin resistance.
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Subjects and Methods |
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Two hundred forty-two nondiabetic (according to American Diabetes Association criteria) subjects (87 males and 155 females) were studied. One hundred seven subjects were nonobese, and 135 were obese [body mass index (BMI) 
30 kg/m2]. Nonobese subjects were recruited from the staff of our hospital; obese subjects were recruited from both hospital staff and the outpatient Obesity and Metabolic Clinic of our institute. Clinical investigation was conducted in accordance with the guidelines in The Declaration of Helsinki. Informed consent was obtained from all participants before entering the study, which was approved by the local research ethics committee. All subjects were kept on a weight-maintaining diet and were not on medications known to interfere with the studied variables. On the day of the study, after a 10-h overnight fast, two systolic and diastolic blood pressure recordings were obtained at 5-min intervals in all subjects.
The clinical characteristics of the subjects are shown in Table 1
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Euglycemic-hyperinsulinemic clamp (29) was performed in a subgroup of 115 subjects representative of the entire cohort (47 males and 68 females; age, 38.6 ± 1.3 yr, mean ± SEM; range, 17–70 yr; BMI, 31.7 ± 0.9 kg/m2; range, 17.5–55.9 kg/m2; 61 nonobese and 54 obese). Clamp studies were performed with insulin infusion at a constant rate (40 mU/m2·min) and with variable glucose infusion to maintain plasma glucose within 10% of the baseline value for 2 h, as previously described (30). The M value (the glucose metabolized, M) was calculated from the average glucose infusion rate (equivalent to metabolized glucose) between 60 and 120 min.
In all 242 subjects, the homeostasis model assessment of insulin-resistance index (HOMAIR) was calculated according to the following formula: fasting glucose (mmol/liter) x fasting insulin (mU/liter)/22.5 (31). HOMAIR values were strongly correlated with clamp M values (r = –0.78; P < 0.0001; n = 115).
Plasma glucose and insulin levels were also measured in all subjects before and 60 and 120 min after a 75-g oral glucose tolerance test (OGTT) and the ISI was calculated according to the following formula: 10,000/
(glucose0 x insulin0 x glucosemean x insulinmean) (32). ISI values were strongly correlated with both M values (r = 0.84; P < 0.0001) and HOMAIR (r = –0.94; P < 0.0001).
Methods
Blood samples for adipocytokines, hormone, and metabolic parameter measurements were drawn after an overnight fast. Plasma glucose was measured by the glucose oxidase method on a Beckman Glucose Analyzer 2 (Beckman Coulter, Inc., Fullerton, CA) and plasma insulin by microparticle enzyme immunoassay (Abbott Laboratories, Abbott Park, IL). Total cholesterol and triglycerides were evaluated by enzymatic methods (Instrumentation Laboratory, Milan, Italy). High-density lipoprotein cholesterol (HDL-C) fraction was separated by the use of Mg2+ and the dextran sulfate method (Sclavo Diagnostics, Siena, Italy).
Adiponectin and leptin were measured by RIA (Linco Research, Inc., St. Charles, MO) in plasma samples immediately frozen and stored at –20 C.
Statistical analyses
Values are given as mean ± SEM. Mean values from two different groups were compared by unpaired Student’s t test or Mann-Whitney test, as appropriate. Mean value differences between groups, after adjusting for several covariates, were evaluated by analysis of covariance test. Simple and multiple regression analyses were used to test the relationships between plasma adiponectin and leptin concentrations and the other measured variables. Clinical features, metabolic parameters, and plasma adiponectin and leptin levels before and after WL were compared by paired Student’s t test.
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Results |
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Plasma adiponectin (P < 0.01) and plasma leptin (P < 0.0001) levels were significantly higher in females (adiponectin, 16.7 ± 0.6 µg/ml; leptin, 36.5 ± 1.9 ng/ml) than in males (14.2 ± 0.6 µg/ml and 10.0 ± 1.4 ng/ml, respectively). These differences remained significant also after data adjustment for both age (P = 0.001 for both adiponectin and leptin) or age and BMI (P < 0.0001 for both).
Plasma adiponectin levels were significantly higher in nonobese (18.3 ± 0.7 µg/ml) than in obese subjects (13.8 ± 0.5 µg/ml; P < 0.0001). This difference remained significant also after data adjustment for age (P < 0.0001) or age and gender (P < 0.0001).
Plasma leptin levels, as expected, were significantly higher in obese (41.7 ± 1.9 ng/ml) than in nonobese (8.4 ± 0.7 ng/ml; P < 0.0001) subjects. This difference remained significant also after data adjustment for age (P < 0.0001) or age and gender (P < 0.0001).
Cross-sectional study
Simple and multiple correlations in all subjects studied.
Plasma adiponectin and leptin levels were inversely correlated (r = –0.16; P = 0.01), also after adjusting data for age and gender (P < 0.001) (Fig. 1). However, when data were corrected also for BMI, this correlation was lost (P = 0.3).
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Plasma leptin levels were positively correlated with BMI (r = 0.75; P < 0.0001), waist circumference (r = 0.70; P < 0.0001), WHR (r = 0.25; P = 0.0003), fasting plasma glucose (r = 0.33; P < 0.0001) and insulin (r = 0.44; P < 0.0001), HOMAIR (r = 0.43; P < 0.0001), and HDL-C (r = 0.28; P < 0.0001) and negatively correlated with age (r = –0.20; P = 0.003), ISI (r = –0.53; P < 0.0001), and total cholesterol/HDL-C (r = –0.24; P = 0.0003). However, at variance with adiponectin, all these leptin correlations were no longer significant (except WHR, P < 0.05) after adjustment for age, gender, and BMI, thus confirming that plasma leptin reflects mainly the effect of body fat mass on these parameters.
Insulin sensitivity, as measured by euglycemic clamp in a subgroup of 115 subjects, was strongly correlated with both plasma adiponectin (r = 0.44; P < 0.0001) and leptin (r = –0.59; P < 0.0001) concentrations. Again, after adjustment for age, gender, and BMI or waist circumference, only plasma adiponectin, but not leptin, was still correlated with the M values (P < 0.001).
Obese vs. nonobese subjects
When subjects were grouped according to BMI into nonobese (BMI < 30 kg/m2; n = 107) and obese (BMI 30 kg/m2; n = 135) groups, plasma adiponectin was correlated with BMI in nonobese subjects (r = –0.27, P < 0.005 and P = 0.001 after adjustment for age and gender) (Fig. 2A), but not in obese subjects (Fig. 2B). Plasma adiponectin, in contrast, was significantly correlated with insulin sensitivity (evaluated by both clamp M and ISI value, Fig. 3, A and B, respectively) and lipid parameters (HDL-C and triglycerides, Fig 3, C and D, respectively) in both nonobese and obese subjects, also after adjustment for age and gender (P < 0.05–0.0001 for all).
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) and obese subjects (r = 0.45; P < 0.0001) (Fig. 2D), also after adjustment for age and gender (P < 0.0001 for both). As far as insulin sensitivity is concerned, in both nonobese and obese subjects, plasma leptin was not correlated with M or ISI (except for the relationship in nonobese subjects with the ISI value, r = –0.22; P < 0.05). Also, no significant correlations, after adjustment for age and gender, were observed between plasma leptin and lipid parameters in both nonobese and obese subjects. Intervention study: plasma adiponectin and leptin and WL
In a subgroup of 95 obese patients, plasma adiponectin and leptin levels were measured before (baseline value) and after WL. WL (–16.8 ± 0.8% of basal weight, range –3.5 to –37.1%) was associated with a significant increase of plasma adiponectin and a significant decrease of leptin concentrations (Table 2). When these changes were calculated as values (plasma concentration after WL minus baseline level), -adiponectin was negatively correlated with baseline adiponectin (r = –0.23, P < 0.05, P < 0.05 after adjustment for age and gender). Furthermore, -adiponectin was significantly correlated with changes in BMI (r = –0.20; P < 0.05; Fig 4A), HDL-C (r = 0.41; P < 0.0001; Fig 4C) and triglycerides (r = –0.34; P < 0.001; Fig 4E), and these relationships remained significant also after adjustment for age and gender (P < 0.05–0.0001 for all). Interestingly, the relationship between -adiponectin and -HDL-C and -triglycerides was independent of changes in adiposity (P < 0.005, after adjustment for age, gender and -BMI or -leptin) and changes in insulin sensitivity (P < 0.001, after adjustment for age, gender, and -ISI).
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-BMI (r = 0.3; P < 0.005; Fig. 4B) but, at variance with adiponectin, no correlations were observed with -HDL-C and -triglycerides (Fig. 4, D and F, respectively).
Moreover, as expected, insulin sensitivity improved significantly after WL (Table 2) and was significantly correlated with -BMI (r = 0.30, P < 0.005, and P < 0.005 after adjustment for age and gender). In contrast, no correlation was present between -ISI and either -adiponectin or -leptin.
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Discussion |
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In the present study, we have investigated the specific role of adiponectin and leptin by analyzing the correlation of their plasma levels with a variety of metabolic and clinical parameters related to the insulin resistance syndrome. Data were also corrected both for fat mass, fat distribution, and insulin sensitivity to overcome the influence of these factors.
First, we studied a cohort of nondiabetic subjects spanning a wide range of BMI (from normal weight to severe obesity) and found that plasma levels of adiponectin and leptin were inversely correlated but that this relationship was no longer present after data adjustment for BMI. In addition, the two adipocytokines had different behaviors: the plasma adiponectin relationship with insulin sensitivity (i.e. M value of glucose disposal at clamp, ISI at OGTT and HOMAIR) and serum lipid profile (total cholesterol/HDL-C ratio, HDL-C, and triglyceride levels) was statistically independent of body fat mass, whereas the correlation between leptin and those parameters was entirely mediated by BMI. This difference between the two adipocytokines was present also when only obese patients were considered: plasma adiponectin was correlated with insulin sensitivity, triglycerides, and HDL-C concentrations but not with the degree of obesity, whereas plasma leptin was only correlated with BMI. These data indicate that also in obese patients, at variance with leptin, the relationship between plasma adiponectin and either insulin sensitivity or serum lipids is independent of body fat mass. Our studies, carried out in subjects unrelated to diabetic patients yet providing results similar to a previous study carried out in a large cohort of subjects that included more than 50% first-degree relatives of type 2 diabetics (27), exclude the influence of the diabetic genetic background on the BMI-independent relationship between plasma adiponectin and both insulin sensitivity and lipid profile.
Despite the strong correlation between adiponectin levels and insulin sensitivity, a wide variability of adiponectin levels was observed, even in subjects having similar insulin sensitivity and/or BMI. Similar observations have already been reported (20, 21, 27) and may be attributed to a number of factors that influence adiponectin synthesis and secretion (including hormones like glucocorticoid, TNF- intracellular mediators like cAMP, and drugs like thiazolidinediones) (33). In addition, common genetic variants of the adiponectin gene may influence circulating adiponectin levels and, therefore, also adiponectin changes after WL (34, 35).
All available evidence is based on correlation studies and suggests that in human beings, adiponectin’s influence on insulin sensitivity is independent of fat mass. To better identify the specific role of fat mass on this relationship, we carried out an intervention study in 95 obese patients, studied before and 6–12 months after WL. As expected, plasma adiponectin levels increased (+22% with respect to baseline levels), and plasma leptin levels decreased (–45%) after WL. Changes were correlated with the baseline levels of each adipocytokine and with the amount of body weight reduction. In these patients, adiponectin changes after WL correlated with triglyceride decrease and HDL-C increase but, surprisingly, not with insulin sensitivity changes, although insulin sensitivity improvement was directly correlated with WL. Moreover, the relationship between plasma adiponectin changes and serum lipid changes was independent from the degree of WL. These data, in concert with the results obtained at the cross-sectional study, strongly suggest that adiponectin levels directly regulate lipid metabolism and that this effect is independent from the patient fat mass, WL, and insulin sensitivity. These observations, if confirmed in larger series, may have important clinical implications. Baseline adiponectin level measurements could be useful in identifying obese patients at high risk of dyslipidemia and cardiovascular disease. The obese individuals with the highest plasma adiponectin levels may represent a subgroup of patients with a lower atherogenic risk because of a better lipid profile and the ability of adiponectin to inhibit the development of endothelial dysfunction and the atherosclerotic vascular changes (36, 37, 38). In contrast, obese individuals with the lowest adiponectin levels should be considered at high risk for cardiovascular disease: a WL program and (when available) adiponectin treatment should be highly recommended in these patients.
The observation that, after WL, changes in adiponectin levels are not related to changes in insulin sensitivity may have different explanations. It is known that adiponectin circulates as a full-length form active in the liver (39) and a globular form active in skeletal muscles (40). The two forms interact with the specific receptors AdipoR1 and AdipoR2 (41). Changes of circulating adiponectin may differently involve the two forms and, therefore, the biological effects in target tissues (42, 43). Because the present assay measures both forms, we have no insight on this issue: it is therefore possible that small changes in total plasma adiponectin levels (such as the 22% we have observed after WL) have important biological effects because these changes involve also the relative prevalence of the specific form. Because data in animal models suggest that the major biological effect of adiponectin occurs in target tissues (i.e. muscle, liver, and fat), where it increases the activity of molecules involved in fatty acid transport and oxidation (44, 45), the present observations suggest that adiponectin may have a direct effect in decreasing tissue fatty acid content and serum lipids and that amelioration of insulin resistance is only a secondary effect.
In conclusion, our studies indicate that in both nonobese and obese subjects, low plasma adiponectin concentrations are associated with insulin resistance, independently of the subject’s BMI. In addition, adiponectin changes after WL are associated with an antiatherogenic amelioration of the lipid profile, an effect that is independent from both the degree of body weight reduction and from the changes in insulin sensitivity. This positive effect on the lipid profile may also help explain the role of adiponectin in protecting against endothelial dysfunction and atherosclerotic vascular changes (36, 37, 38).
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Footnotes |
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Abbreviations: BMI, Body mass index; HDL-C, high-density lipoprotein-cholesterol; HOMAIR, homeostasis model assessment of insulin-resistance index; ISI, insulin sensitivity index; OGTT, oral glucose tolerance test; WHR, waist-to-hip ratio; WL, weight loss.
Received October 10, 2003.
Accepted February 3, 2004.
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T. W.K. Ng, G. F. Watts, M. S. Farvid, D. C. Chan, and P. H. R. Barrett Adipocytokines and VLDL Metabolism: Independent Regulatory Effects of Adiponectin, Insulin Resistance, and Fat Compartments on VLDL Apolipoprotein B-100 Kinetics? Diabetes, March 1, 2005; 54(3): 795 - 802. [Abstract] [Full Text] [PDF]
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D. C. Chan, G. F. Watts, T. W.K. Ng, Y. Uchida, N. Sakai, S. Yamashita, and P. H. R. Barrett Adiponectin and other Adipocytokines as Predictors of Markers of Triglyceride-Rich Lipoprotein Metabolism Clin. Chem., March 1, 2005; 51(3): 578 - 585. [Abstract] [Full Text] [PDF]
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) and obese (•) subjects. Adiponectin was positively correlated with M value, ISI, and HDL-C and negatively correlated with triglycerides in both nonobese and obese subjects. At multiple regression analysis, correlations between plasma adiponectin and M value (P = 0.01 and P = 0.006 for nonobese and obese, respectively), ISIlog (P < 0.0001 for both nonobese and obese), HDL-C (P < 0.01 for both nonobese and obese), and triglycerides (P < 0.05 and P < 0.0001 for nonobese and obese subjects, respectively) remained significant after adjusting data for age and gender.