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Journal of Clinical Endocrinology & Metabolism , doi:10.1210/jc.2006-1368
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The Journal of Clinical Endocrinology & Metabolism Vol. 91, No. 12 5122-5125
Copyright © 2006 by The Endocrine Society

BRIEF REPORT

Serum Resistin and Hepatic Fat Content in Nondiabetic Individuals

Gianluca Perseghin, Guido Lattuada, Francesco De Cobelli, Georgia Ntali, Antonio Esposito, Agata Burska, Elena Belloni, Tamara Canu, Francesca Ragogna, Paola Scifo, Alessandro Del Maschio and Livio Luzi

Internal Medicine (G.P., G.L., G.N., A.B., F.R., L.L.), Section of Nutrition/Metabolism, Departments of Diagnostic Radiology (F.D.C., A.E., E.B., T.C., A.D.M.) and Nuclear Medicine (P.S.), and Unit of Clinical Spectroscopy (G.P., F.D.C., P.S., A.D.M., L.L.), San Raffaele Scientific Institute, 20132 Milan, Italy; and Center "Physical Exercise for Health and Wellness" (G.P., L.L.), Faculty of Exercise Sciences, Università degli Studi di Milano, 20122 Milan, Italy

Address all correspondence and requests for reprints to: Gianluca Perseghin, M.D., Faculty of Exercise Sciences, Università degli Studi di Milano and San Raffaele Scientific Institute, Internal Medicine, Section of Nutrition/Metabolism and Unit of Clinical Spectroscopy, via Olgettina 60, 20132 Milan, Italy. E-mail: perseghin.gianluca{at}hsr.it.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Context: Serum resistin concentration is increased in patients with nonalcoholic fatty liver disease in proportion with the histological severity of the disease, but the relevance of the contribution of fatty liver per se is undetermined.

Objective: The objective of the study was to assess the relationship between serum resistin and the degree of ectopic fat accumulation in vivo in humans.

Design and Setting: The hepatic fat (IHF) content, measured quantitatively by means of 1H magnetic resonance spectroscopy, serum resistin, and biochemical and hormonal metabolic correlates of fatty liver and insulin resistance were assessed in 28 affected patients, and 47 individuals with comparable anthropometric features served as controls. Insulin sensitivity was estimated using the computer homeostatic model assessment (HOMA)-2. A subset of volunteers (n = 18) also underwent 1H magnetic resonance spectroscopy of the calf muscles to assess the intramyocellular lipid content (IMCL).

Results: In patients with fatty liver, the IHF content (13 ± 8 vs. 2 ± 1% wet weight; P < 0.0001) and also the soleus IMCL content (P < 0.05) were increased in comparison with the controls. Patients with fatty liver had lower insulin sensitivity (HOMA2 insulin sensitivity: 59 ± 24 vs. 72 ± 29%; P < 0.04), serum resistin (3.4 ± 0.8 vs. 3.9 ± 1.0 ng/ml; P < 0.02), and adiponectin (P < 0.01) concentrations. Serum resistin was inversely correlated with the IHF content (r = –0.35; P < 0.003) and the soleus IMCL content (r = –0.51; P < 0.05) but not HOMA2 insulin sensitivity.

Conclusion: This study demonstrates that excessive ectopic fat accumulation in the liver and skeletal muscle of insulin-resistant subjects is associated with lower serum resistin concentration and not with hyperresistinemia.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
HISTORICAL STUDIES SUGGESTED that the adipokine hormone resistin may be involved in the pathogenesis of obesity and insulin resistance in animal models (1), but recent works do not support a major role of resistin in humans (2). Additional data also emphasized the importance of resistin as a potential mediator in inflammatory processes (3). Following this line of evidence, Pagano et al. (4) reported that patients with nonalcoholic fatty liver disease (NAFLD) were characterized by higher serum resistin levels in association with the nonalcoholic steatohepatitis (NASH) score, an index that takes into account necrosis, inflammation, and fibrosis in liver biopsies and reflects the severity of the disease, whereas no correlation was found with insulin resistance and the steatosis score, a discrete (three grades) index of liver fat content. The present study was undertaken to clarify the relationship of the hepatic fat accumulation, assessed using 1H magnetic resonance spectroscopy (MRS) as a tool for the quantification of hepatic triglycerides as a continuous variable, with the circulating resistin levels; in addition, ectopic fat accumulation was also assessed at the level of the skeletal muscle site.


   Subjects and Methods
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 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Subjects

Twenty-eight individuals known to have excessive hepatic fat (IHF) content because they participated in a previous survey performed to assess the prevalence of fatty liver among the employees of the San Raffaele Scientific Institute (unpublished data) were recruited for the study. Forty-seven individuals comparable for the anthropometric features, but with normal IHF content, served as control subjects. Normal or higher than normal IHF content was set at 5% wet weight (ww) as suggested by the American Association for the Study of Liver Diseases (5). These individuals were recruited in the outpatients service of the Center of Nutrition/Metabolism of the San Raffaele Scientific Institute. Body weight was stable for at least 6 months, and history of hepatic disease, substance abuse, or daily consumption of more than one alcoholic drink daily (<20 g/d) or the equivalent in beer and wine were exclusion criteria. The anthropometric characteristics of the subjects are summarized in Table 1Go. Subjects were in good health as assessed by medical history, physical examination, hematology, and urinalysis. Recruited subjects gave their informed written consent after explanation of purposes, nature, and potential risks of the study.


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  		TABLE 1. Characteristics of individuals with (IHF content > 5% ww) or without (IHF content < 5% ww) excessive hepatic fat accumulation

 
Experimental protocol

Subjects were instructed to consume an isocaloric diet and to abstain from exercise activity for 3 d before the study. They were studied after an 8- to 10-h overnight fast by means of 1H MRS and indirect calorimetry for the assessment of the IHF content and whole-body energy homeostasis, respectively. Blood drawing and urine collection were performed to measure serum resistin, leptin, adiponectin, insulin, plasma glucose, free fatty acids (FFAs), the lipid profile, biochemical parameters, and urine nitrogen. A subset of volunteers (n = 18) (five with excessive and 13 with normal IHF content) also underwent 1H MRS of the calf muscles to assess the intramyocellular lipid content (IMCL).

1H MRS

Hepatic 1H MRS was performed in all volunteers with the use of a 1.5T whole-body scanner (Gyroscan Intera Master 1.5 MR system; Philips Medical Systems, Best, The Netherlands) as previously described (6, 7). Soleus and tibialis anterior 1H MRS was performed on a GE Signa 1.5 Tesla scanner (General Electric Medical Systems, Milwaukee, WI) as previously described (8).

Indirect calorimetry

Indirect calorimetry was performed continuously for 30 min as previously described (6, 7) with a ventilated hood system (model 2900, metabolic measurement cart; Sensor Medics, Yorba Linda, CA).

Analytical determinations

Glucose (Beckman Coulter, Inc., Fullerton, CA), FFAs, triglycerides, total cholesterol, and high-density lipoprotein (HDL)-cholesterol were measured as previously described (8). Serum resistin was measured by ELISA kit (BioVendor Laboratory Medicine, Inc., Brno, Czech Republic) as previously described (7, 9). The sensitivity of the assay was 0.2 ng/ml of sample. The intraassay coefficient of variation (CV) was less than 3.5% and interassay less than 7%. Plasma levels of insulin (sensitivity 2 µU/ml; intra- and interassay CV < 3.1 and 6%, respectively) and leptin (sensitivity 0.5 ng/ml; intra- and interassay CV < 5 and 9%, respectively) were measured with RIA (Linco Research, St. Charles, MO). Serum adiponectin was measured by ELISA kit (B-Bridge International, Inc., Sunnyvale, CA) with a sensitivity of 25 pg/ml. The intraassay CV was less than 3.7% and interassay less than 6%.

Calculations

Insulin resistance was determined by the updated computer model homeostatic model assessment (HOMA)-2 indexes (10) (available from www.OCDEM.ox.ac.uk). Resting energy expenditure (REE) was calculated by the Weir’s standard equation and from the urinary nitrogen excretion as previously described (6, 7). Glucose, lipid, and protein oxidation were estimated as previously described (6, 7).

Statistical analysis

Data in text and tables are means ± SD. Analyses were performed using the SPSS software (version 10.0; SPSS Inc., Chicago, IL). Comparison between groups was performed using two-tailed independent samples t test, and P < 0.05 was considered to be significant. Variables with skewed distribution assessed using the Kolmogorov-Smirnov test of normality (body mass index, resistin, IHF content, HDL-cholesterol, triglycerides, glucose, TSH, systolic and diastolic blood pressure) were log transformed before the analysis. The relationship between serum resistin and continuous variables was examined by two-tailed Person’s correlation coefficients; partial correlation was used to examine these relationships independently of a group effect.


   Results
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 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
Characteristics of study subjects

Anthropometric features of study groups were not different (Table 1Go). Individuals with excessive IHF content had higher systolic blood pressure and serum triglycerides and lower HDL-cholesterol than controls. In contrast, FFAs and creatinine were not different. REE was not different between groups (1880 ± 262 vs. 1940 ± 338 kcal/die; P = 0.43) and also when normalized for the predicted REE calculated using the Harris Benedict equation (107 ± 11 vs. 109 ± 12% in controls and individuals with excessive IHF content, respectively; P = 0.55); the respiratory exchange ratio, glucose, and lipid oxidation were also not different between groups. Plasma glucose and insulin were not different between groups. Based on HOMA2 insulin sensitivity, individuals with excessive IHF content had reduced insulin sensitivity (P < 0.04), whereas ß-cell insulin sensitivity was not different. Finally, the soleus IMCL content was increased in the subset of individuals with excessive IHF content; in the tibialis anterior muscle, only a trend was found (Table 1Go).

Adipokine concentration

Plasma leptin was not different between groups, whereas serum adiponectin and resistin (3.4 ± 0.8 vs. 3.9 ± 1.0 ng/ml, P < 0.02; Fig. 1AGo) concentrations were lower in the individuals with excessive IHF content. Serum resistin concentration was associated with the IHF content (r = –0.35; P < 0.003; Fig. 1BGo) also when adjusted for the group effect (r = –0.23; P < 0.05). Despite of the low number of patients in which 1H MRS of the calf muscles was performed, resistin was inversely associated also with the soleus IMCL content (r = –0.51; P < 0.05).


Figure 1
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  		FIG. 1. Serum resistin concentration in study groups and its correlation with the IHF content. A, Serum resistin concentration (median ± SD) with quartile cut-offs (dashed lines) is shown to be lower in patients with fatty liver (empty squares) than the controls (filled squares) (independent samples t test, two tails of the log-transformed data; *, P < 0.02). B, Serum resistin concentration is represented by the scatter plot showing a weak but significant correlation between serum resistin and IHF content (r = –0.35; P < 0.003, Pearson correlation of the log-transformed data).

 

   Discussion
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 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
Ectopic fat accumulation in lean tissues is recognized as a marker of insulin resistance. NAFLD was reported in association with impaired insulin-stimulated glucose metabolism and blunted suppression of endogenous glucose production and whole-body lipolysis (11), and excessive IMCL content was associated with peripheral insulin resistance (8). If resistin was involved in the development of insulin resistance, the insulin-resistant subjects with fat accumulation in the ectopic sites should have increased resistin levels. The opposite findings reported here (Fig. 1AGo) may therefore be considered an argument against the hypothesis linking resistin with insulin resistance in humans (2). Our work is in apparent contrast with liver biopsy-derived data showing that patients with NAFLD had increased circulating resistin levels and increased expression in the sc adipose tissue (4). This discrepancy is reconciled by the fact that in the study by Pagano et al. (4), resistin was increased only in the patients with necrosis, inflammation and fibrosis of the liver and resistin reflected the severity of the disease, whereas no correlation was found with insulin resistance and a qualitative and discrete score of steatosis. The strength of the present study is that the IHF content was assessed as a continuous variable using 1H MRS, a tool successfully used for the evaluation of ectopic fat in various organs for more than a decade (12, 13, 14, 15, 16). In this work, its application showed that increased circulating resistin was not associated with fatty liver and suggested that fat accumulation within the liver (Fig. 1BGo) and the soleus muscle is inversely associated with the circulating hormonal concentration. It is likely that in patients with NAFLD, circulating resistin concentration is increased only in those with NASH.

The above-described inverse correlation was weak, even if statistically significant, but we found it also in obese adolescents with excessive IHF content (7), even if in that work the focus of the research was not resistin; in these youngsters, resistin tended to be lower than in the obese adolescents with normal IHF content (4.0 ± 1.1 vs. 5.0 ± 2.2 ng/ml; P = 0.12, as in Ref. 7), and the IHF content and serum resistin were inversely correlated (r = –0.30; P = 0.052). In elite professional athletes, in which the IHF storage may be expected to be depleted, we found that serum resistin concentration was surprisingly increased (9), especially in the athletes involved in aerobic endurance training programs. We believe that all together these data strongly suggest that in humans serum resistin concentration may be inversely associated with the IHF content.

Patients with NASH (4) may represent an exception, and data about type 2 diabetic patients are controversial. Bajaj et al. (16) found a direct proportional relationship between the IHF content and serum resistin concentration in diabetic patients, but more recently Carey et al. (17) reported lower resistin in patients with type 2 diabetes than matched nondiabetic controls, and they suggested that these lower levels may protect the patients against further insulin resistance as it may be in our patients with excessive ectopic fat accumulation. It is possible that similarly to NASH, in type 2 diabetes, the IHF accumulation may be paralleled by a variable degree of necrosis, inflammation, and fibrosis. Epidemiological data, in fact, showed that the prognosis of NAFLD may be worsened by diabetes as a comorbid condition (18). This interpretation supports the hypothesis that high resistin levels in patients with NAFLD and type 2 diabetes are related with increased production in immune and inflammatory cells (19) rather than representing a link with insulin resistance. In contrast with the findings related to resistin, the adipokine circulating concentrations support the possibility that in these patients, low adiponectin may be potentially involved in the pathogenesis of insulin resistance (20). In conclusion, in subjects with excessive ectopic fat accumulation in the liver and skeletal muscle, serum resistin concentration is reduced, arguing against a direct role of resistin as mediator of insulin resistance; whether this represents a compensatory mechanism remains to be determined.


   Footnotes
 
This work was supported by grants from the Italian Minister of Health (RF98.49, RF99.55, RF01.1831). A.B. and G.N. were the recipients of the Marie Curie Host Fellowship of the European Community (Contract HPMT-CT-2001-00329). G.N. is currently a clinical fellow in the Department of Endocrinology, Polikliniki Hospital, Athens, Greece, and a Ph.D. candidate in the Department of Nutrition and Dietetics, Harokopio University, Athens, Greece.

Present address for A.B.: Interfaculty Chair, Department of Laboratory Diagnostics, University of Medicine at Lublin, Lublin, Poland.

Disclosure statement: The authors have nothing to disclose.

First Published Online September 12, 2006

Abbreviations: CV, Coefficient of variation; FFA, free fatty acid; HDL, high-density lipoprotein; HOMA, homeostatic model assessment; IHF, hepatic fat; IMCL, intramyocellular lipid content; MRS, magnetic resonance spectroscopy; NAFLD, nonalcoholic fatty liver disease; NASH, nonalcoholic steatohepatitis; REE, resting energy expenditure; ww, wet weight.

Received June 26, 2006.

Accepted September 5, 2006.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

  1. Steppan CM, Bailey ST, Baht S, Brown EJ, Banerjee RR, Wright CM, Patel HR, Ahima RS, Lazar MA 2001 The hormone resistin links obesity to diabetes. Nature 409:307–312[CrossRef][Medline]
  2. Arner P 2005 Resistin: yet another adipokine tells us that men are not mice. Diabetologia 48:2203–2205[CrossRef][Medline]
  3. Bokarewa M, Nagaev I, Dahlberg L, Smith U, Tarkowski A 2005 Resistin, an adipokine with potent proinflammatory properties. J Immunol 174:5789–5795[Abstract/Free Full Text]
  4. Pagano C, Soardo G, Pilon C, Milocco C, Basan L, Milan G, Donnini D, Faggian D, Mussap M, Plebani M, Avellini C, Federspil G, Sechi LA, Vettor R 2006 Increased serum resistin in nonalcoholic fatty liver disease is related to liver disease severity and not to insulin resistance. J Clin Endocrinol Metab 91:1081–1086[Abstract/Free Full Text]
  5. Neuschwander-Tetri BA, Caldwell SH 2003 Nonalcoholic steatohepatitis: summary of an AASLD single topic conference. Hepatology 37:1202–1219[CrossRef][Medline]
  6. Perseghin G, Lattuada G, De Cobelli F, Esposito A, Costantino F, Canu T, Ragogna F, Scifo P, De Taddeo F, Maffi P, Secchi A, Del Maschio A, Luzi L 2005 Reduced intra-hepatic fat content is associated with increased whole body lipid oxidation in patients with type 1 diabetes. Diabetologia 48:2615–2621[CrossRef][Medline]
  7. Perseghin G, Bonfanti R, Magni S, Lattuada G, De Cobelli F, Canu T, Esposito A, Scifo P, Ntali G, Costantino F, Bosio L, Ragogna F, Del Maschio A, Chiumello G, Luzi L 2006 Insulin resistance and whole body energy homeostasis in obese adolescents with fatty liver disease. Am J Physiol Endocrinol Metab 10.1152/ajpendo. 00017
  8. Perseghin G, Scifo P, De Cobelli F, Pagliato E, Battezzati A, Arcelloni C, Vanzulli A, Testolin G, Pozza G, Del Maschio A, Luzi L 1999 Intramyocellular triglyceride content is a determinant of in vivo insulin resistance in humans: a 1H-13C NMR spectroscopy assessment in offspring of type 2 diabetic parents. Diabetes 48:1600–1606[Abstract]
  9. Perseghin G, Burska A, Lattuada G, Alberti G, Costantino F, Ragogna F, Oggionni S, Scollo A, Terruzzi I, Luzi L 2006 Increased serum resistin in elite endurance athletes with high insulin sensitivity. Diabetologia 49:1893–1900[CrossRef][Medline]
  10. Wallace TM, Levy JC, Matthews DR 2004 Use and abuse of HOMA modeling. Diabetes Care 27:1487–1495[Abstract/Free Full Text]
  11. Marchesini G, Brizi M, Bianchi G, Tomassetti S, Bugianesi E, Lenzi M, McCullough AJ, Natale S, Forlani G, Melchionda N 2001 Nonalcoholic fatty liver disease: a feature of the metabolic syndrome. Diabetes 50:1844–1850[Abstract/Free Full Text]
  12. Longo R, Ricci C, Masutti F, Vidimari R, Croce LS, Bercich L, Tiribelli C, Dalla Palma L 1993 Fatty infiltration of the liver quantification by 1H localized magnetic resonance spectroscopy and comparison with computed tomography. Invest Radiol 28:297–302[Medline]
  13. Szczepaniak LS, Nurenberg P, Leonard D, Browning JD, Reingold JS, Grundy S, Hobbs HH, Dobbins RL 2004 Magnetic resonance spectroscopy to measure hepatic triglyceride content: prevalence of hepatic steatosis in the general population. Am J Physiol Endocrinol Metab 288:E462–E468
  14. Seppala-Lindroos A, Vehkavaara S, Hakkinen AM, Goto T, Westerbacka J, Sovijarvi A, Halavaara J, Yki-Jarvinen H 2002 Fat accumulation in the liver is associated with defects in insulin suppression of glucose production and serum free fatty acids independent of obesity an normal men. J Clin Endocrinol Metab 87:3023–3028[Abstract/Free Full Text]
  15. Petersen KF, Dufour S, Befroy D, Lehrke M, Hendler RE, Shulman GI 2005 Reversal of nonalcoholic hepatic steatosis, hepatic insulin resistance, and hyperglycemia by moderate weight reduction in patients with type 2 diabetes. Diabetes 54:603–608[Abstract/Free Full Text]
  16. Bajaj M, Suraamornkul, Hardies LJ, Pratipanawatr T, DeFronzo RA 2004 Plasma resistin concentration, hepatic fat content, and hepatic and peripheral insulin resistance in pioglitazone-treated type II diabetic patients. Int J Obes 28:783–789[CrossRef][Medline]
  17. Carey AL, Wolsk Petersen E, Bruce CR, Southgate RJ, Pilegaard H, Hawley JA, Pedersen BK, Febbraio MA 2006 Discordant gene expression in skeletal muscle and adipose tissue of patients with type 2 diabetes: effect of interleukin-6 infusion. Diabetologia 49:1000–1007[CrossRef][Medline]
  18. Adams LA, Lymp JF, Sauver JS, Sanderson SO, Lindor KD, Feldstein A, Angulo P 2005 The natural history of nonalcoholic fatty liver disease: a population-based study. Gastroenterology 129:113–121[CrossRef][Medline]
  19. Diehl AM 2002 Nonalcoholic steatosis and steatohepatitis IV. Nonalcoholic fatty liver disease abnormalities in macrophage function and cytokines. Am J Physiol Gastrointest Liver Physiol 282:G1–G5
  20. Bugianesi E, Pagotto U, Manini R, Vanni E, Gastaldelli A, de Iasio R, Gentilcore E, Natale S, Cassader M, Rizzetto M, Pasquali R, Marchesini G 2005 Plasma adiponectin in nonalcoholic fatty liver is related to hepatic insulin resistance and hepatic fat content, not to liver disease severity. J Clin Endocrinol Metab 90:3498–3504[Abstract/Free Full Text]



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