help button home button Endocrine Society JCEM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Journal of Clinical Endocrinology & Metabolism , doi:10.1210/jc.2004-1364
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Submit a related Letter to the Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Housova, J.
Right arrow Articles by Haluzik, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Housova, J.
Right arrow Articles by Haluzik, M.
Related Collections
Right arrow Neuroendocrinology and Pituitary
Right arrow Metabolism
The Journal of Clinical Endocrinology & Metabolism Vol. 90, No. 3 1366-1370
Copyright © 2005 by The Endocrine Society

Serum Adiponectin and Resistin Concentrations in Patients with Restrictive and Binge/Purge Form of Anorexia Nervosa and Bulimia Nervosa

Jitka Housova, Katerina Anderlova, Jarmila Krizová, Denisa Haluzikova, Jaromir Kremen, Tereza Kumstyrová, Hana Papezová and Martin Haluzik

Third Department of Medicine (J.H., K.A., J.Kri., J.Kre., T.K., M.H.) and Departments of Sports Medicine (D.H.) and Psychiatry (H.P.), First Faculty of Medicine, Charles University, Prague 2, Czech Republic

Address all correspondence and requests for reprints to: Martin Haluzik, M.D., Ph.D., Third Department of Medicine, First Faculty of Medicine, Charles University, U Nemocnice 1, 128 08, Prague 2, Czech Republic. E-mail: mhalu{at}lf1.cuni.cz.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
To study the role of adipose tissue-derived hormones in the pathophysiology of eating disorders, circulating levels of adiponectin, resistin, and other hormonal and metabolic parameters were measured in 16 females with the restrictive subtype of anorexia nervosa (R-AN), 10 females with the binge/purge subtype of anorexia nervosa (P-AN), 15 females with bulimia nervosa (BN), and 12 age-matched healthy females (C). Body mass index (BMI), body fat content, and serum leptin levels were severely decreased in R-AN and moderately decreased in P-AN patients, whereas the BN group did not differ from C in these parameters. Serum soluble leptin receptor levels were increased in R-AN and P-AN and unchanged in BN patients. Circulating adiponectin levels were inversely related to BMI and were unchanged in BN patients and increased by 53% in P-AN and by 96% in R-AN relative to C group, respectively. In contrast, resistin levels in malnourished R-AN and P-AN were not different from either C or BN groups and showed no significant relationship to BMI or body fat content. We suggest that increased adiponectin levels reflect decreased body fat content in AN patients. In contrast, circulating resistin levels do not appear to be closely related to the nutritional status.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
IT IS NOW well established that adipose tissue produces numerous metabolically active substances and hormones (1, 2). Many experimental and clinical studies have shown that the adipose tissue-derived hormone leptin is a key player in the regulation of food intake and energy balance (3, 4, 5). Complete leptin deficiency because of leptin gene mutation in humans leads to morbid obesity caused by extreme hyperphagia without major changes in energy expenditure and cortisol levels (6). Paradoxically, the great majority of cases of human obesity is accompanied by increased instead of decreased leptin levels, indicating that there is probably a certain degree of decreased sensitivity to leptin effects (3).

In addition to leptin, a number of other adipose tissue-derived hormones with suggested roles in the regulation of energy metabolism and/or insulin sensitivity have been discovered. Two of the recently discovered hormones produced by adipose tissue have drawn the major attention, adiponectin and resistin. Adiponectin is a protein hormone produced exclusively by adipocytes that appears to be deficient in patients with obesity, diabetes/insulin resistance, and atherosclerosis (1). It has been suggested that adiponectin deficiency might have a causal role in the development of the above mentioned diseases (7). On the contrary, resistin was originally discovered as a potential link between obesity and insulin resistance (8). Later studies did not fully support this original hypothesis (9, 10). Moreover, resistin’s role and the site of production in humans (mostly immunocompetent cells localized in the adipose tissue) appear to be different from mice (adipocytes).

Although most of the studies have focused on the changes of endocrine function of adipocytes in obesity, adipose tissue also has a very important role in patients with malnutrition and decreased body fat content. It has been demonstrated that serum leptin levels are severely decreased in both patients with protein-caloric malnutrition and patients with the restrictive form of anorexia nervosa (AN) (11, 12). Such a secondary leptin deficiency acts as an important peripheral signal of starvation on the hypothalamic level and turns on the complex neurohumoral response to starvation that includes decreased energy expenditure, amenorrhea, and a series of other processes (4).

Here we study the endocrine function of patients with different subtypes of AN and with bulimia nervosa. The restrictive form of AN represents an extreme example of psychosomatic-based malnutrition induced by chronically decreased food intake caused by inappropriate fear of obesity and distorted body image (13). In the binge/purge form of AN, the reduction of food intake is combined with periods of binge eating and/or purging (13). As a result, body fat content of patients with the binge/purge form is usually less severely decreased than in patients with the restrictive form of AN. Bulimia nervosa is an eating disorder characterized, in contrast to AN, by normal or even slightly higher body mass index (BMI). Patients with bulimia nervosa suffer from repeated episodes of binge eating combined with inappropriate compensatory behavior to prevent weight gain such as self-induced vomiting, misuse of laxatives, diuretics, fasting, and excessive exercise (13).

The above described subtypes of eating disorders affect nutritional status very differently, ranging from extreme decrease in body fat content in patients with the restrictive form of AN to practically normal body fat content in patients with bulimia nervosa. Here we measured circulating concentrations of adiponectin and resistin to study their role in the pathophysiology of eating disorders.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Study subjects

Sixteen female patients with restrictive subtype of AN (BMI, 14.56 ± 0.43 kg/m2), 10 female patients with binge/purge subtype of AN (BMI, 17.19 ± 0.26 kg/m2), 15 female patients with bulimia nervosa (BMI, 21.92 ± 0.7 kg/m2), and 12 age- and sex-matched healthy controls (BMI, 22.47 ± 0.93 kg/m2) were included in the study. The diagnosis of eating disorder was based on the Diagnostic Statistical Manual IV diagnostic system (13). A clinical evaluation of the patients was performed by an experienced psychiatrist. The Structured Clinical Interview MINI 5.0 was used for diagnostic assessment of patients. None of the studied subjects suffered from diabetes mellitus, thyroid disorder, and/or acute infectious disease. Patients with any acute or chronic stress situations were excluded. Written informed consent was provided by all participants before being enrolled in the study. The study was approved by the Human Ethical Review Committee, First Faculty of Medicine and General University Hospital, Prague, Czech Republic, and was performed in accordance with the guidelines proposed in the Declaration of Helsinki.

Anthropometric examination and blood sampling

All patients were examined at a basal state before the start of any treatment. All subjects were measured and weighed. The total body fat content was predicted from the skinfold thickness measured by a Best caliper applying the method of Allen et al. (14). Blood samples were withdrawn between 0700 and 0800 h after overnight fasting.

Hormonal and biochemical assays

Serum insulin concentrations were measured by commercial RIA kit (Cis Bio International, Gif-sur-Yvette, France). Sensitivity was 2.0 µIU/ml, and the intra- and interassay variability was 4.2 and 8.8%, respectively. Serum leptin concentrations were measured by commercial ELISA kit (BioVendor, Brno, Czech Republic). Sensitivity was 0.12 ng/ml, and the intra- and interassay variability was 1.7 and 8.0%, respectively. Serum soluble leptin receptor concentrations were measured by commercial ELISA kit (BioVendor). Sensitivity was 0.4 U/ml, and the intra- and interassay variability was 4.4 and 7.2%, respectively. Serum adiponectin concentrations were measured by commercial RIA kit (Linco Research, St. Charles, MO). Sensitivity was 1.0 ng/ml, and the intra- and interassay variability was 1.78 and 9.25%, respectively. Serum resistin concentrations were measured by commercial ELISA kit (BioVendor). Sensitivity was 0.2 ng/ml, and the intra- and interassay variability was 3.1 and 6.5%, respectively.

Plasma glucose levels were measured in by standard laboratory methods. Homeostasis model assessment (HOMA-R) index was calculated as previously described (15) using the following formula: fasting serum insulin (U/ml) x fasting serum glucose (mmol/liter)/22.5.

Statistical analysis

The statistical analysis was performed on SigmaStat software (Jandel Scientific, San Rafael, CA). The results are expressed as means ± SEM. The groups were compared by one-way ANOVA followed by Dunnett’s test or Tukey test, respectively. The correlations between the values were estimated by Pearson correlation test.


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
Anthropometric characteristics

Patients with the restrictive form of AN were extremely malnourished as evidenced by severely decreased BMI and body fat content relative to other groups (Table 1Go). Patients with the binge/purge form of AN had significantly higher BMI and body fat content than the restrictive AN group, but these variables were still significantly lower than those of control and bulimia nervosa groups, respectively (Table 1Go). BMI and body fat content of the bulimia nervosa group were comparable with those of the control group (Table 1Go).


View this table:
[in this window]
[in a new window]
  		TABLE 1. Anthropometric, biochemical, and hormonal parameters of patients with restrictive and binge/purge form of AN, bulimia nervosa, and control group of healthy women

 
Serum glucose, insulin, and HOMA index

Serum glucose levels did not significantly differ among the groups studied, whereas serum insulin levels were decreased in restrictive AN patients relative to both the control and bulimia nervosa groups (Table 1Go). Serum insulin levels in the binge/purge AN group tended to be higher than in restrictive AN patients and lower relative to bulimia nervosa and control groups, respectively, but none of those differences reached statistical significance. HOMA index values paralleled serum insulin levels, being markedly decreased in the restrictive AN group, whereas no significant differences between the rest of the groups were found (Table 1Go).

Serum concentrations of adipose tissue-derived hormones

Circulating leptin concentrations were markedly decreased in restrictive AN patients and less so in binge/purge AN patients relative to both control and bulimia nervosa groups (Table 1Go). Serum leptin levels in the bulimia nervosa group tended to be lower relative to the control group, but this difference did not reach statistical significance (Table 1Go). Serum soluble leptin receptor levels were significantly higher in restrictive and binge/purge AN groups relative to both control and bulimia nervosa groups (Table 1Go).

Serum adiponectin concentrations in patients with both restrictive and binge/purge forms of AN were higher than those of bulimia nervosa and control groups. No difference in adiponectin concentrations were found between the bulimia nervosa and control groups (Table 1Go).

In contrast to marked differences in serum leptin and adiponectin levels between malnourished patients with AN and control and bulimia nervosa subjects, serum resistin concentrations in patients with binge/purge and restrictive forms of AN did not differ from those of control and bulimia nervosa groups, respectively (Table 1Go).

Relationship of adipose tissue-derived hormones with other parameters

The relationships of adipose tissue-derived hormones with other parameters were studied in the combined population of all four groups (Table 2Go). Serum leptin levels correlated positively with BMI and body fat content and were inversely related to serum soluble leptin receptor and adiponectin levels. Serum soluble leptin receptor levels correlated positively with serum adiponectin and were inversely related to BMI, insulin, and leptin levels. Serum adiponectin levels correlated positively with serum soluble leptin receptor levels and were inversely related to BMI, body fat content, serum leptin levels, and blood glucose concentrations. In contrast, serum resistin levels were not significantly related to any of other parameters studied. The above mentioned relationships were calculated also in each group separately (data not shown) and were found similar to those of the combined population.


View this table:
[in this window]
[in a new window]
  		TABLE 2. Relationship of leptin, soluble leptin receptor (LEPR), adiponectin, and resistin with anthropometric, biochemical, and hormonal parameters calculated in combined population with all four groups (restrictive and binge/purge AN bulimia nervosa, and healthy women) included

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
The most important finding of this study is that leptin and adiponectin levels in patients with restrictive and binge/purge types of AN and bulimia nervosa were strongly related to nutritional status, whereas resistin levels were not. This finding may be in part explained by the fact that although leptin and adiponectin are produced almost exclusively by adipocytes (16), the main source of resistin in humans is immunocompetent cells in the adipose tissue (17). It should be noted, however, that our data are based on single blood samples drawn after overnight fasting, and therefore possible nutrition-related changes in the dynamic secretion patterns of these hormones may not have been detected here.

Numerous studies have previously found that leptin levels in malnourished patients are severely decreased, reflecting lowered body fat content (18, 19). In contrast, serum soluble leptin receptor levels in these patients were reported to be increased, which was true also in our study. This increase may represent a protective mechanism that decreases free leptin bioavailability and thus further facilitates energy conservation. Serum leptin levels in patients with the binge/purge form of AN in our study were higher than in the restrictive form but lower than in control and bulimia nervosa groups, which is in agreement with previously published data (20). Interestingly, the difference in serum leptin levels between bulimia nervosa patients and healthy control women in our study did not reach statistical significance. In most but not all previously published papers, serum leptin levels in bulimia nervosa patients were lower than in healthy women despite comparable BMI (21, 22).

Thus, our data do not support the hypothesis that basal leptin levels in patients with bulimia are primarily affected by the eating pattern.

Studies focused on serum adiponectin levels in AN and bulimia nervosa patients brought rather contradictory results. Some authors found increased adiponectin levels either in AN (23, 24) or bulimia nervosa patients (25). In contrast, Iwahashi et al. (26) did not observe any difference in adiponectin levels between AN patients and healthy women, whereas Tagami et al. (27) found even decreased adiponectin levels in both AN and bulimia nervosa patients. Here we found similarly to Delporte et al. (23) and Pannacciulli et al. (24) increased adiponectin levels in AN patients. Moreover, we demonstrated that there was a gradual rise in adiponectin levels related to the nutritional status of AN patients. Less severely malnourished patients with the binge/purge form of AN had a relatively modest increase in circulating adiponectin, whereas a more prominent rise in this parameter was found in severely malnourished restrictive AN patients. In contrast to previously published data, we found no difference in circulating adiponectin levels in bulimia nervosa patients relative to the control group. At present, there is no obvious explanation for such a discrepancy in published data for circulating adiponectin levels in patients with eating disorders. However, the two studies that describe decreased or unchanged adiponectin levels in AN and decreased adiponectin levels in bulimia nervosa, respectively, were performed on a Japanese population, and the anorectic patients included were significantly older than in our study (26, 27).

The finding of increased adiponectin levels in patients with AN may have interesting etiopathogenetic consequences. It has been recently demonstrated in mice that intracerebroventricular administration of adiponectin decreased body weight (28). It is tempting to speculate that hyperadiponectinemia could be a contributing etiopathogenetic factor in patients with AN. However, a more likely possibility is that increased adiponectin levels are rather the consequence of severely decreased body fat and/or other metabolic changes in anorectic patients. Finally, it has been hypothesized that elevated circulating adiponectin concentrations in patients with AN might represent a compensatory mechanism for the reduced insulin-stimulated glucose metabolism (24).

Resistin was originally proposed to be a link between obesity and insulin resistance/diabetes (8). However, we and others have previously demonstrated that fat resistin mRNA expression is severely reduced in morbidly obese ob/ob mice (9, 10, 29). Our recent data show that despite decreased fat mRNA expression, circulating resistin levels are increased in ob/ob mice relative to lean animals and thus could contribute to insulin resistance phenotype (Haluzik, M., and O. Gavrilova, unpublished data). In contrast, resistin’s role in human physiology is currently unclear and probably different from that in mice. There are generally a lot of contradictory data regarding resistin levels in humans ranging from reports showing a positive correlation with BMI and increase in obesity to no such relationship and no change in the groups with different degrees of adiposity (30, 31, 32). To our best knowledge, there are no published data for resistin levels in patients with AN and/or bulimia nervosa. Here we show that in contrast to leptin or adiponectin, circulating resistin levels did not significantly differ in the groups studied herein despite huge distinctions in BMI and body fat content. We therefore suggest that neither malnutrition nor changes in eating patterns is an important factor affecting circulating resistin levels in patients with eating disorders. Thus, resistin does not appear to be a contributing factor in the etiopathogenesis of either anorexia or bulimia nervosa.

In conclusion, we demonstrated that circulating levels of leptin and adiponectin in patients with different eating disorders are primarily determined by their nutritional status. In contrast, resistin levels were unrelated to either anthropometric or insulin sensitivity variables. We suggest that increased adiponectin levels could contribute to metabolic changes and/or decreased food intake in AN but not bulimia nervosa patients, whereas resistin does not appear to be involved in this process.


   Footnotes
 
This work was supported by Grant 7429-3 of IGA MH CR (to M.H.).

First Published Online December 14, 2004

Abbreviations: AN, Anorexia nervosa; BMI, body mass index; HOMA, homeostasis model assessment.

Received July 15, 2004.

Accepted December 6, 2004.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

  1. Havel PJ 2002 Control of energy homeostasis and insulin action by adipocyte hormones: leptin, acylation stimulating protein, and adiponectin. Curr Opin Lipidol 13:51–59[CrossRef][Medline]
  2. Haluzik M, Parizkova J, Haluzik MM 2004 Adiponectin and its role in the obesity-induced insulin resistance and related complications. Physiol Res 53:123–129[Medline]
  3. Maffei M, Halaas J, Ravussin E, Pratley RE, Lee GH, Zhang Y, Fei H, Kim S, Lallone R, Ranganathan S, Kern PA, Friedman JM 1995 Leptin levels in human and rodent: measurement of plasma leptin and ob RNA in obese and weight-reduced subjects. Nat Med 1:1155–1161[CrossRef][Medline]
  4. Ahima RS, Prabakaran D, Mantzoros C, Qu D, Lowell B, Maratos-Flier E, Flier JS 1996 Role of leptin in the neuroendocrine response to fasting. Nature 382:250–252[CrossRef][Medline]
  5. Haluzik M, Dietz KR, Kim JK, Marcus-Samuels B, Shulman GI, Gavrilova O, Reitman ML 2002 Adrenalectomy improves diabetes in A-ZIP/F-1 lipoatrophic mice by increasing both liver and muscle insulin sensitivity. Diabetes 51:2113–2118[Abstract/Free Full Text]
  6. Montague CT, Farooqi IS, Whitehead JP, Soos MA, Rau H, Wareham NJ, Sewter CP, Digby JE, Mohammed SN, Hurst JA, Cheetham CH, Earley AR, Barnett AH, Prins JB, O’Rahilly S 1997 Congenital leptin deficiency is associated with severe early-onset obesity in humans. Nature 387:903–908[CrossRef][Medline]
  7. Okamoto Y, Kihara S, Ouchi N, Nishida M, Arita Y, Kumada M, Ohashi K, Sakai N, Shimomura I, Kobayashi H, Terasaka N, Inaba T, Funahashi T, Matsuzawa Y 2002 Adiponectin reduces atherosclerosis in apolipoprotein E-deficient mice. Circulation 106:2767–2770[Abstract/Free Full Text]
  8. Steppan CM, Bailey ST, Bhat 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]
  9. Savage DB, Sewter CP, Klenk ES, Segal DG, Vidal-Puig A, Considine RV, O’Rahilly S 2001 Resistin/Fizz3 expression in relation to obesity and peroxisome proliferator-activated receptor-gamma action in humans. Diabetes 50:2199–2202[Abstract/Free Full Text]
  10. Way JM, Gorgun CZ, Tong Q, Uysal KT, Brown KK, Harrington WW, Oliver Jr WR, Willson TM, Kliewer SA, Hotamisligil GS 2001 Adipose tissue resistin expression is severely suppressed in obesity and stimulated by peroxisome proliferator-activated receptor gamma agonists. J Biol Chem 276:25651–25653[Abstract/Free Full Text]
  11. Haluzik M, Papezova M, Nedvidkova J, Kabrt J 1999 Serum leptin levels in patients with anorexia nervosa before and after partial refeeding, relationships to serum lipids and biochemical nutritional parameters. Physiol Res 48:197–202[Medline]
  12. Kopp W, Blum WF, Ziegler A, Mathiak K, Lubbert H, Herpertz S, Deter HC, Hebebrand J 1998 Serum leptin and body weight in females with anorexia and bulimia nervosa. Horm Metab Res 30:272–275[Medline]
  13. 1994 Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). 4th ed. Washington, DC: American Psychiatric Association
  14. Allen TH, Peng MT, Chen KP, Huang TF, Chang C, Fang HS 1956 Prediction of total adiposity from skinfolds and the curvilinear relationship between external and internal adiposity. Metabolism 5:346–352[Medline]
  15. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC 1985 Homeostasis model assessment: insulin resistance and ß-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 28:412–419[CrossRef][Medline]
  16. Scherer PE, Williams S, Fogliano M, Baldini G, Lodish HF 1995 A novel serum protein similar to C1q, produced exclusively in adipocytes. J Biol Chem 270:26746–26749[Abstract/Free Full Text]
  17. Patel L, Buckels AC, Kinghorn IJ, Murdock PR, Holbrook JD, Plumpton C, Macphee CH, Smith SA 2003 Resistin is expressed in human macrophages and directly regulated by PPAR {gamma} activators. Biochem Biophys Res Commun 300:472–476[CrossRef][Medline]
  18. Haluzik M, Kabrt J, Nedvidkova J, Svobodova J, Kotrlikova E, Papezova H 1999 Relationship of serum leptin levels and selected nutritional parameters in patients with protein-caloric malnutrition. Nutrition 15:829–833[Medline]
  19. Kilic M, Taskin E, Ustundag B, Aygun AD 2004 The evaluation of serum leptin level and other hormonal parameters in children with severe malnutrition. Clin Biochem 37:382–387[Medline]
  20. Ferron F, Considine RV, Peino R, Lado IG, Dieguez C, Casanueva FF 1997 Serum leptin concentrations in patients with anorexia nervosa, bulimia nervosa and non-specific eating disorders correlate with the body mass index but are independent of the respective disease. Clin Endocrinol (Oxf) 46:289–293[CrossRef][Medline]
  21. Baranowska B, Wolinska-Witort E, Wasilewska-Dziubinska E, Roguski K, Chmielowska M 2001 Plasma leptin, neuropeptide Y (NPY) and galanin concentrations in bulimia nervosa and in anorexia nervosa. Neuroendocrinol Lett 22:356–358[Medline]
  22. Brewerton TD, Lesem MD, Kennedy A, Garvey WT 2000 Reduced plasma leptin concentrations in bulimia nervosa. Psychoneuroendocrinology 25:649–658[CrossRef][Medline]
  23. Delporte ML, Brichard SM, Hermans MP, Beguin C, Lambert M 2003 Hyperadiponectinaemia in anorexia nervosa. Clin Endocrinol (Oxf) 58:22–29[CrossRef][Medline]
  24. Pannacciulli N, Vettor R, Milan G, Granzotto M, Catucci A, Federspil G, De Giacomo P, Giorgino R, De Pergola G 2003 Anorexia nervosa is characterized by increased adiponectin plasma levels and reduced nonoxidative glucose metabolism. J Clin Endocrinol Metab 88:1748–1752[Abstract/Free Full Text]
  25. Monteleone P, Fabrazzo M, Martiadis V, Fuschino A, Serritella C, Milici N, Maj M 2003 Opposite changes in circulating adiponectin in women with bulimia nervosa or binge eating disorder. J Clin Endocrinol Metab 88:5387–5391[Abstract/Free Full Text]
  26. Iwahashi H, Funahashi T, Kurokawa N, Sayama K, Fukuda E, Okita K, Imagawa A, Yamagata K, Shimomura I, Miyagawa JI, Matsuzawa Y 2003 Plasma adiponectin levels in women with anorexia nervosa. Horm Metab Res 35:537–540[CrossRef][Medline]
  27. Tagami T, Satoh N, Usui T, Yamada K, Shimatsu A, Kuzuya H 2004 Adiponectin in anorexia nervosa and bulimia nervosa. J Clin Endocrinol Metab 89:1833–1837[Abstract/Free Full Text]
  28. Qi Y, Takahashi N, Hileman SM, Patel HR, Berg AH, Pajvani UB, Scherer PE, Ahima RS 2004 Adiponectin acts in the brain to decrease body weight. Nat Med 10:524–529[CrossRef][Medline]
  29. Haluzik M, Colombo C, Gavrilova O, Chua S, Wolf N, Chen M, Stannard B, Dietz KR, Le Roith D, Reitman ML 2004 Genetic background (C57BL/6J versus FVB/N) strongly influences the severity of diabetes and insulin resistance in ob/ob mice. Endocrinology 145:3258–3264[Abstract/Free Full Text]
  30. McTernan CL, McTernan PG, Harte AL, Levick PL, Barnett AH, Kumar S 2002 Resistin, central obesity, and type 2 diabetes. Lancet 359:46–47[CrossRef][Medline]
  31. Volarova de Courten B, Degawa-Yamauchi M, Considine RV, Tataranni PA 2004 High serum resistin is associated with an increase in adiposity but not a worsening of insulin resistance in Pima Indians. Diabetes 53:1279–1284[Abstract/Free Full Text]
  32. Heilbronn LK, Rood J, Janderova L, Albu JB, Kelley DE, Ravussin E, Smith SR 2004 Relationship between serum resistin concentrations and insulin resistance in nonobese, obese, and obese diabetic subjects. J Clin Endocrinol Metab 89:1844–1848[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 J. Clin. Endocrinol. Metab.Home page
M. Misra, K. K. Miller, J. Cord, R. Prabhakaran, D. B. Herzog, M. Goldstein, D. K. Katzman, and A. Klibanski
Relationships between Serum Adipokines, Insulin Levels, and Bone Density in Girls with Anorexia Nervosa
J. Clin. Endocrinol. Metab., June 1, 2007; 92(6): 2046 - 2052.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
D. Modan-Moses, D. Stein, C. Pariente, A. Yaroslavsky, A. Ram, M. Faigin, R. Loewenthal, E. Yissachar, R. Hemi, and H. Kanety
Modulation of Adiponectin and Leptin during Refeeding of Female Anorexia Nervosa Patients
J. Clin. Endocrinol. Metab., May 1, 2007; 92(5): 1843 - 1847.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
M. M. Haluzik, Z. Lacinova, M. Dolinkova, D. Haluzikova, D. Housa, A. Horinek, Z. Vernerova, T. Kumstyrova, and M. Haluzik
Improvement of Insulin Sensitivity after Peroxisome Proliferator-Activated Receptor-{alpha} Agonist Treatment Is Accompanied by Paradoxical Increase of Circulating Resistin Levels
Endocrinology, September 1, 2006; 147(9): 4517 - 4524.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
M. J. Bahr, J. Ockenga, K. H. W. Boker, M. P. Manns, and U. J. F. Tietge
Elevated resistin levels in cirrhosis are associated with the proinflammatory state and altered hepatic glucose metabolism but not with insulin resistance
Am J Physiol Endocrinol Metab, August 1, 2006; 291(2): E199 - E206.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
N. Moriconi, M. Kraenzlin, B. Muller, U. Keller, C. P. G. Nusbaumer, S. Stohr, M. Tamm, and J. J. Puder
Body Composition and Adiponectin Serum Concentrations in Adult Patients with Cystic Fibrosis
J. Clin. Endocrinol. Metab., April 1, 2006; 91(4): 1586 - 1590.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Submit a related Letter to the Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Housova, J.
Right arrow Articles by Haluzik, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Housova, J.
Right arrow Articles by Haluzik, M.
Related Collections
Right arrow Neuroendocrinology and Pituitary
Right arrow Metabolism

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