Leptin and adiponectin levels in patients with ankylosing spondylitis. The effect of infliximab treatment. Serum adipokines as biomarkers of beta-cell function in patients with type 1 diabetes: positive association with leptin and resistin and negative association with adiponectin. The influence of very-low-calorie-diet on serum leptin, soluble leptin receptor, adiponectin and resistin levels in obese women. Effect of oncological treatment on serum adipocytokine levels in patients with stage II-III breast cancer. Lifestyle Intervention and Adipokine Levels in Subjects at High Risk for Type 2 Diabetes Periodontal treatment with topical antibiotics improves glycemic control in association with elevated serum adiponectin in patients with type 2 diabetes mellitus. Adipocytokines, obesity, and insulin resistance during combined androgen blockade for prostate cancer. Clinical Significance of Serum Adipokines according to Body Mass Index in Patients with Clinically Localized Prostate Cancer Undergoing Radical Prostatectomy Adipocytokines and the risk of coronary heart disease in healthy middle aged men: the PRIME Study Lower leptin/adiponectin ratio and risk of rapid lung function decline in chronic obstructive pulmonary disease. Body mass index increase, serum leptin, adiponectin, neuropeptide Y and lipid levels during treatment with olanzapine and haloperidol. Effects of 90-day hypolipidemic treatment on insulin resistance, adipokines and proinflammatory cytokines in patients with mixed hyperlipidemia and impaired fasting glucose. Leptin and adiponectin responses in overweight inactive elderly following resistance training and detraining are intensity related. Hyperresistinemia is associated with postmenopausal breast cancer Elevated levels of interleukin 6 are reduced in serum and subcutaneous adipose tissue of obese women after weight loss. The plasma leptin/adiponectin ratio predicts first cardiovascular event in men: a prospective nested case-control study. Circulating cytokines as determinants of weight loss-induced improvements in insulin sensitivity
BACKGROUND Adipose tissue-derived leptin and adiponectin control hunger , energy expenditure , insulin sensitivity , endothelial function , reproduction and immunity and are thought to play a role in autoimmune diseases . However , their role in ankylosing spondylitis ( AS ) is not clearly defined . Tumour necrosis factor ΤNF-α is a potential modulator of adipocytokines . The effect of longterm anti-TNF-α treatment on plasma levels of leptin and adiponectin has not been assessed so far . OBJECTIVES To assess the effect of a 6-month anti-TNF-α treatment on serum leptin and adiponectin levels in AS patients . METHODS Thirty men with AS were included in the study . Thirty age- and weight-matched men served as controls . Clinical and biochemical parameters were assessed and serum levels of leptin and adiponectin were measured with enzyme immunoassay methods prior to and after the 6-month treatment with infliximab . RESULTS Mean age and disease duration of AS patients were 40.6±13.7 and 13.4±8.4 years , respectively . At baseline , AS patients exhibited significantly higher adiponectin ( 15.4±8.3 vs. 8.6±4.2 μg/ml , p<0.05 ) , but no difference in leptin levels ( 7.2±2.9 vs. 8.9±6.4 ng/ml , p = NS ) . Adipocytokines did not correlate with any disease parameter . Body weight of the patients did not change significantly over the 6-month period . Serum levels of leptin and adiponectin did not change significantly after the 6-month treatment . CONCLUSIONS Adiponectin levels were significantly higher in AS patients compared with  controls . Infliximab treatment did not change serum levels of leptin and adiponectin suggesting that the anti-TNF-α treatment may not modulate significantly their levels BACKGROUND We investigated the adipokines adiponectin , leptin and resistin as serum biomarkers of beta-cell function in patients with type 1 diabetes . METHODS One hundred and eighteen patients with type 1 diabetes ( 20.3 ± 7.5 years ) diagnosed < 5 years underwent st and ardized mixed meal test ( MMTT ) for 2 h.  Systemic concentrations of C-peptide , adiponectin , leptin and resistin obtained during MMTT were measured and compared between patient groups by multiple regression analysis . RESULTS Patients were divided by their adipokine levels in subgroups above or below the median level ( ' high versus low ' ) . High adiponectin levels ( > 10.6 µg/mL ) were associated with lower C-peptide compared to the low adiponectin subgroup ( p < 0.03 ) . Increased leptin or resistin concentrations associated positively with beta-cell function even after adjustment for metabolic confounders ( p < 0.04 ) . The described associations between adipokines and C-peptide concentrations persisted in Spearman correlation tests ( p < 0.05 ) . Serum adipokines fell during MMTT ( p < 0.05 ) . CONCLUSIONS Serum adipokine levels differentially correlate with beta-cell function in type 1 diabetes independent of BMI or metabolic control . Serum adipokines should be investigated as biomarkers of beta-cell function in prospect i ve studies and intervention trials in type 1 diabetes The aim of our study was to determine whether adipocyte-derived hormones leptin , adiponectin and resistin contribute to the improvement of insulin sensitivity after very-low calorie diet ( VLCD ) . Therefore , serum levels of these hormones were measured in fourteen obese females before and after three weeks VLCD and in seventeen age- and sex-matched healthy controls .  Body mass index , HOMA index , serum insulin and leptin levels in obese women before VLCD were significantly higher than in control group ( BMI 48.01+/-2.02 vs. 21.38+/-0.42 kg/m(2 ) , HOMA 10.72+/-2.03 vs. 4.69+/-0.42 , insulin 38.63+/-5.10 vs. 18.76+/-1.90 microIU/ml , leptin 77.87+/-8.98 vs. 8.82+/-1.52 ng/ml ) . In contrast , serum adiponectin and soluble leptin receptors levels were significantly lower in obese women before VLCD than in the control group . No differences were found in serum glucose and resistin levels between the obese group before VLCD and the control group . VLCD significantly decreased BMI , HOMA index , serum glucose , insulin and leptin levels and increased soluble leptin receptor levels . The changes in serum adiponectin and resistin levels in obese women after VLCD did not reach statistical significance . We conclude that leptin and soluble leptin receptor levels were affected by VLCD while adiponectin and resistin concentrations were not . Therefore , other mechanisms rather than changes in the endocrine function of the adipose tissue are probably involved in the VLCD-induced improvement of insulin sensitivity Adipose tissue-derived hormones ( adipocytokines ) , such as adiponectin , leptin , resistin and visfatin , and the pancreatic hormone insulin , have been suggested to play a role in carcinogenesis . we therefore hypothesized that the oncological treatment of breast cancer may alter the serum levels of these adipocytokines and insulin . In this study , we aim ed to compare the serum levels of adipocytokines and insulin between the pre- and post-treatment period in patients with breast cancer . In this prospect i ve study , 20 consecutive patients with stage II and III breast cancer underwent breast-conserving surgery or total mastectomy and /or axillary dissection .  The patients received adjuvant chemotherapy and radiotherapy , if necessary . Blood sample s were obtained during the preoperative period and postoperatively after completion of the adjuvant therapy . There was no statistically significant difference between the pre- and post-treatment levels of visfatin , adiponectin and leptin . However , the serum insulin and resistin levels and insulin resistance were found to be statistically significantly increased following treatment ( P<0.05 ) . Post-treatment resistin levels were positively correlated with insulin resistance ( r=0.45 , P<0.05 ) . Therefore , oncological treatment of stage II and III breast cancer did not affect visfatin , adiponectin and leptin levels , but statistically significantly increased resistin levels and insulin resistance . In addition , the post-treatment resistin levels were positively correlated with insulin resistance , suggesting that resistin may be involved in the development of insulin resistance in breast cancer patients following treatment OBJECTIVE —We investigated whether circulating adipokine concentrations can be altered by lifestyle intervention according to general recommendations in subjects at risk for diabetes as well as the potential of leptin , adiponectin , and resistin as biomarkers for lifestyle-induced improvements in glucose metabolism and insulin resistance . RESEARCH DESIGN AND METHODS —In the Study on Lifestyle intervention and Impaired glucose tolerance Maastricht , 147 men and women with impaired glucose tolerance ( IGT ) were r and omized to either a combined diet- and -exercise intervention or a control program . At baseline and after 1 year , an oral glucose tolerance test , an exercise test , and anthropometric measurements were performed . After 1 year , complete data of 103 subjects ( 50 intervention and 53 control subjects ) were obtained . RESULTS —Lifestyle intervention reduced plasma leptin concentrations ( −14.2 % ) in IGT subjects but did not alter plasma adiponectin ( −0.3 % ) or resistin ( −6.5 % ) concentrations despite marked improvements in glucose tolerance and insulin resistance . CONCLUSIONS —Changes in leptin concentration were related to improvements in insulin sensitivity independent of changes in body composition OBJECTIVES Chronic inflammation of periodontitis aggravates glycemic control in type 2 diabetic patients through aggravation of insulin resistance . Increased or decreased release of various inflammatory mediators , such as high sensitivity C-reactive protein ( hs-CRP ) , tumor necrosis factor (TNF)-α , interleukin (IL)-6 and adipokines , such as adiponectin , leptin , and resistin , are presumed to be responsible for developing and progressing insulin resistance . The purpose of this study was to examine the effects of periodontal treatment on glycemic control , serum inflammatory mediators and adipokines in type 2 diabetes patients with periodontitis . METHODS Twenty-one type 2 diabetic patients with periodontitis received periodontal treatment with topical antibiotics ( intervention group ) and 8 patients did not receive periodontal treatment ( control group )  . Periodontal examination , including probing pocket depth ( PPD ) and bleeding on probing ( BOP ) , and blood sampling  were performed at baseline , 2 and 6 months after periodontal treatments . Glycated hemoglobin ( HbA1c ) , hs-CRP , TNF-α , IL-6 , adiponectin , leptin , and resistin were analyzed . RESULTS In the intervention group , improvements of PPD and BOP , decrease in HbA1c and elevation of serum adiponectin were observed , while in the control group , all parameters were not changed . Generalized linear model revealed that changes of serum adiponectin and TNF-α and change of BOP correlated significantly with the reduction of HbA1c at 6 months after periodontal treatments . CONCLUSION The results demonstrated that periodontal treatment improves periodontal status and glycemic control with elevation of serum adiponectin in type 2 diabetic patients . The results suggest that HbA1c is reduced by amelioration of insulin resistance due to elevated serum adiponectin after periodontal treatments OBJECTIVES Gonadotropin-releasing hormone agonists increase fat mass , decrease insulin sensitivity , and increase serum triglycerides . To better characterize the metabolic effects of gonadotropin-releasing hormone agonist treatment , we prospect ively evaluated the changes in body composition , insulin sensitivity , and levels of adiponectin , resistin , C-reactive protein ( CRP ) , and plasminogen activator inhibitor type 1 ( PAI-1 ) . We also assessed the relationships among changes in adipocytokines , body composition , and insulin sensitivity . METHODS In this prospect i ve , 12-week study , 25 nondiabetic men with locally advanced or recurrent prostate cancer and no radiographic evidence of metastases were treated with leuprolide depot and bicalutamide . The outcomes studied included changes from baseline to week 12 in body composition , insulin sensitivity , and levels of adiponectin , resistin , CRP , and PAI-1 . RESULTS The mean + /- st and ard error percentage of fat body mass increased by 4.3 % + /- 1.3 % from baseline to week 12 ( P = 0.002 ) . The insulin sensitivity index decreased by 12.9 % + /- 7.6 % ( P = 0.02 ) . The serum adiponectin levels increased by 37.4 % + /- 7.2 % from baseline to week 12 ( P < 0.001 ) . In contrast , the resistin , CRP , and PAI-1 levels did not change significantly . Changes in body composition tended to be associated with changes in adiponectin , but not insulin sensitivity . CONCLUSIONS Combined and rogen blockade with leuprolide and bicalutamide significantly increased fat mass and adiponectin levels and decreased insulin sensitivity but did not alter the resistin , CRP , or PAI-1 levels . This pattern of metabolic changes appears distinct from the classic metabolic syndrome Purpose The aim of this study was to investigate the clinical significance of 7 circulating adipokines according to body mass index ( BMI ) in Korean men with localized prostate cancer ( PCa ) undergoing radical prostatectomy ( RP ) .  Material s and Methods Sixty-two of 65 prospect ively enrolled patients with clinical ly localized PCa who underwent RP between 2015 and 2016 were evaluated . Patients were classified into 2 groups according to their BMI : non-obese ( < 25 kg/m2 ) and obese ( ≥25 kg/m2 ) . The adipokines evaluated were interleukin-2 , insulin-like growth factor 1 ( IGF-1 ) , chemerin , C-X-C motif chemokine 10 , adiponectin , leptin , and resistin . Multivariate logistic regression analysis was used to identify the independent predictors of advanced tumor stage . Results We found that obese patients with PCa who underwent RP had a higher incidence of tumors with a high Gleason score ( ≥8 ) , pathological T3 ( pT3 ) stage , and positive extraprostatic extension than patients with a normal BMI . Additionally , patients with obesity showed significantly lower serum adiponectin and higher serum leptin levels , but did not show differences in other adipokines . Multivariate analysis demonstrated that IGF-1 ( odds ratio [OR]=1.03 ) was identified as a predictor of advanced tumor stage ( ≥pT3 ) in the overall population . However , only leptin remained an independent predictive factor for advanced tumor stage ( ≥pT3 ) ( OR=1.15 ) in patients with obesity . Conclusions In conclusion , our results indicate that a higher leptin level in obese men can be considered a risk factor for aggressive PCa . This prospect i ve study provides greater insight into the role of circulating adipokines in Korean patients with PCa undergoing RP , particularly in patients with obesity Background : Adipokines play an important role in glucose , lipid and lipoprotein metabolisms , as well as in coagulation and inflammatory processes . So far , studies have evaluated the association of individual adipokines with future coronary heart disease ( CHD ) event and provided mixed results . Objectives : We sought to investigate the association of a set of adipocytokines , including total adiponectin , adipsin , resistin , leptin and plasminogen activator inihibitor-1 ( PAI-1 ) , with future CHD events in apparently healthy men . Methods : We built a nested case – control study within the PRIME Study , a multicenter prospect i ve cohort of 9779 healthy European middle-aged men .  Total adiponectin , adipsin , resistin , leptin and PAI-1  were measured in the baseline plasma sample of 617 men who developed a first CHD event ( coronary death , myocardial infa rct ion , stable or unstable angina ) during 10 years of follow-up and in 1215 study -matched controls , by multiplex assays using commercial kits . HRs for CHD were estimated by conditional logistic regression analysis . Results : Median concentrations of total adiponectin , adipsin and resistin were similar in cases and in controls , whereas those of leptin and PAI-1 were higher in cases than in controls , 6.30 vs 5.40 ng ml−1 , and 10.09 vs 8.48 IU ml−1 , respectively . The risk of future CHD event increased with increasing quintiles of baseline leptin and PAI-1 concentrations only in unadjusted analysis ( P-value for trend < 0.003 and < 0.0001 , respectively ) . However , these associations were no longer significant after adjustment for usual CHD risk factors including hypertension , diabetes , smoking , total cholesterol , triglycerides and HDL cholesterol . Conversely , baseline CRP and IL-6 levels remained associated with CHD risk in multivariate analysis . Conclusions : In apparently healthy men  , circulating total adiponectin , adipsin , resistin , leptin and PAI-1 were not independent predictors of future CHD event RATIONALE The rate of annual change in FEV1 is highly variable among patients with chronic obstructive pulmonary disease ( COPD ) . Reliable blood biomarkers are needed to predict prognosis . OBJECTIVES To explore plasma biomarkers associated with an annual change in FEV1 in patients with COPD . METHODS Plasma sample s of 261 subjects , all Japanese , with COPD from the 5-year Hokkaido COPD cohort study were analyzed as a hypothesis-generating cohort , and the results were vali date d using data of 226 subjects with and 268 subjects without airflow limitation , mainly white , from the 4-year COPD Quantification by Computed Tomography , Biomarkers , and Quality of Life ( CBQ ) study conducted in Denmark . The plasma sample s were measured using Human CardiovascularMAP ( Myriad RBM , Austin , TX ) , which could analyze 50 biomarkers potentially linked with inflammatory , metabolic , and tissue remodeling pathways , and single ELISAs were used to confirm the results . MEASUREMENTS AND MAIN RESULTS Higher plasma adiponectin levels and a lower leptin/adiponectin ratio at enrollment were significantly associated with an annual decline in FEV1 even after controlling for age , sex , height , and body mass index in the Hokkaido COPD cohort study ( P = 0.003 , P = 0.004 , respectively ) . A lower plasma leptin/adiponectin ratio was also significantly associated with an annual decline in FEV1 in subjects with airflow limitation in the CBQ study ( P = 0.014 ) , the patients of which had largely different clinical characteristics compared with the Hokkaido COPD cohort study . There were no significant associations between lung function decline and adipokine levels in subjects without airflow limitation . CONCLUSIONS A lower leptin/adiponectin ratio was associated with lung function decline in patients with COPD in two independent Japanese and Western cohort studies of population s of different ethnicity . Measure of systemic adipokines may provide utility in predicting patients with COPD at higher risk of lung function decline INTRODUCTION Body mass index ( BMI ) increase is an undesired effect associated with antipsychotics , and crucial for patients ' global health and treatment compliance . We aim ed to investigate the relation between BMI during olanzapine or haloperidol treatments and leptin , neuropeptide Y ( NPY ) , adiponectin and lipid serum levels . METHODS In this 9-month , r and omized and naturalist study , 34 male patients , 18 on olanzapine and 16 on haloperidol group were enrolled , all were under monotherapy .  Patient outcome was evaluated with positive and negative syndrome scale ( PANSS ) at every 3-month period . In each visit , BMI , leptin , NPY , lipid , olanzapine or haloperidol levels were also monitored . RESULTS AND DISCUSSION Leptin levels positively correlated with BMI  in olanzapine ( r=0.64 , p<0.001 ) and haloperidol ( r=0.73 , p<0.001 ) groups ; only in olanzapine patients , the former also correlated with PANSS score ( r=0.54 , p<0.05 ) . NPY levels negatively correlated with olanzapine levels ( r=− 0.65 , p<0.01 ) . Adiponectin levels had not significantly varied . CONCLUSION Antipsychotics probably interfere on leptin and NPY signalling ways and disturb these hormones in eating behaviour control OBJECTIVE Concerns regarding worsening insulin sensitivity associated with statin treatment have recently emerged . Therefore the aim of this study was to assess and compare the effects of 90-day monotherapies with fenofibrate and atorvastatin , as well as combined therapy , on fasting plasma glucose , insulin resistance index , adipokines ( leptin , resistin , adiponectin ) and levels of proinflammatory cytokines ( TNF-α , IL-6 ) in patients with impaired fasting glucose ( IFG ) and mixed hyperlipidemia . MATERIAL S AND METHODS 67 patients were r and omly assigned to four treatment arms : monotherapy with atorvastatin , monotherapy with fenofibrate , combined therapy ( fenofibrate and torvastatin ) or therapeutic lifestyle change . The study lasted for 90 days . All participants received counseling regarding proper diet and physical activity . RESULTS Compared to the control subjects , prediabetic patients exhibited elevated plasma levels of leptin , resistin , TNF-α and IL-6 , and a lower plasma level of adiponectin . All therapeutic interventions result ed in significant alterations in the lipid profile . Insulin resistance index ( HOMA-IR ) was reduced after treatment with fenofibrate . The effect of atorvastatin on insulin resistance was comparable to therapeutic lifestyle change alone . Therapy with hypolipidemic drugs caused increases in adiponectin levels and decreases in leptin and resistin . An additive effect of the combined treatment on plasma IL-6 level was also observed . CONCLUSIONS Fenofibrate-based treatment was associated with improved insulin sensitivity . Atorvastatin did not cause a deterioration in insulin sensitivity . Hypolipidemic therapies result ed in significant changes in the proinflammatory cytokine network as well as in adipokine levels . At the end of the study the measured parameters nearly resembled those of the healthy subjects CONTEXT Adiponectin and leptin are closely related to weight control and energy balance , whereas exercise affects elderly metabolic regulation and functional capacity . OBJECTIVE The objective of this study was to investigate leptin and adiponectin responses in elderly males after exercise training and detraining .  DESIGN The study design was a 1-yr r and omized controlled trial . SETTING The study was performed at the Laboratory of Physical Education and Sport Science Department . PARTICIPANTS Fifty inactive men [ age , 65 - 78 yr ; body mass index ( BMI ) , 28.7 - 30.2 kg/m2 ] were recruited from a volunteer data base by word of mouth and fliers sent to medical practitioners , physiotherapists , and nursing homes in the local community . INTERVENTION(S ) Participants were r and omly assigned to a control ( n = 10 ) , low-intensity ( n = 14 ) , moderate-intensity ( n = 12 ) , or high-intensity training ( HI ; n = 14 ) group . Resistance training ( 6 months , 3 d/wk , 10 exercises/three sets ) was followed by 6 months of detraining . MAIN OUTCOME MEASURE(S ) Strength , exercise energy cost , skinfold sum , body weight , maximal oxygen consumption , resting metabolic rate ( RMR ) , and plasma leptin and adiponectin were determined at baseline and after training and detraining . RESULTS Strength , maximal oxygen consumption , RMR , and exercise energy cost increased ( P < 0.05 ) after training in an intensity-dependent manner . Skinfold sum and BMI were reduced by resistance training ( P < 0.05 ) , with HI being more effective ( P < 0.05 ) than moderate-intensity/low-intensity training . Leptin was diminished ( P < 0.05 ) by all treatments , whereas adiponectin increased ( P < 0.05 ) only in HI . Detraining maintained training-induced changes only in HI . The percent leptin decrease was associated ( P < 0.05 ) with the percent BMI decrease and the percent RMR increase , whereas the percent adiponectin increase was associated ( P < 0.05 ) with the percent BMI decrease . CONCLUSIONS Resistance training and detraining may alter leptin and adiponectin responses in an intensity-dependent manner . Leptin and adiponectin changes were strongly associated with RMR and anthropometric changes Objective The constellation of obesity , insulin resistance , and serum adipocytokine levels is associated with the risk and prognosis of postmenopausal breast cancer ( PBC ) . Altered secretion of resistin may underlie the association between overweight/obesity and PBC . We thus explored the association of serum resistin with PBC , taking into account established risk factors , including adipokines and anthropometric , metabolic , and inflammatory markers . Methods In a case-control study , we studied 102 postmenopausal women with pathologically confirmed , incident invasive breast cancer and 102 control participants matched on age and time of diagnosis between 2003 and 2010 at the Veterans ’ Administration General Hospital of Athens ( NIMTS Hospital ) .  Serum resistin , adiponectin , leptin , metabolic ( homeostasis model assessment score of insulin resistance ) and inflammatory ( tumor necrosis factor-&agr ; , interleukin-6 , and high-sensitivity C-reactive protein ) parameters , and tumor markers ( carcinoembryonic antigen and CA 15 - 3 ) were determined . Results The mean serum resistin level was significantly higher in case participants than in control participants ( P < 0.001 ) in both univariate and multivariable analyses , adjusting for age , date of diagnosis , education , family history of cancer , use of exogenous hormones , alcohol consumption , smoking status , physical activity , reproductive markers , metabolic markers , anthropometric ( body mass index and weight circumference ) markers , inflammatory markers , and adipokines ( odds ratio , 1.17 ; 95 % CI , 1.03 - 1.34 ; P = 0.02 ) . In case participants , resistin level correlated significantly with tumor markers and inflammatory parameters , but not with metabolic and anthropometric variables . Conclusions Further prospect i ve , longitudinal , and mechanistic studies are needed to determine whether hyperresistinemia is involved in the development of PBC or reflects changes during PBC progression and therefore could be used as a biomarker for PBC . Targeting resistin inhibition could be an effective therapeutic strategy in breast cancer by down-regulating the inflammatory microenvironment in breast tissue The aim of this study was to investigate the potential role of adipose cytokines in the obesity-associated insulin resistance . To that end , we compared : 1 ) serum concentrations of interleukin 6 ( IL-6 ) , tumor necrosis factor alpha ( TNFalpha ) , and leptin in eight healthy lean control females and in and roid obese female without ( n = 14 ) and with ( n = 7 ) type 2 diabetes ; and 2 ) the levels of these cytokines both in serum and in sc adipose tissue in the 14 obese nondiabetic women before and after 3 weeks of a very low-calorie diet ( VLCD ) .  As compared with lean controls , obese nondiabetic and diabetic patients were more insulin resistant and presented increased values for leptin , IL-6 , TNFalpha , and C-reactive protein . In the whole group , IL-6 values were more closely related to the parameters evaluating insulin resistance than leptin or TNFalpha values .  VLCD result ed in weight loss and decreased body fat mass ( approximately 3 kg ) . Insulin sensitivity was improved with no significant change in both serum and adipose tissue TNFalpha levels . In contrast , VLCD induced significant decreases in IL-6 and leptin levels in both adipose tissue and serum . These results suggest that , as for leptin , circulating IL-6 concentrations reflect , at least in part , adipose tissue production . The reduced production and serum concentrations after weight loss could play a role in the improved sensitivity to insulin observed in these patients OBJECTIVE The plasma leptin/adiponectin ( L/A ) ratio has been proposed as a preferential marker of atherosclerosis susceptibility compared to leptin and adiponectin alone . We determined the extent to which the L/A ratio predicts incident cardiovascular disease ( CVD ) taking account of clinical risk factors , microalbuminuria , the total cholesterol/HDL cholesterol ( TC/HDL-C ratio ) , triglycerides , high sensitive C-reactive protein ( hs-CRP ) and insulin sensitivity ( homeostasis model assessment ( HOMA(ir ) ) ) . METHODS A community-based prospect i ve nested case-control study was carried out in 103 non-diabetic men who developed a first cardiovascular event ( cases ) and 106 male control subjects ( no clinical ly manifest CVD and no lipid lowering drug use at baseline ; median follow-up of 3.0 and 10.5 years , respectively ) .  Plasma leptin , adiponectin , the leptin/adipnectin ( L/A ) ratio , as well as hs-CRP , HOMA(ir ) and the TC/HDL-C ratio were determined at baseline . RESULTS Plasma leptin levels and the L/A ratio were higher in cases vs. controls ( p=0.002 for both ) , but the difference in adiponectin was not significant ( p=0.10 ) . Age-adjusted incident CVD was associated with plasma leptin , adiponectin and the L/A ratio ( p=0.045 to p=0.001 ) . The relationships of incident CVD with plasma leptin ( p=0.19 ) and adiponectin ( p=0.073 ) lost statistical significance after additional adjustment for smoking , waist circumference , hypertension , microalbuminuria , the TC/HDL-C ratio , hs-CRP and HOMA(ir ) . In this fully adjusted analysis , the L/A ratio remained predictive of incident CVD ( hazard ratio : 1.40 ( 95 % CI 1.05 - 1.87 ) , p=0.024 ) . CONCLUSION This study suggests that the L/A ratio may be a preferential marker of a first cardiovascular event in men compared to plasma leptin and adiponectin levels alone Dietary calorie restriction and exercise promote weight loss and may have additive effects for improving insulin sensitivity , independent of weight loss . It is not known if these effects are attributable to changes in circulating cytokines . We evaluated the hypothesis that modest , matched weight loss induced by calorie restriction and exercise have additive effects on circulating cytokines and these changes correlate with improvements in insulin sensitivity . Overweight and sedentary women and men ( n = 52 , 45–65 years ) were r and omized to undergo 7 % weight loss by using 3–6 months of calorie restriction , exercise , or a combination of both calorie restriction and exercise . Concentrations of cytokines and hormones were measured in fasting and oral glucose tolerance test blood sample s. Insulin sensitivity was estimated based on oral glucose tolerance test for glucose and insulin . With all groups combined , fasting leptin ( p < 0.0001 ) and high molecular weight adiponectin ( p = 0.04 ) decreased and pentraxin-3 increased ( p < 0.0001 ) , in a manner that correlated with improvements in insulin sensitivity ( all p ≤ 0.0002 ) . These changes , combined with decreases in glucose-dependent insulinotropic polypeptide from the oral glucose tolerance test , explained 63 % of the variance ( p < 0.0001 ) in insulin sensitivity improvements . Exercise and calorie restriction had additive effects on leptin , with a similar trend for high molecular weight adiponectin . Monocyte chemoattractant protein-1 and C-reactive protein concentrations did not change . Calorie restriction and exercise had opposite effects on soluble tumor necrosis factor receptor-1 .  Modest weight loss in overweight adults  decreases serum leptin and high molecular weight adiponectin , and increases pentraxin-3 concentrations in a manner that correlates with increased insulin sensitivity . Exercise has additive effects to those induced by calorie restriction for reductions in leptin and possibly adiponectin . These changes may contribute to the additive effects of calorie restriction and exercise for improving insulin sensitivity
Subgroup analyses suggested that Asian and African AS patients as well as patients aged < 40 years had higher serum leptin and resistin levels when compared to controls .
Serum adiponectin levels were higher in AS patients compared to controls in subgroup of age ≥ 40 , and serum resistin levels in subgroup of BMI ≥ 25 .
Measurement method was a source of heterogeneity for resistin .
Publication bias was not observed and the robustness of study results was confirmed by sensitivity analysis .
Conclusion : Serum resistin , but not leptin or adiponectin levels may be closely associated with the development of AS .
HighlightsSerum levels of resistin are associated with the pathogenesis of AS.In specific subgroups , leptin and adiponectin may be related to AS.Measuring type is one of sources of heterogeneity for the studies about resistin
Objectives : Various studies have research ed the serum levels of leptin , adiponectin and resistin in patients with ankylosing spondylitis ( AS ) , but the results were inconclusive .
The purpose of this study was to systematic ally evaluate the correlations between serum levels of these adipokines and AS .