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Journal of Clinical Endocrinology & Metabolism , doi:10.1210/jc.2005-0742
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The Journal of Clinical Endocrinology & Metabolism Vol. 90, No. 9 5324-5328
Copyright © 2005 by The Endocrine Society

BRIEF REPORT

Circulating Resistin Levels Are Not Associated with Fat Redistribution, Insulin Resistance, or Metabolic Profile in Patients with the Highly Active Antiretroviral Therapy-Induced Metabolic Syndrome

Diana Barb1, Sanjivini G. Wadhwa1, Juergen Kratzsch, Alina Gavrila, Jean L. Chan, Catherine J. Williams, Adolf W. Karchmer and Christos S. Mantzoros

Divisions of Endocrinology, Diabetes, and Metabolism (D.B., A.G., J.L.C., C.J.W., C.S.M.) and Infectious Disease (S.G.W., A.W.K.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215; and Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, University of Leipzig (J.K.), 04109 Leipzig, Germany

Address all correspondence and requests for reprints to: Dr. Christos S. Mantzoros, Division of Endocrinology, Diabetes, and Metabolism, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Stoneman 816, Boston, Massachusetts 02215. E-mail: cmantzor{at}bidmc.harvard.edu.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Context: The mechanisms underlying the development of the highly active antiretroviral therapy (HAART)-induced metabolic syndrome remain to be fully elucidated.

Objective: The objective of this study was to investigate whether the adipocyte-secreted hormone, resistin, is associated with anthropometric and metabolic abnormalities of the HAART-induced metabolic syndrome.

Design, Setting, and Patients: We conducted a cross-sectional study of 227 HIV-positive patients (37 women and 190 men) recruited from the infectious diseases clinics. On the basis of history, physical examination, dual-energy x-ray absorptiometry, and single-slice computed tomography, patients were classified into four groups: non-fat redistribution (n = 85), fat accumulation (n = 42), fat wasting (n = 35), and mixed fat redistribution (n = 56).

Main Outcome Measures: The main outcome measures were serum resistin levels and anthropometric and metabolic variables.

Results: Mean serum resistin levels were not significantly different among subjects with fat accumulation, fat wasting, or mixed fat redistribution or between these groups and the non-fat redistribution group. We found a weak, but significant, positive correlation between resistin and percent total body fat (r = 0.20; P < 0.01), total extremity fat (r = 0.18; P < 0.01), and abdominal sc fat (r = 0.19; P < 0.01), but not abdominal visceral fat (r = –0.10; P = 0.16) or waist to hip ratio (r = –0.05; P = 0.43). When adjustments were made for gender (women, 3.92 ± 2.71 ng/ml; men, 2.96 ± 2.61 ng/ml; P = 0.05), correlations between resistin and the above parameters were no longer significant. Importantly, resistin levels were not correlated with fasting glucose, insulin, homeostasis model assessment of insulin resistance index, triglycerides, or cholesterol levels in the whole group.

Conclusions: Resistin is related to gender, but is unlikely to play a major role in the insulin resistance and metabolic abnormalities of the HAART-induced metabolic syndrome.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
ALTHOUGH HIGHLY ACTIVE antiretroviral therapy (HAART) prolongs survival in HIV-infected individuals, a metabolic syndrome often complicates its use. The latter increases morbidity and mortality, mainly due to cardiovascular disease (1). Lipodystrophic changes in this syndrome consist of body fat redistribution (FR; lipoatrophy, lipohypertrophy, or a combination of both) and are associated with insulin resistance (IR), hyperglycemia, and dyslipidemia. These metabolic abnormalities accompanying FR occur in more than half of the HAART-treated patients (2, 3). It has been suggested that HAART may interfere with adipocyte differentiation (1, 2) and may directly (4) or through FR affect the expression and circulating levels of TNF{alpha}, IL-6, leptin, and adiponectin (2). Nevertheless, the etiology of the HAART-induced metabolic syndrome has not been fully elucidated.

Resistin, an adipocyte-secreted cystein-rich peptide, also called adipocyte-secreted factor or FIZZ-3 (found in inflammatory zone 3), has been postulated to link obesity with diabetes (5, 6). The administration of resistin to animals has resulted in impaired glucose and lipid metabolism in some studies (5, 7), but these findings are challenged by subsequent reports of no associations between adipose tissue resistin expression and IR (8, 9). Findings in humans have also been variable. Elevated resistin levels have been noted in obese (10) and diabetic (11) subjects, and increased resistin has been associated with IR in lean and obese subjects (12). Other studies, however, have found no association between circulating resistin levels and IR (10, 11, 13, 14, 15).

In a recent study of patients with the HAART-induced metabolic syndrome, resistin levels decreased after administration of rosiglitazone, an insulin sensitizer, but the physiological relevance of this finding remains uncertain, because the researchers report no correlation between resistin and IR or markers of inflammation and coagulation (16). To further elucidate the relationship between resistin and IR in the HAART-induced metabolic syndrome, we examined the relationship among resistin levels, body composition, and IR in a cross-sectional study of 227 consecutively enrolled, HIV-infected patients.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Subjects were recruited from the infectious diseases and general medicine clinics at our institution from August 2000 through January 2004. All subjects provided informed consent to participate. Inclusion criteria were age greater than 16 yr, documented HIV infection, and a cumulative exposure to antiretroviral therapy for a minimum of 6 months. Data were collected during a study visit at the General Clinical Research Center. Each subject provided a detailed medical history and underwent physical examination and anthropometric measurements. Fasting blood samples were obtained for measurement of resistin, insulin, glucose, and lipids. CD4 counts and HIV RNA levels were obtained within 2 months of the study visit. Dual-energy x-ray absorptiometry was used to measure body composition (fat and fat-free mass). Abdominal visceral and sc fat were assessed by single-slice computed tomography at the L4 level.

Using previously published criteria (17), based on physical examination, measurement of waist and upper arm circumferences, waist to hip ratio (WHR), triceps and subscapular skinfolds, total body fat, and total abdominal and visceral fat (17), three blinded investigators adjudicated subjects into one of four groups: non-FR, fat accumulation (FA), fat wasting (FW), or mixed FR (MFR). One subject was excluded from analysis because of incomplete data, and eight subjects were excluded because the adjudication committee did not unanimously agree upon their classification. Thus, 218 subjects were used for the between-group statistical analysis, and all 227 subjects were used for the correlation analysis.

Insulin levels were measured by RIA (Diagnostic System Laboratories, Inc., Webster, TX; sensitivity, 1.3 µIU/ml; inter- and intraassay coefficients of variation, 4.7–12.2% and 4.5–8.3%, respectively). IR was estimated using the homeostasis model: homeostasis model assessment of IR (HOMA-IR) = (fasting insulin x fasting glucose)/22.5. Serum resistin concentrations were measured at the Institute of Laboratory Medicine, Clinical Chemistry, and Molecular Diagnostics (Leipzig, Germany) using an in-house ELISA (sensitivity, 0.4 ng/ml). The average intra- and interassay coefficients of variation for three control samples (23.6, 6.7, and 1.9 ng/ml) were 6.9% and 8.1%, respectively (n = 12). Lipid and lipoprotein levels were measured as previously described (17).

Statistical analysis

SPSS 11.0 (SPSS, Inc., Chicago, IL) and SAS 8.0 (SAS Institute, Cary, NC) were used for analysis. We compared the four groups using one-way ANOVA with Bonferroni correction for continuous variables and {chi}2 tests for categorical variables. We used Spearman correlation coefficients to assess associations between resistin and anthropometric and metabolic variables, cumulative HIV medication use, CD4 count, and HIV RNA. We adjusted for gender using Spearman partial correlations. P < 0.05 was declared statistically significant. All statistical tests were two-tailed. The study had sufficient power (80% at the conventional two-tailed {alpha} = 0.05 level) to detect a level of correlation of r ≥ 0.18 (16).


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
Table 1Go shows baseline characteristics of the 218 subjects considered for analysis in the non-FR or FR groups. Subjects in the non-FR group were younger. There were more women in the FA group (P < 0.05) than in the non-FR group. Subjects in the MFR (P < 0.05) and FW (P = 0.069) groups were diagnosed with HIV infection earlier than those in the non-FR group. There were no differences in current CD4 or HIV RNA levels among the groups.


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  		TABLE 1. Characteristics of HIV subjects (n = 218)

 
Differences in anthropometric and body composition parameters were consistent with the adjudication process among the FR groups (Table 1Go). Subjects in the FA group had significantly greater weight, body mass index, total body fat, total extremity fat, abdominal total fat, and abdominal sc fat (all P < 0.001) compared with all other groups and significantly higher abdominal visceral fat compared with the non-FR and FW groups (P < 0.001). They also had higher glucose levels (P < 0.05) compared with all other groups and the highest prevalence of diabetes (Table 1Go). Conversely, the FW group had lower total body and extremity fat (P < 0.01), abdominal total fat, and abdominal sc fat (P < 0.05) than the non-FR group. The MFR group had higher total abdominal and visceral fat and lower total extremity fat than the non-FR group (P < 0.01).

All three FR groups as well as the combined FR group had higher fasting insulin levels than the non-FR group (P < 0.05; Table 1Go). FA and MFR groups had significantly higher HOMA-IR indexes than the non-FR group (P < 0.05). The prevalence of diabetes was higher in the combined FR groups than in the non-FR group (23.9% vs. 2.4%; P < 0.01). Fasting triglycerides levels were higher in the MFR group compared with the non-FR group (P < 0.001; Table 1Go). Although total and low-density lipoprotein cholesterol did not differ between groups, high-density lipoprotein cholesterol was lower in the MFR and FW groups than in the non-FR (P < 0.001) and FA groups (P < 0.005).

There were no differences in fasting resistin levels between the FR and non-FR groups or among the FR groups. However, we found a gender difference in resistin levels, with women having higher levels than men (women, 3.92 ± 2.71 ng/ml; men, 2.96 ± 2.61 ng/ml; P = 0.05). To further evaluate predictors of resistin, we performed correlation analysis between resistin and anthropometric and metabolic variables, HIV medication exposure, and disease duration (Table 2Go). In bivariate analyses, resistin was significantly and positively correlated with percent body fat (r = 0.20; P < 0.01), total extremity fat (r = 0.18; P < 0.01), and abdominal sc fat (r = 0.19; P < 0.01), but not with abdominal visceral fat (r = –0.10; P = 0.16) or WHR (r = –0.05; P = 0.43). In addition, there was a negative correlation between serum resistin levels and lean mass (r = –0.14; P < 0.05). We found no correlation of serum resistin with fasting insulin, glucose, HOMA-IR, triglycerides, cholesterol levels, duration of HIV infection, cumulative antiretroviral treatment, CD4 count, or HIV RNA levels (Table 2Go). Cumulative or current exposure to a protease inhibitor (PI)-based HAART regimen was not associated with resistin levels (data not presented). Because a significant association between resistin and gender was noted, partial correlation analyses were performed with adjustment for gender and revealed no independent correlations between resistin and percent body fat, abdominal sc fat, or lean mass (Table 2Go). Analyses excluding diabetic patients showed similar results (data not shown).


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  		TABLE 2. Spearman correlation coefficients of resistin with metabolic and anthropometric factors, HIV medication use, disease severity and duration, unadjusted and adjusted for gender (n = 227, 37 women and 190 men)

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
The HAART-induced metabolic syndrome occurs in more than half of the patients treated with PIs (3). The mechanisms underlying the FR and IR in HAART-treated, HIV-infected patients are not completely understood. The most firmly established risk factor for the development of this syndrome is treatment with PIs and/or nucleoside reverse transcriptase inhibitors, with combination therapy most strongly associated with severe lipoatrophy (1).

PIs inhibit sterol regulatory enhancer-binding protein-1 and adipocyte expression of peroxisome proliferator-activated receptor-{gamma} (PPAR{gamma}), a nuclear factor that has an important role in adipogenesis and lipid and glucose metabolism (1, 2). Nucleoside reverse transcriptase inhibitors inhibit mitochondrial DNA polymerase within adipocytes, which results in mitochondrial injury and inhibition of adipogenesis and adipocyte differentiation (1, 2). In addition, HIV-related factors, such as HIV-1 accessory proteins, may increase tissue sensitivity to glucocorticoids and inhibit PPAR{gamma} activity (2). Finally, changes in FR may alter the expression and circulating levels of adipocyte-secreted molecules that alter energy homeostasis and insulin responsiveness (2). For example, leptin and adiponectin are decreased in subjects with the HAART-induced lipoatrophy (17, 18), whereas TNF-{alpha} is increased (2).

Resistin, a novel PPAR{gamma}-responsive adipocytokine (5, 8, 16, 19), has been postulated to play a role in IR, inflammation, and regulation of adipose tissue mass by altering adipocyte differentiation (6). Although the receptors for resistin remain to be described, recent studies suggest that resistin may induce the expression of suppressor of cytokine signaling-3, a known inhibitor of leptin and insulin signaling (20). The clinical relevance of this observation remains to be better elucidated.

The absence of an association between serum resistin and IR, as assessed by HOMA-IR in this study, is consistent with our previous data in HIV-negative subjects (13) and with other recent studies in humans (10, 11, 14, 15, 16). Moreover, hyperinsulinemic glucose clamp studies showed no correlation between serum resistin and whole body glucose disposal rate in HIV-negative subjects (14, 19). Nevertheless, results from studies evaluating resistin in humans remain divergent; some researchers have reported increased levels in obesity and diabetes (10, 11), and others have reported no change in resistin under these conditions (13). These discrepancies may reflect differences in the study population and experimental design and/or differences in the sensitivity of the assays used (16). Alternatively, gender could be a confounding factor.

The positive correlation among resistin, total fat mass, and abdominal sc fat in this study is consistent with previous reports in humans (14, 15, 21), but after adjustment for gender, the correlations between resistin and percent body fat and abdominal sc fat are no longer significant. These data suggest that gender is an important determinant of resistin levels in humans. This sexual dimorphism of resistin and other adipocytokines, including leptin and adiponectin, has been previously reported in studies of non-HIV-positive subjects (21, 22). Our findings that resistin levels are similar in HIV-infected subjects with or without FR and that resistin is not associated with markers of central obesity, IR, or hyperlipidemia do not support a role for this molecule in the HAART-induced metabolic syndrome. Although some studies have reported higher resistin mRNA expression in visceral compared with peripheral fat (23, 24), our data do not show a significant correlation between circulating resistin levels and abdominal visceral fat and do not support a role for resistin in mediating the effect of visceral fat on IR in the HAART-induced metabolic syndrome.

Although the cross-sectional design of this study prevents the firm establishment of the lack of a causal relationship between resistin and the HAART-induced metabolic syndrome, it is one of the first to probe for an association. Only one recent study has evaluated resistin in 24 HIV-infected subjects. It demonstrated that resistin levels decreased with rosiglitazone administration, but were not associated with IR, metabolic parameters, or inflammatory markers (16). The researchers suggested that the relatively small size of their study might have prevented demonstrations of statistical significance. The previous study was adequately powered (>80%) to demonstrate associations of r ≥ 0.55 at an {alpha} = 0.05 level. Our study confirms their data in a larger sample, which provides similar power (80%) to demonstrate significance at the 0.05 level even if lower correlations of r≥0.18 are present, i.e. correlation coefficients that may be of clinical relevance.

In conclusion, circulating resistin levels are related to adiposity, possibly through an underlying association with gender, but are unlikely to play a major role in the IR and metabolic abnormalities associated with the HAART-induced metabolic syndrome.


   Footnotes
 
This work was supported by an American Diabetes Association clinical research grant; National Institutes of Health Grants DK-58785-R01 (to C.S.M.), M01-RR-01032 (to Beth Israel Deaconess Medical Center General Clinical Research Center), and K30-HL-04095 (to Harvard Medical School); and Merck Research Laboratories.

First Published Online June 14, 2005

1 D.B. and S.G.W. contributed equally to this paper. Back

Abbreviations: FA, Fat accumulation; FR, fat redistribution; FW, fat wasting; HAART, highly active antiretroviral therapy; HOMA-IR, homeostasis model assessment of insulin resistance; IR, insulin resistance; MFR, mixed fat redistribution; PI, protease inhibitor; PPAR-{gamma}, peroxisome proliferator-activated receptor-{gamma}; WHR, waist to hip ratio.

Received April 6, 2005.

Accepted June 3, 2005.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

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