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. Leptin and adiponectin levels in patients with ankylosing spondylitis. The effect of infliximab treatment. Periodontal treatment with topical antibiotics improves glycemic control in association with elevated serum adiponectin in patients with type 2 diabetes mellitus. L-carnitine supplementation and adipokines in patients with end-stage renal disease on regular hemodialysis. Effects of ursodeoxycholic acid in combination with vitamin E on adipokines and apoptosis in patients with nonalcoholic steatohepatitis. 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. Effect of dieting on plasma leptin, soluble leptin receptor, adiponectin and resistin levels in healthy volunteers Clinical Significance of Serum Adipokines according to Body Mass Index in Patients with Clinically Localized Prostate Cancer Undergoing Radical Prostatectomy Circulating adipokines and mRNA expression in adipose tissue and the placenta in women with gestational diabetes mellitus Hyperresistinemia is associated with postmenopausal breast cancer Lifestyle Intervention and Adipokine Levels in Subjects at High Risk for Type 2 Diabetes Effects of 90-day hypolipidemic treatment on insulin resistance, adipokines and proinflammatory cytokines in patients with mixed hyperlipidemia and impaired fasting glucose. Adipokines and biochemical changes in Egyptian obese subjects: possible variation with sex and degree of obesity The effect of enteral nutrition on adipokines in patients with acute pancreatitis Favorable effects of low-fat and low-carbohydrate dietary patterns on serum leptin, but not adiponectin, among overweight and obese premenopausal women: a randomized trial Resistin and adiponectin in major depression: the association with free cortisol and effects of antidepressant treatment. Exercise and obesity in fibromyalgia: beneficial roles of IGF-1 and resistin? Effects of supplementation with curcumin on serum adipokine concentrations: A randomized controlled trial. Adipocytokines and the risk of coronary heart disease in healthy middle aged men: the PRIME Study Circulating levels of adiponectin, resistin, and visfatin after mud-bath therapy in patients with bilateral knee osteoarthritis Effect of exercise training combined with phytoestrogens on adipokines and C-reactive protein in postmenopausal women: a randomized trial. The effect of testosterone replacement therapy on adipocytokines and C-reactive protein in hypogonadal men with type 2 diabetes.
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 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 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 Chronic hemodialysis ( HD ) patients frequently encounter carnitine depletion , elevated adipose tissue-derived hormones/cytokines , that may contribute to accelerated arteriosclerosis . 10 non-diabetic HD patients were studied over 28 weeks . In the 12 weeks treatment period 1 g L-carnitine was given iv after each HD session . Measurements of plasma free- and acylcarnitines , insulin , leptin , adiponectin , resistin and ghrelin were performed at baseline , at weeks 2 , 4 , 8 , 12 ( treatment period ) and at weeks 24 - 28 ( post-treatment period ) . L-carnitine supplementation result ed in progressive increase of free- and acylcarnitine levels . Plasma levels of insulin , resistin , leptin and ghrelin remained at the already elevated baseline values . L-carnitine therapy induced a significant increase in plasma adiponectin from 20.2 ± 12.7 μg/ml ( baseline ) to 32.7 ± 20.2 μg/ml in week 2 ( p<0.05 ) and 35.4 ± 19.6 μg/ml in week 12 ( p < 0.03 ) , which remained unchanged in the post-carnitine period . Plasma insulin levels correlated positively with leptin ( r = 0.525 , p<0.0001 ) and resistin ( r = 0.284 , p<0.005 ) ; adiponectin levels correlated inversely with leptin ( r = -0.255 , p<0.02 ) and resistin ( r = -0.213 , p<0.04 ) irrespective of carnitine status . Plasma levels of adipokines and related hormones are greatly elevated in patients on regular HD  . L-carnitine administration further augmented the plasma levels of protective adiponectin , therefore it may have a role in preventing cardiovascular complications of uremia BACKGROUND / AIMS Adipokines and hepatocellular apoptosis participate in the pathogenesis of nonalcoholic steatohepatitis ( NASH ) . In a r and omized trial ursodeoxycholic acid ( UDCA ) with vitamin E ( VitE ) improved serum aminotransferases and hepatic histology . The present work evaluates the effect of this combination on adipokines and hepatocellular apoptosis . METHODS Circulating levels of adiponectin , resistin , leptin , interleukin (IL)-6 , IL-8 , retinol binding protein-4 , monocyte chemoattractant protein-1 and tumour necrosis factor-alpha were measured by enzyme-linked immunoassays at the beginning and after 2 years of treatment with either UDCA+VitE , UDCA+placebo ( P ) or P+P.  Apoptosis was assessed by immunohistochemistry for activated caspase-3 and circulating levels of apoptosis-associated cytokeratin 18 fragments ( M30 ) . RESULTS Levels of adiponectin increased in patients treated with UDCA+VitE , whereas they decreased in the two other groups ( P<0.04 ) and correlated with the improvement of liver steatosis ( P<0.04 ) . M30 levels worsened in the P/P group and improved in the other two groups . They correlated with hepatocellular apoptosis ( P<0.02 ) and steatosis ( P<0.02 ) as well as negatively with adiponectin levels ( P<0.04 ) . CONCLUSIONS UDCA+VitE improves not only aminotransferase levels and liver histology of patients with NASH , but also decreases hepatocellular apoptosis and restores circulating levels of adiponectin . These results suggest that the UDCA+VitE combination has metabolic effects in addition to its beneficial cytoprotective properties 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 Recent findings demonstrating important effects of the adipokines on metabolism , energy homeostasis and body weight regulation have prompted research on the possible role of negative energy balance in altering adipocytokine regulation . The goal of this study was to evaluate the effects of a hypocaloric diet in healthy normal‐weight volunteers . An additional goal was to help clarify the contribution of restricted caloric intake to altered plasma adipokine levels in the eating disorders anorexia nervosa and bulimia nervosa 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 HighlightsChemerin and leptin are increased , omentin‐1 and visfatin are decreased in at term GDM‐obese women .  Chemerin and omentin‐1 are expressed mainly by the maternal VAT . Leptin is expressed mainly in maternal SAT.Circulating chemerin and leptin in at term pregnancy correlate with BMI and HOMA‐IR.Chemerin and leptin could contribute to insulin resistance and low grade inflammation that characterizes GDM women complicated by obesity . Weight control during pregnancy is necessary to avoid adverse metabolic complications for the mother and the offspring . & NA ; Maternal adipose tissue and the placenta secrete various molecules commonly called adipokines such as chemerin , omentin‐1 , visfatin , adiponectin , and leptin that are important players in the pathogenesis of insulin resistance . Gestational diabetes mellitus ( GDM ) is defined as a state of glucose intolerance characterized by & bgr;‐cell dysfunction and insulin resistance . To examine whether circulating adipokines and their mRNA expression in the adipose tissue and the placenta are altered in GDM pregnancy , we compared 15 GDM women [ obese ( BMI > 30 ) and non‐obese ( BMI < 30 ) ] to 23 NGT ( normal glucose tolerance ) women [ obese and non‐obese ] , at the time of the Cesarean section .  Circulating chemerin and leptin were higher ( p = 0.009 and p = 0.005 , respectively ) and circulating omentin‐1 , visfatin , as well as the adiponectin/leptin ratio were lower ( p = 0.039 , p = 0.007 and p = 0.011 , respectively ) in GDM‐obese compared to NGT‐non‐obese women . Chemerin and leptin correlated positively with BMI and HOMA‐IR and omentin‐1 correlated negatively with BMI . Serum TNF‐&agr ; was significantly elevated in all obese compared to non‐obese pregnant women and correlated positively with BMI . Adiponectin levels were reduced ‐although not significantly‐ in GDM‐ and NGT‐obese women compared to their non‐obese counterparts . Resistin , RPB4 and IL‐6 levels did not differ significantly between groups . Chemerin mRNA expression in subcutaneous adipose tissue ( SAT ) and visceral adipose tissue ( VAT ) was significantly higher compared to placenta in all women ( 6‐to 24‐times , p < 0.05 ) . Chemerin‐VAT mRNA expression in GDM‐obese tended to be significantly higher compared to NGT‐non‐obese women ( 3‐times , p = 0.005 ) . Omentin‐1 mRNA expression was significantly higher in VAT compared to SAT ( 50‐ to 100‐times , p < 0.01 ) and its expression in placenta was negligible in all women . Although , leptin was expressed significantly higher in SAT compared to VAT and the placenta in all women ( 5‐ to 46‐times , p < 0.05 ) , only its mRNA expression in VAT of obese ( GDM and NGT ) differed significantly when compared to NGT‐non‐obese women ( 3‐times higher , p < 0.02 ) . Visfatin mRNA expression was comparable in all tissues . In conclusion , chemerin and leptin are elevated and omentin‐1 and visfatin levels are decreased in GDM women complicated by obesity . This finding together with the positive association of chemerin and leptin with markers of insulin resistance , suggests that these adipokines and more especially chemerin and leptin accompanied by their adipose tissue expression could contribute to the increased insulin resistance and low grade inflammation that characterizes GDM‐obese women 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 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 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 The purpose of this study was firstly to evaluate the adipokines and biochemical changes in obese subjects in relation to different grade s of obesity and in relation to gender difference ( males versus females ) and secondly to evaluate the role of TNF-α in obesity . From January 2013 to February 2014 , a total number of 120 non-diabetic subjects of both sexes were recruited and r and omly selected from Dr. Abd-Elhamid Elsheikh center for physiotherapy and weight control , El-menofia-Egypt . Those subjects were classified according to their sex into two main groups ; the female group and the male group . The female group ( 60 women ) was distributed according to BMI into group 1 ( 15 lean women ) , group 2 ( 15 class I obese women ) , group 3 ( 15 class II obese women ) , and group 4 ( 15 class III obese women ) . The male group ( 60 men ) was also distributed according to the BMI into group 1 ( 15 lean men ) , group 2 ( 15 class I obese men ) , group 3 ( 15 class II obese men ) , and group 4 ( 15 class III obese men ) . All individuals enrolled in the study were su bmi tted to weight and height measurements with subsequent calculation of body mass index . Fasting blood sample s were collected from all participants for quantitative determination of blood glucose , serum lipid , TNF-α , leptin , and adiponectin levels . One-way analysis of variance followed by LSD post hoc test was used for comparison of variables . In obese subjects of both sexes , it was found that circulating leptin and TNF-α levels were significantly high ( P < 0.05 ) and positively correlated to BMI . In contrast to leptin , adiponectin concentrations were significantly low ( P < 0.05 ) and inversely correlated to BMI . Regarding gender difference , although serum leptin and adiponectin levels were higher in women than men , men showed higher atherogenic parameters . We conclude that leptin , TNF-α , and adiponectin were related to both BMI and grade s of obesity . Furthermore , TNF-α may play a role in obesity The mechanism behind the beneficial effects of enteral nutrition ( EN ) for patients with acute pancreatitis ( AP ) is largely unknown . Adipokines , as mediators of metabolism and inflammation , may be a possible mechanism . The study aim ed to investigate the effect of EN on adipokines early in the course of AP . Patients with AP were r and omised to EN or nil-by-mouth ( NBM ) .  Blood sample s were taken on the first 4 d of admission and adipokine concentrations for adiponectin , leptin , omentin , resistin and visfatin were determined by ELISA assays . A linear mixed model analysis was run to determine differences in adipokine concentrations between the two study groups . A total of thirty-two patients were included in the study .  Omentin concentrations were significantly higher in patients who received EN compared with NBM across the first 4 d of admission ( mean difference : 11·6 ( 95 % CI 1·0 , 22·3 ) ng/ml ; P = 0·033 ) . Leptin concentrations were significantly higher in patients who received EN compared with NBM after adjusting for age , sex and BMI ( mean difference : 2·3 ( 95 % CI 0·1 , 4·5 ) ng/ml ; P = 0·037 ) . No significant difference in adiponectin , resistin or visfatin concentrations were observed between the two study groups . EN significantly increases omentin and leptin concentrations in AP . Future research should be directed towards underst and ing whether these adipokines are responsible for the therapeutic benefits of EN Purpose The most effective dietary pattern for breast cancer prevention has been greatly debated in recent years . Studies have examined hypocaloric diets , with particular emphasis on macronutrient composition , yielding inconclusive data . The objective of this study was to examine the effects of calorie-restricted low-fat and low-carbohydrate diets ( LFD and LCD , respectively ) on circulating adipokines among overweight and obese premenopausal women . Methods Seventy-nine overweight and obese premenopausal women were r and omized to either LFD or LCD , with increased physical activity , for 52 weeks . Serum adiponectin , leptin and the adiponectin-to-leptin ratio ( A/L ) were measured at baseline , and at weeks 34 and 52 to assess intervention effects . Results While there were no significant changes in serum adiponectin concentrations following the LCD and LFD interventions , leptin concentrations significantly decreased by week 34 of the intervention period ( LCD : 35.3 % , P = 0.004 ; LFD : 30.0 % , P = 0.01 ) , with no difference by intervention arm . At week 52 , these reductions were statistically non-significant , indicating a return to baseline levels by the end of the intervention . While there were non-significant increases in the A/L ratio following the LCD and LFD intervention arms , the overall trend , across groups , was marginally significant ( P = 0.05 ) with increases of 16.2 % and 35.1 % at weeks 34 and 52 , respectively . Conclusions These findings suggest that caloric-restricted LCD and LFD dietary patterns favorably modify leptin and possibly the A/L ratio , and lend support to the hypothesis that these interventions may be effective for obesity-related breast cancer prevention through their effects on biomarkers involved in metabolic pathways . Trial registration Clinical Trial Registration Number : NCT01559194 Major depression is associated with an increased risk for myocardial infa rct ion . Adipokines have been shown to link obesity with metabolic disturbances . Based on this finding the present study was design ed to investigate the effect of antidepressive treatment with either amitriptyline or paroxetine on circulating concentrations of resistin and adiponectin in depressed patients , and to establish , whether these adipokines are associated with the activation of the hypothalamic-pituitary-adrenal (HPA)-system . Thirty-seven depressed in- patients were treated in a double-blind , r and omized protocol with either amitriptyline or paroxetine over a period of five weeks . After six drug free days blood was drawn on day 1 and again 36 days after antidepressive treatment for the measurement of resistin and adiponectin , fasting glucose and insulin concentrations . For quantification of free cortisol levels saliva was obtained daily at 0800 hours during weeks 1 and 5 . While resistin concentrations decreased in patients remitting under amitriptyline and paroxetine ( p<0.03 ) , no changes were observed in non-remitters . At baseline , though not during treatment , circulating resistin concentrations correlated positively with free cortisol levels and with BMI ( p<0.01 ) . Adiponectin levels , however , did not change during treatment and were not associated with free cortisol concentrations but were instead positively related to QUICKI ( p<0.03 ) . In conclusion , the present data revealed resistin but not adiponectin to be related to free cortisol concentrations and to decline in remitters to antidepressive treatment Introduction Severe fatigue is a major health problem in fibromyalgia ( FM ) . Obesity is common in FM , but the influence of adipokines and growth factors is not clear . The aim was to examine effects of exercise on fatigue , in lean , overweight and obese FM patients . Methods In a longitudinal study , 48 FM patients ( median 52 years ) exercised for 15 weeks .  Nine patients were lean ( body mass index , BMI 18.5 to 24.9 ) , 26 overweight ( BMI 25 to 29.9 ) and 13 obese .  Fatigue was rated on a 0 to 100 mm scale ( fibromyalgia impact question naire [ FIQ ] fatigue ) and multidimensional fatigue inventory ( MFI-20 ) general fatigue ( MFIGF ) . Higher levels in FIQ fatigue and MFIGF indicate greater degree of fatigue . Free and total IGF-1 , neuropeptides , adipokines were determined in serum and cerebrospinal fluid ( CSF ) . Results Baseline FIQ fatigue correlated negatively with serum leptin ( r = -0.345 ; P = 0.016 ) and nerve growth factor ( NGF ; r = -0.412 ; P = 0.037 ) . In lean patients , baseline MFIGF associated negatively with serum resistin ( r = -0.694 ; P = 0.038 ) . FIQ Fatigue associated negatively with CSF resistin ( r = -0.365 ; P = 0.073 ) . Similarly , FIQ fatigue ( r = -0.444 ; P = 0.026 ) and MFIGF correlated negatively with CSF adiponectin ( r = -0.508 ; P = 0.01 ) . In lean patients , FIQ fatigue ( P = 0.046 ) decreased after 15 weeks . After 30 weeks , MFIGF decreased significantly in lean ( MFIGF : P = 0.017 ) , overweight ( MFIGF : P = 0.001 ) , and obese patients ( MFIGF : P = 0.016 ) . After 15 weeks , total IGF-1 increased in lean ( P = 0.043 ) patients . ∆Total IGF-1 differed significantly between lean and obese patients ( P = 0.010 ) . ∆Total IGF-1 related negatively with ∆MFIGF after 15 weeks ( r = -0.329 ; P = 0.050 ) . After 30 weeks , ∆FIQ fatigue negatively correlated with ∆NGF ( r = -0.463 ; P = 0.034 ) and positively with ∆neuropeptide Y ( NPY ) ( r = 0.469 ; P = 0.032 ) . Resistin increased after 30 weeks ( P = 0.034 ) . ∆MFIGF correlated negatively with ∆resistin ( r = -0.346 ; P = 0.031 ) , being strongest in obese patients ( r = -0.815 ; P = 0.007 ) . In obese patients , ∆FIQ fatigue after 30 weeks correlated negatively with ∆free IGF-1 ( r = -0.711 ; P = 0.032 ) . Conclusions Exercise  reduced fatigue  in all FM patients , this effect was achieved earlier in lean patients . Baseline levels of resistin in both serum and CSF associated negatively with fatigue . Resistin was increased after the exercise period which correlated with decreased fatigue . Changes in IGF-1 indicate similar long-term effects in obese patients . This study shows reduced fatigue  after moderate exercise in FM and indicates the involvement of IGF-1 and resistin in these beneficial effects . Trial registration Clinical Trials.gov : OBJECTIVE Previous experimental studies have suggested curcumin as a safe phytochemical that can improve insulin resistance through effects on adiponectin and leptin . This study aim ed to investigate the effect of curcumin on circulating adiponectin and leptin concentrations in patients with metabolic syndrome . METHODS In this pilot , r and omized , double-blind , placebo-controlled trial , subjects who met the criteria of metabolic syndrome according to the National Cholesterol Education Program Adult Treatment Panel III criteria were r and omly assigned to curcumin ( n = 59 ; 1000 mg/d ) or a placebo ( n = 58 ) for 8 wk . Serum adiponectin and leptin concentrations were determined before and after intervention . The pooled effect size for the impact of curcumin supplementation on serum adiponectin and leptin levels was also estimated using r and om-effects meta analysis . RESULTS Eight-week supplementation with curcumin was associated with a significant increase in serum adiponectin levels ( P < 0.001 ) and a reduction in serum leptin concentrations ( P < 0.001 ) . Serum leptin : adiponectin ratio was also improved by curcumin ( P < 0.001 ) . These beneficial effects of curcumin remained significant after adjustment for changes in serum lipids and glucose concentrations and baseline differences in body mass index and serum levels of glucose and glycated hemoglobin as potential confounders of treatment response . Meta analysis suggested that curcumin supplementation can increase adiponectin levels by 76.78 % ( 95 % CI : 6.14 - 147.42 ; P = 0.0330 ) , and reduce leptin by 26.49 % ( 95 % CI : -70.44 to 17.46 ) , however this latter effect size did not reach statistical significance ( P = 0.238 ) . CONCLUSIONS Curcumin can improve serum levels of adiponectin and leptin in patients with metabolic syndrome . This trial was registered at the UMIN Clinical Trials Registry ( http://www.umin.ac.jp/ctr/ ) under Trial No. UMIN000018339 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 Adipocytokines , including adiponectin , resistin , and visfatin may play an important role in the pathophysiology of osteoarthritis ( OA ) .  Spa therapy is one of the most commonly used non-pharmacological approaches for OA , but its mechanisms of action are not completely known . The aim of the present study was to assess whether a cycle of mud-bath therapy ( MBT ) influences the serum levels of adiponectin , resistin , and visfatin in patients with knee OA . As part of a prospect i ve r and omized , single blind-controlled trial evaluating the efficacy of MBT in knee OA , we included in this study 95 out patients . One group ( n = 49 ) received a cycle of MBT at the spa center of Chianciano Terme ( Italy ) in addition to the usual treatment , and one group ( control group ; n = 46 )  continued their regular care routine alone . Patients were assessed at basal time and at the end of the study ( 15 days ) for clinical and biochemical parameters . Clinical assessment s included spontaneous pain on a visual analog scale ( VAS ) score and the Western Ontario and McMaster Universities index ( WOMAC ) subscores for knee OA evaluated as total pain score ( W-TPS ) , total stiffness score ( W-TSS ) , and total physical function score ( W-TPFS ) . Adiponectin , resistin and visfatin serum levels were assessed by enzyme immunoassay methods . At the end of the mud-bath therapy , serum adiponectin levels showed a significant decrease ( p < 0.001 ) , while no significant modifications were found in the control group at day 15 . Serum resistin showed a significant decrease ( p < 0.0001 ) in the MBT group at the end of the study and a significant increase in the control patients ( p < 0.001 ) . No significant modifications of visfatin were found in MBT . Furthermore , we tested the relationships between demographic and clinical parameters and adipocytokine concentrations measured in the MBT group at basal and at the end of the study . In conclusion , the present study shows that a cycle of MBT can modify serum levels of adiponectin and resistin but not the circulating levels of visfatin . In view of the recent evidence s about the involvement of adiponectin and resistin in the pathogenesis and progression of OA , the decrease of these adipokines after mud-bath therapy may play a protective role in the course of the disease . However , it remains to be clarified which of the mechanisms of action of MBT may have determined the changes in serum levels of adiponectin and resistin that we observed Phytoestrogens and training could be effective to reduce cardiovascular and type 2 diabetes mellitus risk factors in postmenopausal women . Nevertheless , the impact of their combination on adipokines and systemic inflammation was never investigated . The objective was to verify if 6 months of mixed training combined with phytoestrogens could have an additional effect on adipokine levels and systemic inflammation in obese postmenopausal women . Fifty-two obese women aged between 50 and 70 years were r and omly assigned to ( 1 ) exercise with placebo ( EX + PL ; n = 25 ) or ( 2 ) exercise with phytoestrogens ( EX + PHY ; n = 27 ) . Body weight , waist circumference , fat mass , and lean body mass ( dual-energy x-ray absorptiometry ) were assessed . Fasting plasma glucose and insulin , adiponectin , leptin , and C-reactive protein ( CRP ) levels were obtained after a 12-hour overnight fast . Total energy intake was measured with a 3-day dietary record . All measurements were performed before and after the 6-month intervention . Although energy intake remained unchanged , body composition was improved in all women ( all Ps < .02 ) . Plasma CRP and leptin levels decreased in both groups similarly ( all Ps < .03 ) , whereas plasma adiponectin and insulin did not change with exercise combined with placebo or phytoestrogens . Correlation analyses showed that homeostasis model assessment of insulin resistance ( r = -0.58 , P = .02 ) and fasting insulin levels ( r = -0.42 , P = .02 ) at baseline were both correlated with changes in leptin levels . Baseline fasting glucose ( r = -0.36 , P = .03 ) and adiponectin ( r = 0.45 , P = .005 ) levels were associated with changes in CRP concentrations . Although mixed exercise program combined with phytoestrogens does not seem to provide any additional effect , mixed training improves systemic inflammation and leptin concentrations in obese postmenopausal women OBJECTIVE Serum testosterone levels are known to inversely correlate with insulin sensitivity and obesity in men . Furthermore , there is evidence to suggest that testosterone replacement therapy reduces insulin resistance and visceral adiposity in type 2 diabetic men . Adipocytokines are hormones secreted by adipose tissue and contribute to insulin resistance . We examined the effects of testosterone replacement treatment on various adipocytokines and C-reactive protein ( CRP ) in type 2 diabetic men . DESIGN Double-blinded placebo-controlled crossover study in 20 hypogonadal type 2 diabetic men . Patients were treated with testosterone ( sustanon 200 mg ) or placebo intramuscularly every 2 weeks for 3 months in r and om order followed by a washout period of 1 month before the alternate treatment phase . METHODS Leptin , adiponectin , resistin , tumour necrosis factor-alpha ( TNF-alpha ) , interleukin (IL)-6 and CRP levels were measured before and after each treatment phase . Body mass index ( BMI ) and waist circumference were also recorded . RESULTS At baseline , leptin levels significantly correlated with BMI and waist circumference . There was a significant inverse correlation between baseline IL-6 and total testosterone ( r=-0.68 ; P=0.002 ) and bioavailable testosterone levels ( r=-0.73 ; P=0.007 ) . CRP levels also correlated significantly with total testosterone levels ( r=-0.59 ; P=0.01 ) . Testosterone treatment reduced leptin ( -7141.9 + /- 1461.8 pg/ml ; P=0.0001 ) and adiponectin levels ( -2075.8 + /- 852.3 ng/ml ; P=0.02 ) . There was a significant reduction in waist circumference . No significant effects of testosterone therapy on resistin , TNF-alpha , IL-6 or CRP levels were observed . CONCLUSION Testosterone replacement treatment decreases leptin and adiponectin levels  in type 2 diabetic men . Moreover , low levels of testosterone in men are associated with pro-inflammatory profile , though testosterone treatment over 3 months had no effect on inflammatory markers
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 .