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Background: Adipokines are key mediators of inflammation in metabolic syndrome perpetuating the effect of excess nutrient intake by setting a self-maintaining vicious circle. Here, we assess levels of adiponectin and leptin in a cohort of individuals with MetS undergoing dietary and behavioral counselling. Specifically, we investigate their role as predictors of metabolic syndrome remission after 1 year., Methods: Patients with MetS (n = 127) received behavioral and dietary recommendations and were followed-up for 1 year. Serum was available for 108 individuals, levels of adiponectin and leptin were tested at baseline, at 6 months (t1) and after 1 year (t2). Adiponectin/leptin (A/L) ratio was also calculated and tested for predictive ability., Result: At the end of the follow-up period, 59 patients did not show enough criteria to define MetS anymore. When considered alone, adiponectin and leptin levels did not show difference over follow-up. Their ratio instead was significantly reduced at t1 and t2 with respect to baseline. Remitters also showed lowers level of leptin and A/L ratio as compared to non-remitters at t1. At this timepoint, A/L ratio independently predicted MetS remission at 1 year [OR 9.082 95%CI (1.394-59.160), p = 0.021]. Bootstrap resampling analysis internally validated our findings., Conclusions: Preliminary results from our pilot study suggest that MetS remission after counselling associates with changes in adipokine balance. A/L ratio decreases overtime and its value at 6 months can independently predict MetS remission., Competing Interests: Declaration of competing interest LL is coinventors on the International Patent (WO/2020/226993) filed in April 2020 and relating to the use of antibodies which specifically bind IL-1α to reduce various sequelae of ischemia–reperfusion injury to the central nervous system. LL has received speaker fees outside of this work from Daichi-Sankyo. AB received honoraria from Effetti s.r.l. (Milan, Italy) to collaborate on the medical website www.inflammology.org, outside the present work. S.K. declares research grants to the institution from the Jubiläumsstiftung SwissLife, the Lindenhof Foundation, the Novartis Foundation for Medical-biological Research, the Swiss Heart Foundation, the Swiss Society of Cardiology, and the Theodor-Ida-Herzog-Egli Foundation, and equipment and materials from Roche Diagnostics outside the submitted work. Further, he has received travel support from the European Atherosclerosis Society, the European Society of Cardiology, the European Society of Clinical Investigation, Sphingotec GmbH, the 4TEEN4 Pharmaceuticals GmbH, and PAM Theragnostics GmbH. The other authors report no conflict of interest., (Copyright © 2024. Published by Elsevier B.V.)

Metabolic syndrome (MetS) is a global health challenge characterized as a group of risk factors for developing atherosclerotic cardiovascular disease. Although visceral adipose tissue, adipocyte dysfunction, chronic low-grade inflammation, and insulin resistance are fundamental to MetS, the exact biochemical mechanisms underlying this disease state remain unclear. Numerous biomarkers, however, have been proposed to improve our understanding of its complex pathophysiology and facilitate diagnosis. This review examines these biomarkers and clarifies their potential roles in the pathogenesis, diagnosis, prediction, progression, and severity of MetS and MetS-related disorders., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Unlabelled: Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome (MetS). Up to a third of NAFLD subjects are at risk for developing nonalcoholic steatohepatitis (NASH). Many rodent models fail to replicate both MetS and NASH. The purpose of this study was to develop a reliable mouse model of NASH and MetS using a diet containing cholesterol, saturated fat and carbohydrate that is reflective of Western diets of North Americans., Experimental Design: We used adult male C57BL/6 J 4- to 5-week-old mice and administered a solid diet containing 0.2% cholesterol, 45% of its calories from fat, with 30% of the fat in the form of partially hydrogenated vegetable oil. We also provided carbohydrate largely as high-fructose corn syrup equivalent in water. In a separate cohort, we gave the identical diet in the absence of cholesterol. Glucose and insulin tolerance testing was conducted throughout the feeding period. The feeding was conducted for 16 weeks, and the mice were sacrificed for histological analysis, markers of MetS, liver inflammation, circulating lipids, as well as liver staining for fibrosis and alpha smooth muscle actin (α-SMA)., Results: We found that cholesterol significantly increased serum leptin, interleukin-6, liver weight and liver weight/body weight ratio, fibrosis and liver α-SMA., Conclusions: Mice administered a diet accurately reflecting patterns associated with humans afflicted with MetS can reliably replicate features of MetS, NASH and significant liver fibrosis. The model we describe significantly reduces the time by several months for development of stage 3 hepatic fibrosis., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Background: Although there are several studies on the prevalence of metabolic syndrome (MetS) in childhood cancer survivors (CCS), the association between MetS components and serum adipocytokine level has not been elucidated., Methods: The charts of 49 patients (27 male, 22 female) who had attended the CCS clinic of the Department of Pediatrics, Kyoto University Hospital, between April 2009 and March 2010 were retrospectively reviewed. Median age was 10.7 years, and the median interval since the completion of chemotherapy was 5.1 years. The diagnosis of MetS was made based on the Japanese criteria for either children or adults., Results: Three (6.1%) of 49 patients fulfilled the criteria for MetS, and 28 (57.1%) had at least one component of MetS. High leptin level was seen in 18 patients (36.7%), and low total adiponectin level was seen in 20 (40.8%). The number of patients with high leptin was correlated with body mass index z-score (>2.0), abdominal circumference/height (≥0.5), diastolic blood pressure and fasting blood sugar. The number of patients with low total adiponectin was correlated with systolic blood pressure and triglyceride. When the patients were divided into three groups based on the number of positive MetS components (0, 1 and 2-4), leptin and adiponectin tended to be higher and lower in the third group, respectively., Conclusions: Adipocytokines may play a role in the pathogenesis of MetS occurring in CCS. It is recommended that adipocytokines be evaluated together with MetS components at the CCS follow-up clinics., (© 2013 The Authors. Pediatrics International © 2013 Japan Pediatric Society.)

Background: Circulating leptin:adiponectin ratio (L:A) is a potential surrogate marker for cardiometabolic diseases; however, the relationship of the L:A with the occurrence of metabolic syndrome (MetS) has not yet been fully explored in the general Japanese population., Methods: We enrolled 678 Japanese subjects (208 men and 470 women, mean age: 58.8±14.4 [SD] yr; mean body mass index: 23.6±3.3 kg/m(2)) in this study, and determined their MetS status by using the National Cholesterol Education Program-Adult Treatment Panel (NCEP-ATP) recommendations with minor modifications for the Japanese population. Biochemical markers such as leptin and adiponectin present in blood were measured. The statistical analyses performed were gender-based., Results: A in subjects with MetS was significantly higher than that in subjects without MetS, regardless of gender. The L:A also showed a significant and gradual increase corresponding to the increase in the number of components of MetS present in both the genders (trend P<0.01). The cut-off level of the L:A to detect MetS was 0.59 (sensitivity: 0.72, specificity: 0.70) in men and 1.04 (sensitivity: 0.72, specificity: 0.69) in women., Conclusions: These results suggest that the L:A can serve as a clinically useful marker for detecting MetS characteristics in the general Japanese population. The clinical application of this laboratory index for detecting MetS should be assessed in future studies.

The serum adiponectin/leptin ratio (A/L ratio) is a surrogate marker of insulin sensitivity. Pre-eclampsia (PE) is associated with maternal metabolic syndrome and occasionally impaired fetal growth. We assessed whether the A/L ratio in first-trimester maternal serum was associated with PE and/or birth weight. Adiponectin and leptin were quantitated in first-trimester blood samples (gestational week 10+3–13+6) from 126 women who later developed PE with proteinuria (98 mild PE; 21 severe PE; 7 HELLP syndrome), and 297 controls, recruited from the Copenhagen First-Trimester Screening Study. The A/L ratio was reduced in PE pregnancies, median 0.17 (IQR: 0.12–0.27) compared with controls, median 0.32 (IQR: 0.19–0.62) (p < 0.001). A multiple logistic regression showed that PE was negatively associated with log A/L ratio independent of maternal BMI (odds ratio = 0.315, 95% CI = 0.191 to 0.519). Adiponectin (AUC = 0.632) and PAPP-A (AUC = 0.605) were negatively associated with PE, and leptin (AUC = 0.712) was positively associated with PE. However, the A/L ratio was a better predictor of PE (AUC = 0.737), albeit not clinically relevant as a single marker. No significant association was found between A/L ratio and clinical severity of pre-eclampsia or preterm birth. PE was associated with a significantly lower relative birth weight (p < 0.001). A significant negative correlation was found between relative birth weight and A/L ratio in controls (β = −0.165, p < 0.05) but not in PE pregnancies), independent of maternal BMI. After correction for maternal BMI, leptin was significantly associated with relative birth weight (β = 2.98, p < 0.05), while adiponectin was not significantly associated. Our findings suggest that an impairment of the A/L ratio (as seen in metabolic syndrome) in the first trimester is characteristic of PE, while aberrant fetal growth in PE is not dependent on insulin sensitivity, but rather on leptin-associated pathways. [ABSTRACT FROM AUTHOR]

Abstract Background Dietary fatty acid (FA) content has been shown to influence the development of post-traumatic osteoarthritis (PTOA) in obesity. We used the fat-1 transgenic mouse to examine the hypothesis that endogenous reduction of ω-6 to ω-3 FA ratio, under the same dietary conditions, would mitigate metabolic inflammation and the pathogenesis of PTOA in obese male and female mice. Methods Male and female fat-1 and wild-type littermates were fed either a control diet or an ω-6 FA-rich high-fat diet and underwent destabilization of the medial meniscus (DMM) surgery to induce PTOA. OA severity, synovitis, and osteophyte formation were determined histologically, while biomarker and lipidomic analyses were performed to evaluate levels of adipokines, insulin, pro-/anti-inflammatory cytokines, and FAs in serum and joint synovial fluid. Multivariable models were performed to elucidate the associations of dietary, metabolic, and mechanical factors with PTOA. Results We found that elevated serum levels of ω-3 FAs in fat-1 mice as compared to wild-type controls fed the same diet resulted in reduced OA and synovitis in a sex- and diet-dependent manner, despite comparable body weights. The fat-1 mice showed trends toward decreased serum pro-inflammatory cytokines and increased anti-inflammatory cytokines. Multivariable analysis for variables predicting OA severity in mice resulted in correlations with serum FA levels, but not with body weight. Conclusions This study provides further evidence that circulating FA composition and systemic metabolic inflammation, rather than body weight, may be the major risk factor for obesity-associated OA. We also demonstrate the potential genetic use of ω-3 FA desaturase in mitigating PTOA in obese patients following injury.

The serum adiponectin/leptin ratio (A/L ratio) is a surrogate marker of insulin sensitivity. Pre-eclampsia (PE) is associated with maternal metabolic syndrome and occasionally impaired fetal growth. We assessed whether the A/L ratio in first-trimester maternal serum was associated with PE and/or birth weight. Adiponectin and leptin were quantitated in first-trimester blood samples (gestational week 10+3–13+6) from 126 women who later developed PE with proteinuria (98 mild PE; 21 severe PE; 7 HELLP syndrome), and 297 controls, recruited from the Copenhagen First-Trimester Screening Study. The A/L ratio was reduced in PE pregnancies, median 0.17 (IQR: 0.12–0.27) compared with controls, median 0.32 (IQR: 0.19–0.62) (p < 0.001). A multiple logistic regression showed that PE was negatively associated with log A/L ratio independent of maternal BMI (odds ratio = 0.315, 95% CI = 0.191 to 0.519). Adiponectin (AUC = 0.632) and PAPP-A (AUC = 0.605) were negatively associated with PE, and leptin (AUC = 0.712) was positively associated with PE. However, the A/L ratio was a better predictor of PE (AUC = 0.737), albeit not clinically relevant as a single marker. No significant association was found between A/L ratio and clinical severity of pre-eclampsia or preterm birth. PE was associated with a significantly lower relative birth weight (p < 0.001). A significant negative correlation was found between relative birth weight and A/L ratio in controls (β = −0.165, p < 0.05) but not in PE pregnancies), independent of maternal BMI. After correction for maternal BMI, leptin was significantly associated with relative birth weight (β = 2.98, p < 0.05), while adiponectin was not significantly associated. Our findings suggest that an impairment of the A/L ratio (as seen in metabolic syndrome) in the first trimester is characteristic of PE, while aberrant fetal growth in PE is not dependent on insulin sensitivity, but rather on leptin-associated pathways.

Background: Obesity is a major risk factor for diabetes mellitus and cardiovascular diseases. Nevertheless, some obese patients have normal parameters of blood arterial pressure, carbohydrate, and lipid metabolism ("metabolically healthy obesity", MHO).Aim: To study adipocytokine levels and to assess the effect of weight loss on cardiometabolic risk factors in patients with metabolically healthy obesity.Materials and methods: We conducted a comparative analysis of the main metabolic parameters and adipocytokine levels in 44 female patients with MHO (according to the IDF criteria of the metabolic syndrome, 2005: obese patients with no more than one additional cardiometabolic risk factor) and in 33 women with metabolically unhealthy obesity (MUHO). We also assessed changes of these indices in the patients who reduced their body weight by ≥ 5% at 6 months.Results: At baseline, body mass index (BMI) and the levels of basal insulin, C-reactive protein (CRP), tumor necrosis factor alfa (TNF-α), adiponectin and retinol-binding protein-4 (RBP-4) in the MHO and MUHO groups were comparable. A significant difference between these groups was observed for the HOMA index (3.0 and 4.4, respectively; p < 0.05), alanine aminotransferase (ALT) (23.49 and 37.39 U/l; p = 0.001), interleukin-6 (0.76 and 1.5 pg/ml; p < 0.05), chemerin (322.4 and 369.2 ng/ml; p < 0.05), and the duration of obesity (18 and 22.6 years; p < 0.05). At 6 months, in those MHO patients, who reduced body weight by ≥ 5% of the initial (66%), there was a significant increase of adiponectin by 4.54 ± 0.83 µg/ml (p < 0.05) and a reduction of waist circumference (WC) by -8.6 ± 1 cm (p > 0.05), НОМА index by -1.13 ± 0.42 (p < 0.05), CRP by -1.7 ± 0.4 mg/l (p < 0.05), RBP-4 by 2.9 ± 1.0 ng/ml (p < 0.05), and сhemerin by -46.6 ± 17.0 ng/ml (p < 0.05). In the MHO group, we found a positive correlation between changes in the adiponectin levels and the degree of reduction in body weight (p < 0.01), changes in RBP-4 and WC (p < 0.05), and changes in the levels of interleukin-6 and high-density lipoprotein (p < 0.05).Conclusion: Compared to the complicated obesity, MHO is associated with a shorter disease history, and lower levels of the HOMA index, interleukin-6, and chemerin levels. The body mass decrease in MHO is associated with a decrease in the proinflammatory adipocytokine levels and of the HOMA index that determines the need for treatment of obesity, regardless of its phenotype.

Background: Obesity and metabolic syndrome are considered the risk factors of colorectal adenoma (CRA) and colorectal cancer (CRC). Chemerin is a novel adipocytokine associated with the development of gastric cancer, esophageal cancer, hepatocellular carcinoma, and CRC. However, the relationship between chemerin levels and CRA remains unclear. Objective: This study is aimed at investigating the -association between serum chemerin levels and the development of CRA. Methods: We conducted a total colonoscopy-based cross-sectional case-control study of 80 male patients with CRA and 80 male age-matched control individuals without CRA, according to their endoscopic findings. Serum chemerin concentrations were measured using a sandwich enzyme-linked immunosorbent assay kit, and the OR of CRA was calculated via logistic regression analysis. Results: The mean serum chemerin level of the CRA group was significantly higher than that of the control group (7.9 ± 0.41 vs. 5.16 ± 0.34 ng/mL, p < 0.001). Serum chemerin level was positively correlated to the development of CRA (r = 0.34). Multivariate logistic regression analysis revealed that a high chemerin level was independently associated with the development of CRA (OR 2.82, 95% CI 1.39–5.72). Conclusions: Our findings indicated that increased serum chemerin levels are positively associated with the presence of CRA in men. Chemerin may play an important role in the development of CRA. [ABSTRACT FROM AUTHOR]

BPA, one of the environmental endocrine disruptors, and fructose, reason of liver steatosis which is frequently encountered in the daily diet, contribute to the formation of metabolic syndrome (MetS). This study examines the possible effects of concurrent fructose and BPA administration on MetS and determines the effects of melatonin on this process. In the seven identified groups, a total of forty-two adult male Sprague Dawley rats were treated by following fructose, BPA, and melatonin amounts, separately and together: group 1 (control), group 2 (10% aqueous fructose), group 3 (25 mg/kg BPA), group 4 (10% fructose + 25 mg/kg BPA), group 5 (10% fructose + 20 mg/kg melatonin), group 6 (25 mg/kg BPA + 20 mg/kg melatonin), and group 7 (10% fructose + 25 mg/kg BPA + 20 mg/kg melatonin). At the end of 60 days, histochemical, immunohistochemical, and biochemical procedures were performed on liver tissue. As a result, it was seen that BPA and fructose + BPA induced morphological alteration and inflammation and increased intracellular lipid quantity and amount of collagen and reticular fibers. The percentage of apoptotic liver cells stained by annexin V-FITC/PI was lower in group 7 compared to the group 4 (p < 0,001) and also in group 6 compared to the group 3 (p = 0.014). Both BPA and fructose application caused an increase in lipid peroxidation level due to the increase of oxidative stress. Application of melatonin induced antioxidant enzyme activity and reduced lipid peroxidation level. Our results indicate that fructose and BPA administration triggered the formation of MetS, whereas melatonin healed these variations, although not entirely. [ABSTRACT FROM AUTHOR]

Background/aim: Recent data draw attention to the effect of body composition, insulin resistance, and adipocytokines to acne vulgaris (AV) development. The aim of this study was to assess the association of AV with insulin resistance and adipocytokine levels and to evaluate the effect of isotretinoin on insulin resistance and adipocytokine levels. Materials and methods: In 29 AV patients and 29 healthy volunteers, body mass index (BMI) and body fat mass (BFM), lipid, adiponectin, leptin, resistin, retinol binding protein-4 (RBP4), and insulin levels were measured and insulin resistance was assessed by HOMA-IR index in serum samples taken twice from patients before and after isotretinoin treatment. Results: In AV patients, pretreatment HOMA-IR and adipocytokine levels were not found to correlate with disease severity. With five months of isotretinoin treatment, higher HOMA-IR values were found (P = 0.028). Isotretinoin therapy maintained lower mean resistin levels (P = 0.016), higher mean RBP4 levels (P = 0.040), but not affected the mean adiponectin and leptin levels (P = 0.113, P = 0.125, respectively). Conclusions: All data suggests that five months of isotretinoin therapy in AV patients causes insulin resistance and the increase in insulin resistance is not dependent on age, BMI, BFM, and lipid levels of these patients. [ABSTRACT FROM AUTHOR]

Background: The deep subcutaneous adipose tissue (dSAT) is closely related to the obesity-associated complications similarly to the characteristics of visceral adipose tissue (VAT). However, the association between dSAT and metabolic syndrome (MS) is unclear. The purpose of our study was to evaluate the association of distinct abdominal adipose tissue with the cardiometabolic risk factors and MS. Methods: Abdominal computed tomography (CT) images were obtained in 365 asymptomatic subjects (187 subjects with MS and 178 without MS). The axial images segmented into superficial and deep SAT by manually tracing the fascia superficialis at L4-5 levels. The concentrations of serum inflammatory cytokines and adipokines were also measured. Results: The MS group had significantly lower adiponectin levels but significantly higher levels of resistin, leptin, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), intercellular adhesion molecule (ICAM), monocyte chemotactic protein-1 (MCP-1), and oxLDL than the control group (p < 0.05). All inflammatory cytokines and adipokines were associated with the sum of VAT and dSAT areas (VDAT) (P for trend < 0.05), but no significant correlation was found between inflammatory cytokines and sSAT. dSAT was significantly associated with MS in both men and women (OR 2.371; p < 0.001) whereas the ORs between sSAT and MS were not significant (p = 0.597). The age-adjusted ORs between VDAT and MS (OR of 8.359 in men and 3.183 in women, p < 0.001) were higher than those of VAT (OR of 7.941 in men and 2.570 in women, p < 0.05) and dSAT (OR of 2.954 in men and 1.856 in women, p < 0.05). Conclusions: We demonstrated that dSAT was associated with increased inflammation and oxidative stress, suggesting that dSAT is an important determinant of MS. Therefore, abdominal subcutaneous fat should be considered as two functionally distinct compartments rather than a single entity. [ABSTRACT FROM AUTHOR]

"Less is more" - this is becoming the global quote on event of alarming rise in the prevalence of obesity among all age groups. The perspective of adipose tissue as merely a fat depot has changed in recent times. Focus is now being laid on the metabolic and inflammatory functions of the adipose tissue which is modulated through adipocytokines. Adipocytokines have been found to control insulin sensitivity, inflammatory activity, neuroendocrine activity, cardiovascular function, food and water intake, breeding, and bone metabolism. Few of these adipokines play a role in the positive metabolism promoting good health, while few of them pose adverse effects. Omentin is a recently identified novel adipocytokine and it falls under the category of being a good adipokine. Plasma omentin-1 levels are signifi cantly decreased in patients with obesity, insulin resistance, and diabetes that contribute to the major components of the metabolic syndrome and other disease conditions like atherosclerosis, autoimmune disorders etc and that the review focuses on the comprehensive effects of omentin on all the major systems of the body. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Visfatin, a newly discovered adipocytokine, is thought to play a role in the pathogenesis of metabolic-syndrome-related cancers. The aim of this study was to assess the clinical significance of serum levels and tissue expression of visfatin in relation to endometrial cancer (EC). Methods: A total of 234 EC patients were included in this study. Serum visfatin, metabolic and anthropometric parameters were measured in EC patients and controls. Serum visfatin levels were detected using ELISA. Tissue expression of visfatin was analyzed using immunohistochemistry in tissue microarrays. The correlation between clinicopathological variables and visfatin in EC tissues and the prognostic value of visfatin for overall survival was evaluated. Results: Serum levels of visfatin were significantly higher in EC patients than in controls (P <0.05). In univariate and multivariate logistic regression models, a positive association between EC and serum visfatin, BMI, waist-to-hip ratio, diabetes, and hypertension was evident (P <0.05). Visfatin expression was significantly higher in EC tissue than in normal endometrial tissue (P =0.001). Moreover, serum visfatin levels were significantly positively correlated with tissue expression of visfatin in EC patients (P <0.05). High visfatin expression in EC tissues was significantly associated with advanced FIGO stage (P =0.016) and myometrial invasion ≥1/2 (P =0.023). The overall survival rate of EC patients was significantly higher in the group with negative visfatin expression than with positive visfatin expression (P =0.035). Conclusions: Visfatin is a potential serum biomarker and prognostic factor for EC that may indicate high risk for EC and EC progression. It may also be a novel potential therapeutic target for EC. [Copyright &y& Elsevier]

Highlights: [•] Ellagic acid suppressed specifically resistin secretion in vivo. [•] Ellagic acid improved hepatic steatosis and serum lipid composition in KK-Ay mice. [•] Ellagic acid increased mRNA expressions of ppara and cpt1a in the liver. [•] Our study proposes a preventive against metabolic syndrome by ellagic acid. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the relationship between the adiponectin levels and various characteristics of the metabolic syndrome (MS) in a sample of the Tunisian population. Three hundred and fifty-four individuals were included in this study. Body mass index, blood pressure, HDL-cholesterol, triglycerides, glucose, insulin, and adiponectin concentrations were measured. Insulin resistance was assessed by homeostasis model assessment of insulin resistance (HOMA-IR). MS was identified with the NCEP-ATP III criteria. Subjects with MS showed significantly lower adiponectin levels compared to those without MS. For both genders, the prevalence and the number of MS components increased significantly as the adiponectin concentrations decreased. Subjects with the lowest adiponectin quartile had an increased risk of MS adjusted for age, gender, and HOMA-IR. Our findings suggest that hypoadiponectinemia is strongly associated with the risk of MS independent of insulin resistance. [ABSTRACT FROM AUTHOR]

Background: To investigate the relationship between serum levels of cystatin C and adiponectin in patients with type 2 diabetes. Methods: We examined serum cystatin C and adiponectin levels in 234 patients with type 2 diabetes who visited our hospital. Results: The serum level of cystatin C was positively correlated with age ( P < 0.001), duration of diabetes ( P = 0.013), serum creatinine ( P < 0.001), uric acid ( P < 0.001), and adiponectin (p = 0.001), while it was inversely correlated with estimated glomerular filtration rate ( P < 0.001). Serum adiponectin was significantly higher in patients with high serum cystatin C levels than in those with normal cystatin C levels (8.3 ± 4.7 and 6.2 ± 3.2 μg/mL, respectively; P < 0.001). Adiponectin was also significantly higher in male patients with high cystatin C levels, but not in females. In multiple regression analysis, serum adiponectin was also independently and significantly correlated to age, diastolic blood pressure, high-density lipoprotein cholesterol, triglyceride and serum cystatin C. Conclusions: Serum adiponectin level was correlated with serum cystatin C level on simple and multiple regression analyses in patients with type 2 diabetes. Although circulating adiponectin is increased in advanced kidney disease, it might be biologically inactive due to binding to cystatin C and thus not display an anti-arteriosclerotic effect. [ABSTRACT FROM AUTHOR]

Abstract: Background: To date the role of resistin in colorectal cancer (CRC) is far from being elucidated. The aim of this study was to investigate the association between serum resistin levels and CRC in relation to known risk/protective factors including anthropometric, metabolic, inflammatory parameters as well as lifestyle individual characteristics. Methods: 40 CRC patients and 40 controls were enrolled. Body weight, height, waist circumference and blood pressure were recorded. Fasting plasma glucose, lipids, C-reactive protein (CRP) and resistin levels were measured. Metabolic Syndrome (MS) was defined according to the harmonized definition. Results: Resistin levels were significantly higher in CRC patients than in controls (p=0.028) and gradually increased with tumor stage progression (p=0.042). A high resistin level was statistically significant determinant of CRC after adjusting for age, sex, body mass index and lifestyle parameters (p=0.029). Resistin showed a strong association with CRP levels (p≤0.0001). In stepwise regression analysis CRP remained the only independent predictor of both resistin levels (p=0.001) and CRC risk (p=0.021). Conclusions: These results clarify the nature of the association between resistin and CRC risk suggesting that the proinflammatory state of cancer, rather than the clinical diagnosis of CRC itself or its link with obesity and MS, may govern this association. [Copyright &y& Elsevier]

Abstract: Aims: To determine the effects of food restriction (FR) on the expression of Sirt1 and its down-stream factors related to lipid and glucose metabolism in obese and hypertensive rats (SHRSP/IDmcr-fa), as a model of human metabolic syndrome. Main methods: Male, 10-week-old SHRSP/IDmcr-fa rats were treated with 85% FR for 2weeks. Metabolic parameters, serum adipocytokines and distribution of serum adiponectin multimers were investigated. Sirt1 expression was determined in epididymal adipose tissue, liver and skeletal muscle. We also determined the expression of PPARα, γ and other adipocyte-related genes in epididymal adipose tissue, and glucose transporters (GLUT2 and GLUT4) in the liver and skeletal muscle. Key findings: FR improved the general conditions as well as blood chemistry of SHRSP/IDmcr-fa rats. In the epididymal adipose tissue of the FR rats, Sirt1 expression was enhanced, as was adiponectin, whereas leptin was downregulation, findings that were paralleled by the serum protein levels. Furthermore, the serum ratio of high to total adiponectin was increased in the FR group. The mRNA expression of Sirt1 was upregulated in the adipose tissue in the FR group. Sirt1 mRNA expression was downregulated, while PPARα and GLUT2 expression was enhanced in the liver. No differences were found in terms of Sirt1, PPAR or GLUT4 expression in skeletal muscle. Significance: These results indicate that FR corrects adipokine dysfunction by activating PPARγ via Sirt1 in adipose tissue. Furthermore, glucose and lipid metabolism are activated by upregulation of GLUT2 via the activation of PPARα in the liver. [Copyright &y& Elsevier]

Background: Our previous studies have indicated a close association between visceral fat accumulation and hepatic steatosis in nonalcoholic fatty liver disease (NAFLD). This study investigated whether visceral fat accumulation was related to the pathogenesis and disease progression of nonalcoholic steatohepatitis (NASH)/NAFLD. Methods: First, a total of 550 subjects who underwent a health checkup and measurement of visceral fat accumulation, done with a bioelectrical impedance analyzer (X-SCAN; Owa Medical, Fukuoka, Japan), were included. The relationship between visceral fat accumulation and biochemical parameters was examined. Second, a total of 74 patients with NASH/NAFLD who underwent liver biopsy were reviewed. Visceral fat accumulation was determined by abdominal computed tomography. The association between visceral fat accumulation and the histopathological grade/stage determined by the NAFLD activity score and Brunt's classification was evaluated. Results: There was a significant relationship between visceral fat accumulation and glucose, triglyceride, and alanine aminotransferase (ALT; r = 0.423, P < 0.01). In stepwise regression analysis, visceral fat area (VFA), serum triglyceride level, and serum low-density lipoprotein (LDL)-cholesterol level were selected as predictor variables for serum ALT level, in a continuous manner (serum ALT level = −1.359 + 0.143 × VFA + 0.046 × triglyceride + 0.059 × LDL, R = 0.217, P < 0.001). In patients with NASH, there was no correlation between histological grade and the visceral fat volume. Visceral fat accumulation in patients with stage 3/4 advanced NASH was greater than that in patients with stage 1/2 early NASH ( P < 0.05). Conclusions: These results suggest that visceral fat accumulation plays a role in steatosis and fibrosis in the pathogenesis and prognosis of NAFLD. [ABSTRACT FROM AUTHOR]

Background/Aims: To clarify the impact of visceral obesity on hepatitis C virus (HCV)-infected patients, we examined the relationship between insulin resistance development and visceral fat accumulation. Methods: We analyzed 87 HCV-infected patients with mild fibrosis (stage 1 or 2) in comparison with 125 sex- and age-matched patients with non-alcoholic fatty liver disease (NAFLD). The degree of visceral fat area (VFA; cm2) at the umbilical level was measured by abdominal computed tomography and divided into two grades: no visceral obesity, VFA<100 and visceral obesity, VFA≥100. Insulin resistance was evaluated by homeostasis model assessment of insulin resistance (HOMA-IR) and the quantitative insulin sensitivity check index (QUICKI). Pancreatic β-cell function was evaluated by homeostasis model assessment of β-cell function (HOMA-β). Serum soluble tumour necrosis factor (TNF)-receptors 1 and 2 and adiponectin were measured. Results: Insulin resistance evaluated by HOMA-IR and QUICKI was correlated with visceral fat accumulation, and was higher in HCV patients than in NAFLD patients with visceral obesity. HOMA-β was higher in HCV patients than in NAFLD patients for each VFA grade. Serum-soluble TNF-receptors 1 and 2 were higher in HCV patients than in NAFLD patients with visceral obesity. Conclusions: Hepatitis C virus infection is a risk factor for development of insulin resistance, particularly in patients with visceral obesity. [ABSTRACT FROM AUTHOR]

Objective. Adipocytokines are bioactive substances derived from adipose tissues, especially visceral fat, and play a crucial role in the development of metabolic syndrome. The aims of this study were to estimate serum levels of adipocytokines (adiponectin, resistin and TNF-α) and to examine the associations between adipocytokine levels and metabolic syndrome in menopausal women. Methods. We recruited 28 postmenopausal women with features of metabolic syndrome. For the purpose of comparing adipocytokine levels, 30 postmenopausal women without metabolic syndrome were recruited by matching age and body mass index (BMI). Serum levels of adipocytokines (adiponectin, resistin, TNF-α) were then determined, and any potential correlations between adipocytokine levels and metabolic syndrome were investigated. Results. There were no significant differences in adiponectin or resistin levels in women with metabolic syndrome when compared with the control group. Conversely, TNF-α levels were significantly higher in women with metabolic syndrome. Furthermore, multivariate logistic regression analysis indicated that TNF-α was significantly associated with metabolic syndrome. Conclusion. Our results suggest that, among the adipocytokines (adiponectin, resistin and TNF-α), serum TNF-α levels may serve as a useful biomarker for diagnosing metabolic syndrome in menopausal women. [ABSTRACT FROM AUTHOR]

Abstract: The rapid increase of obese population in the United States has made obesity into epidemic proportion. Obesity is a strong risk factor for metabolic syndrome, type 2 diabetes mellitus, cardiovascular diseases, cancer and other diseases. Compelling evidence has demonstrated that increased adipose tissue mass is not only the consequence of obesity, but also plays a central role in the development of obesity-associated diseases. Recent studies have profoundly changed the concept of adipose tissue from being an energy depot to an active endocrine organ. The development of obesity alters adipocyte-derived hormones or cytokines expression, which provide a link between obesity and impaired insulin sensitivity and metabolic defects in other tissues. This review summarizes the current knowledge on how major adipose-derived hormones or adipocytokines influence insulin sensitivity. [Copyright &y& Elsevier]

In Western culture, excess visceral fat accumulation or obesity has reached epidemic proportions, resulting in metabolic syndrome. However, more than 10 years of research has shown that adipocytes also function as endocrine cells that release various bioactive substances, so called "adipocytokines or adipokines", that play a major role in the regulation of food intake, insulin sensitivity, energy metabolism, and the vascular microenvironment. Adiponectin, an adipocytokine, is considered to improve insulin sensitivity. Recently, monocyte chemoattractant protein (MCP)-1 has been reported to be a novel adipocytokine involved in the development of obesity-associated insulin resistance and atherosclerosis. Nuclear receptors, especially peroxisome proliferator-activated receptor-α (PPARα) and PPARγ are ligand-activated transcription factors that regulate the metabolism of glucose and lipids. PPARγ is strongly expressed in adipocytes and plays a significant role in the transcriptional activation of adipocytokines including adiponectin. PPARα, another PPAR isoform, is involved in the control of lipid metabolism in the liver and skeletal muscle. PPARα activation causes lipid clearance via β-oxidation enhancement. We showed that various dietary terpenoids and other natural ingredients regulate the transcription of PPAR target genes, induces the expression and secretion of adiponectin, and inhibits those of MCP-1 in adipocytes and β-oxidation in liver. These findings indicate that dietary factor acts as an agonist of PPARs and is a valuable medical and food component for the gradual improvement of metabolic syndrome. [ABSTRACT FROM AUTHOR]

Adipocytokines involved in inflammation and the acute phase responders have been found to be increased in the metabolic syndrome (MS). The aim of the study was to compare the 'normal' weight women's fibrinogen, hsCRP, adiponectin, TNF-α, vascular cell adhesion molecule (VCAM) with obese patients with MS, and to evaluate the association between fibrinogen, hsCRP, adiponectin, TNF-αα, VCAM and insulin resistance. The study included 52 obese women who met the criteria for MS defined as in 2001, the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) ATP III and 24 normal women. Serum concentrations of glucose (FBG), triglyceride, total and HDL-Cholesterol were determined by enzymatic procedures, serum insulin was measured by chemiluminescence, plasma levels of adiponectin, TNF-α and VCAM by Elisa, hsCRP by immunoturbimetric assay and fibrinogen by coagulation method. Measurements of insulin resistance were obtained using the homeostasis model assessment. Mean plasma levels of adiponectin, TNF-α, VCAM, fibrinogen and hsCRP were found 6.11±2.39 mg/ml, 3.10±3.30 pg/ml, 14.21±4.00 ng/ml, 375.49±49.67 mg/dl, 0.33±0.10 mg/dl in the obese with MS; 6.20±2.48 mg/ml, 3.01±1.68 pg/ml, 12.63±2.54 ng/ml, 304.06±49.52 mg/dl, 0.30±0.19 mg/dl in the normal women, respectively. Mean fasting insulin level and HOMA-IR were measured 13.80±6.32 mU/ml and 3.69±1.90 mU/ml, respectively in obese with MS. In normal women, fasting insulin level and HOMA-IR were measured 8.30±3.08 mU/ml and 1.49±0.37, respectively. Mean levels of adiponectin were positively correlated with mean TNF-α levels in the obese with MS (r=0.472, p=0.001). VCAM was negatively correlated with TNF-α levels (r=-0.301, p=0.038) in the obese with MS. This study demonstrated that TNF-α showed a positive association with adiponectin and a negative association with VCAM in the obese women with MS. [ABSTRACT FROM AUTHOR]

Aims Metabolic syndrome is characterized by its association with certain cardiovascular disease risk factors. The aim of this study was to investigate the relationships between metabolic syndrome and markers of subclinical atherosclerosis, serum adiponectin and endogenous androgen concentrations in Japanese men with Type 2 diabetes. Methods Using the 2005 International Diabetes Federation (IDF) definition, we assessed the prevalence of the metabolic syndrome in 424 consecutive men with Type 2 diabetes aged 40–75 years in a cross-sectional study. We compared characteristics including ultrasonographic carotid atherosclerosis markers, pulse-wave velocity (PWV), and serum adiponectin, free testosterone, and dehydroepiandrosterone sulphate (DHEA-S) concentrations in diabetic patients with and without the metabolic syndrome. Results The prevalence of the metabolic syndrome in Japanese men with Type 2 diabetes was 46.9%. Men with the metabolic syndrome had higher urinary albumin excretion rate than those without. Carotid intima-media thickness (0.97 ± 0.26 vs. 0.91 ± 0.18 mm), plaque score [3.3 (1.5–8.1) vs. 3.8 (1.3–6.2)], PWV (1818 ± 331 vs. 1749 ± 331 cm/s) and ankle-brachial index (1.10 ± 0.14 vs. 1.08 ± 0.16) did not differ significantly between patients with and without the metabolic syndrome. Similarly, serum adiponectin [3.70 (2.06–6.09) vs. 4.65 (3.09–7.02) µg/ml], free testosterone (36.4 ± 10.7 vs. 34.7 ± 11.1 pmol/l), and DHEA-S concentrations (3.29 ± 1.83 vs. 3.17 ± 1.63 µmol/l) did not differ significantly between groups, Conclusions The metabolic syndrome, as defined by the IDF, is not significantly associated with subclinical atherosclerosis markers, serum adiponectin, or endogenous androgen concentrations in Japanese men with Type 2 diabetes. [ABSTRACT FROM AUTHOR]

Adipose tissue, which classically has been considered as an energy-storing organ, is now viewed as a massive source of bioactive substances such as leptin, tumor necrosis factor (TNF)-α, and adiponectin. Adiponectin was discovered to be the most abundant adipose-specific transcript. Its function had been unclear, but epidemiological and clinical studies have demonstrated that serum levels of adiponectin are inversely associated with body weight, especially abdominal visceral fat accumulation. In addition, adiponectin was inversely related to cardiovascular risk factors, such as insulin resistance, blood pressure, and low-density lipoprotein (LDL) cholesterol and triglyceride levels, and was positively related to high-density lipoprotein (HDL) cholesterol levels. Moreover, low adiponectin concentration is associated with a high incidence of cardiovascular disease (CVD), diabetes, some kinds of cancer, and other various diseases. These associations suggest the clinical significance of adiponectin, and a number of investigations are now being conducted to clarify the biological functions of adiponectin. Recent studies have revealed that adiponectin exhibits antiinflammatory, antiatherogenic, and antidiabetic properties. In addition, adiponectin has been thought to be a key molecule in “metabolic syndrome,” which is an epidemiological target for preventing cardiovascular disease. Various functions of adiponectin may possibly serve to prevent and treat obesity-related diseases and CVD. Furthermore, enhancement of adiponectin secretion or action may become a promising therapeutic target. [ABSTRACT FROM AUTHOR]

Metabolic syndrome is a highly atherogenic state in which hyperglycemia, dyslipidemia and hypertension cluster in one individual. Intra-abdominal visceral fat accumulation plays a key role in the development of these disorders and the occurrence of metabolic syndrome. We have investigated adipocyte functions intensively in the past 10 years and have revealed that these cells act as endocrine cells secreting a variety of bioactive substances, termed adipocytokines. Among adipocytokines, tumor necrosis factor-α, plasminogen activator inhibitor type 1 and heparin-binding epidermal growth factor-like growth factor are produced in adipocytes as well as other organs and may contribute to the development of vascular diseases. Visfatin was identified recently as a visceral-fatspecific protein that might be involved in the development of obesity-related diseases, such as diabetes mellitus and cardiovascular disease. In contrast to these adipocytokines, adiponectin, an adipose tissue-specific, collagen-like protein, has been noted as an important antiatherogenic and antidiabetic protein or as an anti-inflammatory protein. The functions of adipocytokine secretion might be regulated dynamically by nutritional state. Visceral fat accumulation causes dysregulation of adipocyte functions, including oversecretion of tumor necrosis factor-a, plasminogen activator inhibitor type 1, heparinbinding epidermal growth factor-like growth factor and visfatin and hyposecretion of adiponectin simultaneously, which results in the development of a variety of metabolic and circulatory diseases. In this article, the importance of adipocytokines, focusing particularly on adiponectin, is discussed with respect to lifestyle-related diseases, such as diabetes mellitus and cardiovascular disease. [ABSTRACT FROM AUTHOR]

We determined the relationship between abdominal circumference and the concentration of nitric oxide (NO), an endothelial cell product known to play an important role in the regulation of vascular tone and thrombocyte activations. Subjects were 177 men and 339 women aged 40 or over who were free from a history of diabetes or malignancy. Analysis of covariance was applied to examine the gender-specific and smoking-status-specific associations of abdominal fat volume measured as waist circumference, waist-hip ratio, and waist-to-stature ratio, with serum NO level represented by the concentration of NO metabolites (NOx; nitrate plus nitrite). Although men showed no statistical association between abdominal fat accumulation and NOx concentration, abdominal adiposity seemed to inversely affect the serum NOx concentration of never- and current-smoking women. Our results suggest that a reduction in NO bioactivity occurs with abdominal fat accumulation in women. The underlying biological mechanism might involve adipocytokines secreted from visceral fat, but is yet to be elucidated. [ABSTRACT FROM AUTHOR]

In this study, we fed obese model mice black soybean seed coat powder (BSCP) and evaluated the antiobesity effects. As a control, normal yellow soybean seed coat powder (YSCP) was used. C57BL/6J, a high-fat diet-induced obesity model mouse, was fed a high-fat diet containing BSCP or YSCP (20% fat) to induce obesity. The results showed that in the BSCP group, it caused significant suppression of body weight gain and suppression of white adipose tissue weight compared with the YSCP group. Moreover, it significantly decreased serum leptin levels, which correlated with visceral fat mass, and increased antidiabetic adipocytokine and adiponectin levels. Therefore, this suggests the pigmented components contained in BSCP have an antiobesity effect in obese model mice. It is suggested that this material, which can be prepared without extraction with an organic solvent and is suitable for use as a food material, could be a functional food material with a practicable antiobesity effect. [ABSTRACT FROM AUTHOR]