Adiponectin Levels (adiponectin + level)

Distribution by Scientific Domains
Distribution within Medical Sciences

Kinds of Adiponectin Levels

  • plasma adiponectin level
  • serum adiponectin level


  • Selected Abstracts


    Leptin,a predictor of abnormal glucose tolerance and prognosis in patients with myocardial infarction and without previously known Type 2 diabetes

    DIABETIC MEDICINE, Issue 8 2008
    M. Wallander
    Abstract Aims High levels of leptin and low adiponectin are associated with Type 2 diabetes mellitus (T2DM) and cardiovascular (CV) disease. We studied the prognostic implications of leptin and adiponectin in patients with acute myocardial infarction (AMI) without previously known Type 2 DM. Methods One hundred and eighty-one patients were included. Based on an oral glucose tolerance test at hospital discharge (day 4,5), 168 (67% men) had normal or abnormal glucose tolerance (AGT), defined as impaired glucose tolerance or T2DM. Sex- and age-matched healthy persons served as control subjects (n = 185). The associations between fasting serum leptin and adiponectin (day 2) and newly discovered AGT and CV events (CV mortality, non-fatal stroke, reinfarction or severe heart failure) during a median follow-up of 34 months were investigated. Results Compared with control subjects, patients of both genders had significantly higher levels of leptin 2 days after an AMI. These levels were higher than those obtained at hospital discharge and 3 months later. Circulating levels of (ln) leptin 2 days after the AMI predicted AGT at discharge (odds ratio 2.03, P = 0.042). Ln leptin at day 2 was the only biochemical variable that significantly predicted CV events both on univariate [hazard ratio (HR) 1.60, P = 0.018] and on multivariate analysis (HR 1.75, P = 0.045). Adiponectin levels did not differ between patients and control subjects and did not relate to AGT or CV events. Conclusions Elevated circulating levels of leptin on the first morning after an AMI are associated with the presence of AGT at discharge and with a poorer long-term prognosis. [source]


    Low plasma adiponectin concentration is associated with myocardial infarction in young individuals

    JOURNAL OF INTERNAL MEDICINE, Issue 2 2010
    J. Persson
    Abstract., Persson J, Lindberg K, Gustafsson TP, Eriksson P, Paulsson-Berne G, Lundman P. (Danderyd University Hospital; Karolinska Institutet, Novum; Karolinska University Hospital, Karolinska Institutet; Atherosclerosis Research Unit; Karolinska Institutet, Stockholm, Sweden). Low plasma adiponectin concentration is associated with myocardial infarction in young individuals. J Intern Med 2010; 268: 194,205. Objective., The importance of adiponectin in coronary heart disease remains to be elucidated. Therefore, the associations between plasma adiponectin levels and i) myocardial infarction and ii) genetic variation within the adiponectin gene were investigated. Methods., The study included young survivors (age <60 years) of a first myocardial infarction and gender- and age-matched controls (244 pairs). Adiponectin concentrations were analysed by radioimmunoassay. Two polymorphisms, rs266729 and rs1501299, of the adiponectin gene ADIPOQ were genotyped. Results., Adiponectin levels were inversely associated with myocardial infarction [odds ratio (OR) 9.3, 95% confidence interval (CI) 4.7,18.2, for the lowest quartile compared to the highest quartile]. This persisted after adjustment for history of hypertension, HDL cholesterol, smoking and body mass index (BMI) (OR 3.1, 95% CI 1.3,7.6). The rs266729 polymorphism was associated with adiponectin levels. Plasma adiponectin concentrations were lower in individuals with the rare G/G genotype [median 4.3 mg mL,1, interquartile range (IQR) 2.8,6.2] compared to the C/G (median 5.8 mg mL,1, IQR 3.9,8.0; P = 0.035) and C/C genotypes (median 5.5 mg mL,1, IQR 4.0,7.5; P = 0.083). Conclusion., Low plasma adiponectin concentrations are associated with myocardial infarction in individuals below the age of 60, and this remains significant after adjustment for history of hypertension, HDL cholesterol, smoking and BMI. In addition, adiponectin levels differ according to rs266729 genotype. [source]


    Circulating adiponectin reflects severity of liver disease but not insulin sensitivity in liver cirrhosis

    JOURNAL OF INTERNAL MEDICINE, Issue 3 2005
    S. KASER
    Abstract. Background., The adipocytokine adiponectin has been proposed to play important roles in the regulation of energy homeostasis, insulin sensitivity and shows anti-inflammatory properties. Aim., In this study we investigated the role of circulating adiponectin in different chronic liver diseases, its regulation by systemic anti-tumour necrosis factor (TNF)- , treatment and its hepatic metabolism. Patients and methods., Plasma adiponectin levels were determined in 87 patients with liver cirrhosis of different aetiologies, seven patients with alcoholic steatohepatitis undergoing systemic anti-TNF- , treatment, in 11 patients with liver cirrhosis receiving transjugular intrahepatic portosystemic shunt implantation and in 21 healthy controls. Results., Adiponectin levels were significantly higher in all subjects with liver cirrhosis of different aetiologies when compared with healthy controls and increased dependent on Child-Pugh classification. In subjects with alcoholic steatohepatitis, systemic anti-TNF- , treatment caused a significant decrease in circulating adiponectin. Adiponectin concentrations were similar in portal, hepatic and peripheral veins. No correlation between adiponectin levels and insulin resistance was found in any patient group. Conclusions., Our data suggest that circulating adiponectin is increased in liver cirrhosis independent of the aetiology of liver disease. We suggest that high adiponectin levels in chronic liver disease might reflect one of the body's anti-inflammatory mechanisms in chronic liver diseases. [source]


    CB1 Receptor Blockade and its Impact on Cardiometabolic Risk Factors: Overview of the RIO Programme with Rimonabant

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 2008
    A. J. Scheen
    Rimonabant, the first selective CB1 receptor antagonist in clinical use, has been extensively investigated in the Rimonabant in Obesity (RIO) programme, comprising four 1,2 year placebo-controlled randomised clinical trials recruiting more than 6600 overweight/obese patients with or without co-morbidities. Rimonabant 20 mg daily consistently reduced body weight, waist circumference, triglycerides, blood pressure, insulin resistance and C-reactive protein levels, and increased HDL cholesterol concentrations in both non-diabetic and type-2 diabetic overweight/obese patients. Adiponectin levels were increased, an effect that correlated with HDL cholesterol augmentation, while small dense LDL cholesterol levels were decreased in patients receiving rimonabant 20 mg compared with those receiving placebo in RIO Lipids. Furthermore, in RIO Diabetes, a 0.7% reduction in glycated haemoglobin (HbA1c) levels was observed in metformin- or sulphonylurea-treated patients with type-2 diabetes, an effect recently confirmed in the 6-month SERENADE (Study Evaluating Rimonabant Efficacy in drug-NAļve DiabEtic patients) trial in drug-naļve diabetic patients. Almost half of metabolic changes occurred beyond weight loss, in agreement with direct peripheral effects. The positive effects observed after 1 year were maintained after 2 years. Rimonabant was generally well-tolerated, but with a slightly higher incidence of depressed mood disorders, anxiety, nausea and dizziness compared with placebo. In clinical practice, rimonabant has to be prescribed to the right patient, i.e. overweight/obese subjects with cardiometabolic risk factors and with no major depressive illness and/or ongoing antidepressive treatment, in order to both maximise efficacy and minimise safety issues. New trials are supposed to confirm the potential role of rimonabant in patients with abdominal adiposity, atherogenic dyslipidaemia and/or type-2 diabetes, i.e. at high cardiometabolic risk. [source]


    Adiponectin levels among patients with chronic hepatitis B and C infections and in response to IFN-, therapy

    LIVER INTERNATIONAL, Issue 4 2005
    Jin-Ying Lu
    Abstract: Aims: The study was designed to survey the change of adiponectin levels before and after interferon-, (IFN-,) therapy in patients with chronic hepatitis B and C infections. Methods: Twenty-one biopsy-proved patients with chronic hepatitis B (10 cases) and hepatitis C (11 cases) were given IFN-, for a total of 24 weeks. Fasting plasma glucose, insulin and adiponectin levels were obtained before and 12 weeks after completion of IFN-, therapy. Insulin suppression test was conducted before and within 1 week after IFN-, therapy. Results: The change of adiponectin levels differed significantly between responders (eight cases) and non-responders (13 cases) to IFN-, treatment (,4.8±2.2 vs. 0.5±1.0 ,g/ml, P=0.03). After adjusting for age, gender and change in body mass index, the study found the change of adiponectin levels still significantly related to the response to IFN-, (P=0.04). When hepatitis B virus (HBV) and hepatitis C virus (HCV)-infected patients were separately analyzed, the adiponectin levels reported a trend to decrease in HCV responders (11.9±3.2 vs. 10.8±3.0 ,g/ml, P=0.02, n=4) and HBV responders (17.7±4.1 vs. 9.2±1.0 ,g/ml, P=0.10, n=4). In addition, a significant decrease of steady-state plasma glucose in insulin suppression test was noted in responders (13.6±1.8,11.7±1.2 mmol/l, P=0.03), but not in non-responders (12.3±1.1,11.0±1.0 mmol/l, P=0.20), after IFN-, therapy. Conclusions: IFN-, resulted in a decrease of serum adiponectin levels but an improvement of insulin resistance in responders to the treatment. The result contradicts previous concept of the relationship between insulin resistance and adiponectin levels. Whether and how the augmented immune response, which was supposed to result from the disappearance or the profound down-regulation of the virus or viral antigens in responders to IFN-, treatment, contributes to the lowering of adiponectin levels needs to be further investigated. [source]


    Adiponectin levels are high in children with classic congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency

    ACTA PAEDIATRICA, Issue 5 2009
    Thomas MK Völkl
    Abstract Objective: It has been shown that adiponectin serves as an insulin-sensitizing adipokine. Serum concentrations of adiponectin are low in children with obesity, and increase with fat mass loss, indicating that adiponectin can serve as a biomarker. Since the prevalence of overweight and obesity is increased in children with congenital adrenal hyperplasia (CAH), our study aimed to evaluate serum levels of adiponectin in a cohort of CAH children and adolescents, and their associations with clinical parameters such as chronological age (CA), body mass index (BMI), Tanner stage (TS), medication and metabolic control. Patients and methods: We studied 51 patients, aged between 5.6 and 19.6 years (median 11.8; 30 females, 21 males), cross-sectionally. All patients had genetically confirmed CAH and received standard steroid substitution therapy. Adiponectin was measured by an enzyme linked immunoassay. Since BMI SDS of the CAH cohort were significantly higher compared to the reference population, we built matched pairs with healthy Caucasian subjects from a normal representative cohort for sex, Tanner stage, chronologic age and BMI. Results: Adiponectin concentrations were significantly higher in CAH patients (median 11 ,g/L) compared to the matched controls (6.7 ,g/L, p < 0.0001). Correlation analyses in CAH patients revealed a significant inverse relationship between adiponectin and CA, TS, BMI, serum DHEAS and serum testosterone, but no correlation with hydrocortisone and fludrocortisone dosage. Conclusion: Currently, the importance of the elevated adiponectin concentrations in CAH children for risk assessment is not clear. However, our data imply that besides adequate metabolic control of glucocorticoid substitution, a long-term follow-up of other metabolic markers of insulin resistance should be conducted in CAH patients. [source]


    Adiponectin levels in adolescent girls with polycystic ovary syndrome (PCOS)

    CLINICAL ENDOCRINOLOGY, Issue 6 2009
    Orit Pinhas-Hamiel
    Summary Objective, To determine serum adiponectin concentrations in adolescent girls with and without polycystic ovary syndrome (PCOS) and to assess possible correlations of adiponectin levels with insulin and androgen levels. Design, Prospective case,control study. Setting, Endocrine clinics in the community. Patients, Forty-four adolescent girls were grouped as follows: 14 were overweight [body mass index (BMI) standard deviation score >1·645] with PCOS; 16 were lean (BMI SDS <1·036) with PCOS; and 14 were lean (BMI SDS <1·036) without PCOS. Intervention, Blood samples were collected from all girls between 8 and 11 am, after an overnight fast. Main outcome measures, Serum levels of adiponectin, leptin, insulin, Müllerian-inhibiting substance, luteinizing hormone, follicle-stimulating hormone, testosterone, 17-alpha-hydroxyprogesterone, androstendione, dehydroepiandrosterone sulphate (DHEAS) and 17,-oestradiol. Results, Adiponectin concentrations were significantly decreased in obese adolescents with PCOS (10·5 ± 5·5 ,g/ml) compared with that in lean girls with or without PCOS (16·9 ± 8·64 and 18·0 ± 7·4 ,g/ml respectively). Leptin levels were significantly elevated in obese adolescents with PCOS compared with the levels in normal weight adolescents with PCOS, and compared with that in normal weight controls. Insulin levels were markedly higher in obese adolescents with PCOS compared with that in normal weight adolescents (12·3 ± 12·2 vs. 4·5 ± 2·9, P < 0·05), and compared with that in normal weight PCOS adolescents (7·4 ± 4·9); however, this difference was not statistically significant. Insulin levels did not differ between normal weight adolescents with PCOS and normal controls. Adiponectin concentrations correlated inversely with BMI, leptin and insulin. Conclusions, Hypoadiponectinaemia is evident only in obese adolescents with PCOS and therefore does not seem to be involved in the pathogenesis of PCOS in this age group. [source]


    Plasma adiponectin in heart transplant recipients

    CLINICAL TRANSPLANTATION, Issue 1 2009
    Pierre Ambrosi
    Abstract:, Background:, The association between plasma adiponectin and metabolic syndrome may be impaired in heart transplant recipients, since renal failure is frequent among these patients. Thus, we studied the relationship between metabolic syndrome and plasma adiponectin in transplanted heart recipients. Methods:, Ninety-five heart transplant recipients were prospectively included 8.3 ± 5.6 yr after transplantation in this cross-sectional study. All patients had physical examination, echocardiography or routine biennial coronary angiography, and laboratory measurements. Results:, Metabolic syndrome was found in 31% of these patients. Plasma adiponectin was significantly lower in patients with metabolic syndrome (12.5 ± 8.3 ,g/mL) than in patients without (16.7 ± 9.4 ,g/mL, p = 0.03). Adiponectin levels were usually in the normal or high range (< 4 ,g/mL in only two patients). Low creatinine clearance was associated with higher plasma adiponectin (R=,0.26, p = 0.01). Plasma adiponectin was not significantly different between the 28 patients with angiographic evidence of graft vasculopathy (13.9 ± 9.5 ,g/mL) and the 67 patients without (16.1 ± 9.1 ,g/mL, p = 0.3). Conclusions:, Contrasting with a high frequency of metabolic syndrome in these patients, adiponectin levels were usually in the normal or high range, probably as a consequence of renal failure. This suggests that adiponectin is not a major determinant for insulin resistance among these patients. [source]


    Adiponectin changes in HCV-Genotype 4: relation to liver histology and response to treatment

    JOURNAL OF VIRAL HEPATITIS, Issue 10 2009
    M. Derbala
    Summary., Recently, attention has been focussed on adiponectin and its changes in different types of chronic liver disease. Its relation to hepatic fibrosis and insulin resistance in post-hepatitis liver disease is not clear. The aim of this study was to clarify the adiponectin changes in genotype 4 hepatitis C virus (HCV)-infected patient in relation to liver histology and insulin resistance, and its usefulness as a predictor of hepatic fibrosis and response to treatment. Total adiponectin and its high molecular weight (HMW) form as well as insulin levels were studied in 92 chronic HCV, genotype 4 and 66 healthy control volunteers. Neither total adiponectin (r = 0.101, P = 0.220) nor HMW adiponectin (r = 0.081, P = 0.328) correlated with viral load. Total and not HMW adiponectin was significantly correlated with hepatic fibrosis and inflammation (r = 0.267, P = 0.002, r = 0.278, P < 0.001, respectively). In addition, total adiponectin (r = 0.224, P = 0.002) and HMW adiponectin (r = 0.266, P < 0.0006) significantly correlated with insulin resistance. As fibrosis did not correlate with insulin resistance (r = 0.081, P = 0.204), the correlation between total adiponectin and fibrosis was not mediated by insulin resistance. Multivariable regression analysis, (including pretreatment cases and controls) revealed that total adiponectin was significantly associated with gender, being lower among male subjects (X2 = 13.04, P = 0.0001). The multivariable regression model supported the lack of association between insulin resistance and total adiponectin levels (X2 = 1.88, P = 0.171), while non cirrhotics had significantly lower total adiponectin levels than cirrhotics (X2 = 10.90, P = 0.004) and lower level of inflammation significantly lower total adiponectin levels than more severe inflammation (X2 = 8.95, P = 0.003). Total or HMW adiponectin did not yield receiver operating characteristic (ROC) curves with area under the curve (AUC) >75%, thus the cutoff points have poor sensitivity/specificity as predictors of fibrosis. However, as a predictor of end-of-treatment response, the ROC curve of adiponectin index gave yield an AUC = 81.4%. We can conclude that total adiponectin level, in HCV genotype 4 patients, increases with progression of hepatic fibrosis regardless of insulin resistance. Its high molecular form does not have such correlation. The adiponectin changes are not related to viral load, insulin resistance or other demographic data suggesting that this change is histologically related. In spite of this, no adiponectin cutoff level had reasonable sensitivity/specificity for predicting hepatic fibrosis stage, while this may be used as a predictor for antiviral response possibly reflecting improvement in hepatic inflammation post treatment. [source]


    Effects of castration on insulin levels and glucose tolerance in the mouse differ from those in man

    THE PROSTATE, Issue 15 2010
    Takamitsu Inoue
    Abstract BACKGROUND Plasma insulin concentration is increased in prostate cancer patients during androgen deprivation therapy (ADT) and hyperinsulinemia has been associated with aggressive prostate cancer behavior. To investigate the possible role of castration-induced hyperinsulinemia as a mechanism that may attenuate the beneficial effects of ADT in patients with prostate cancer, a murine model would be useful. We therefore investigated long-term metabolic effects of castration in several mouse models. METHODS We studied the long-term influence of castration on energy intake, body weight, glucose tolerance, plasma-insulin, plasma insulin-like growth factor-1 (IGF-1), plasma adiponectin, and plasma leptin in C57BL/6, Swiss nu/nu, and CB17 scid mice receiving various diets. In each case, mice were randomized to have either bilateral orchiectomy or a sham operation. RESULTS Energy intake, body weight, blood glucose levels in glucose tolerance test, plasma insulin, plasma IGF-1, and plasma leptin level in all had a trend to be decreased in castrated as compared to sham operated mice. Plasma adiponectin level was increased in the castrated mice. CONCLUSIONS The effects of castration on glucose, insulin, and related markers in several mouse models studied does not coincide with clinical observations; further studies in this area will require clinical research and/or the use of alternate models such as the dog. Prostate 70: 1628,1635, 2010. © 2010 Wiley-Liss, Inc. [source]


    Serum adiponectin and resistin levels in major depressive disorder

    ACTA PSYCHIATRICA SCANDINAVICA, Issue 3 2010
    S. M. Lehto
    Lehto SM, Huotari A, Niskanen L, Tolmunen T, Koivumaa-Honkanen H, Honkalampi K, Ruotsalainen H, Herzig K-H, Viinamäki H, Hintikka J. Serum adiponectin and resistin levels in major depressive disorder. Objective:, To examine the role of the adipose-tissue-derived low-grade inflammation markers adiponectin and resistin in major depressive disorder (MDD) in a population-based sample. Method:, Serum levels of adiponectin and resistin were measured from 70 DSM-IV MDD subjects and 70 healthy controls. Depression severity was assessed with the 29-item Hamilton Depression Rating Scale. Results:, The MDD group had lowered serum adiponectin levels. Regression modelling with adjustments for age, gender, overweight, several socioeconomic and lifestyle factors, coronary heart disease and metabolic syndrome showed that each 5.0 ,g/ml decrease in serum adiponectin increased the likelihood of MDD by approximately 20% (P = 0.01). The resistin levels correlated with atypical (P = 0.02), but not with typical depressive symptoms (P = 0.12). Conclusion:, Our findings suggest that the lowered adiponectin levels in MDD are depression-specific and not explained by conventional low adiponectin-related factors such as such as coronary heart disease and metabolic disorders. [source]


    The effect of thiazolidinediones on adiponectin serum level: a meta-analysis

    DIABETES OBESITY & METABOLISM, Issue 5 2008
    N. Riera-Guardia
    Background and aims:, Adiponectin is a hormone mainly produced by white adipose tissue. Decreased levels of adiponectin are linked with visceral obesity, insulin resistance states, and cardiovascular diseases. Recently, several studies have pointed out an increase in adiponectin serum levels in subjects undergoing treatment with thiazolidinediones (TZD). The aim of this study is to systematically review the current state of evidence of the effect of TZD on adiponectin serum level with special attention to avoid publication bias. Materials and methods:, An extensive literature search was performed. Meta Analysis Version 2.0 computer program was used to calculate statistical differences in means and 95% confidence interval (CI). Publication bias was assessed using different statistical approaches. Results:, In the meta-analysis including 19 studies the overall standardized mean difference was 0.94 (95% CI, 0.81,1.06) which means that subjects treated with TZDs on average had means of adiponectin concentration that were about 1 standard deviation higher than the comparison groups even after controlling for possible biases. Conclusions:, The results obtained agree with a moderate increase of serum adiponectin. The results clearly reveal an increase of endogenous serum adiponectin levels by intake of TZDs and may point to a potential new option to manage obesity-related diseases. [source]


    Lack of association between serum adiponectin levels and the Pro12Ala polymorphism in Asian Indians

    DIABETIC MEDICINE, Issue 4 2007
    V. Radha
    Abstract Aims, The aim of the study was to investigate the association of serum adiponectin levels with the Pro12Ala polymorphism of the peroxisome proliferator activated receptor-, (PPARG) gene in Asian Indians. Methods, We selected 400 diabetic subjects, 200 with the Pro12Pro genotype (100 male and 100 female) and 200 with the Pro12Ala genotype (100 male and 100 female) and 400 age- and sex-matched normal glucose tolerance subjects with similar genotype profiles from the Chennai Urban Rural Epidemiology Study. Fasting serum adiponection levels were measured using radioimmunoassay. The Pro12Ala polymorphism was genotyped by PCR,restriction fragment length polymorphism using BstUI. Results, All clinical and biochemical parameters were similar in the subjects with the Pro12Pro and Pro12Ala genotypes. There was no significant difference in serum adiponectin values between subjects with the Pro12Pro and Pro12Ala genotypes (males 5.4 vs. 5.8 µg/ml, P = 0.546; females 6.9 vs. 7.2 µg/ml, P = 0.748). Adiponectin values did not differ among these two genotypes even when categorized based on their diabetes status (normal glucose tolerance Pro12Pro 7.9 vs. Pro12Ala 7.7 µg/ml, P = 0.994; diabetes Pro12Pro 4.7 vs. Pro12Ala 5.4 µg/ml, P = 0.622). Conclusion, The Pro12Ala polymorphism of the PPARG gene is not associated with serum adiponectin levels in Asian Indians. [source]


    Effect of bariatric surgery on circulating chemerin levels

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2010
    C. Ress
    Eur J Clin Invest 2010; 40 (3): 277,280 Abstract Background, Subclinical inflammation in obesity is critical for development of several obesity-associated disorders. We set out to investigate the effect of pronounced weight loss on circulating chemerin levels, a chemoattractant protein that also influences adipose cell function by paracrine and autocrine mechanisms. Material and methods, Thirty-two obese patients undergoing bariatric surgery were tested before and on an average of 18 months after gastric banding or gastric bypass surgery. Results, Pronounced weight loss after bariatric surgery was accompanied by improvements in parameters of lipid and glucose metabolism and increased adiponectin levels. Chemoattractant chemerin significantly decreased from 175·91 ± 24·50 to 145·53 ± 26·44 ng mL,1 after bariatric surgery (P , 0·01). Concomitantly, hs-CRP as a marker of subclinical inflammation was significantly reduced after weight reduction (P , 0·01). Conclusions, We hypothesize that weight-loss induced reduction in circulating chemerin might in conjunction with other factors be associated with diminished recruitment of macrophages in adipose tissue and reduction of subclinical inflammation, which again could partly explain beneficial long-term effects of weight reduction in obese subjects. [source]


    The metabolic syndrome: metabolic changes with vascular consequences

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2007
    A. M. J. Wassink
    Abstract Despite criticism regarding its clinical relevance, the concept of the metabolic syndrome improves our understanding of both the pathophysiology of insulin resistance and its associated metabolic changes and vascular consequences. Free fatty acids (FFA) and tumour necrosis factor-alpha (TNF-,) play prominent roles in the development of insulin resistance by impairing the intracellular insulin signalling transduction pathway. Obesity is an independent risk factor for cardiovascular disease and strongly related to insulin resistance. In case of obesity, FFAs and TNF-, are produced in abundance by adipocytes, whereas the production of adiponectin, an anti-inflammatory adipokine, is reduced. This imbalanced production of pro- and anti-inflammatory adipokines, as observed in adipocyte dysfunction, is thought to be the driving force behind insulin resistance. The role of several recently discovered adipokines such as resistin, visfatin and retinol-binding protein (RBP)-4 in the pathogenesis of insulin resistance is increasingly understood. Insulin resistance induces several metabolic changes, including hyperglycaemia, dyslipidaemia and hypertension, all leading to increased cardiovascular risk. In addition, the dysfunctional adipocyte, reflected largely by low adiponectin levels and a high TNF-, concentration, directly influences the vascular endothelium, causing endothelial dysfunction and atherosclerosis. Adipocyte dysfunction could therefore be regarded as the common antecedent of both insulin resistance and atherosclerosis and functions as the link between obesity and cardiovascular disease. Targeting the dysfunctional adipocyte may reduce the risk for both cardiovascular disease and the development of type 2 diabetes. Although lifestyle intervention remains the cornerstone of therapy in improving insulin sensitivity and its associated metabolic changes, medical treatment might prove to be important as well. [source]


    Inhibition of adiponectin production by homocysteine: A potential mechanism for alcoholic liver disease,

    HEPATOLOGY, Issue 3 2008
    Zhenyuan Song
    Although recent evidence suggests that down-regulation of production of the adipocyte hormone adiponectin has pathophysiological consequences for the development of alcoholic liver disease (ALD), the underlying mechanisms are elusive. Abnormal hepatic methionine-homocysteine metabolism induced by prolonged alcohol exposure has been reported both in clinical and experimental studies of ALD. Here, we conducted both in vivo and in vitro experiments to examine the effects of prolonged alcohol exposure on homocysteine levels in adipose tissue, its potential involvement in regulating adiponectin production, and the consequences for ALD. Chronic alcohol exposure decreased the circulating adiponectin concentration and adiponectin messenger RNA (mRNA) and protein levels in epididymal fat pads. Alcohol feeding induced modest hyperhomocysteinemia and increased homocysteine levels in the epididymal fat pad, which was associated with decreased mRNA levels of cystationine ,-synthase. Betaine supplementation (1.5%, wt/vol) in the alcohol-fed mice reduced homocysteine accumulation in adipose tissue and improved adiponectin levels. Moreover, exogenous homocysteine administration reduced gene expression, protein levels, and secretion of adiponectin in primary adipocytes. Furthermore, rats fed a high-methionine diet (2%, wt/wt) were hyperhomocysteinemic and had decreased adiponectin levels in both plasma and adipose tissue, which was associated with suppressed AMP-activated protein kinase activation in the liver. Mechanistic studies revealed that both inactivation of the extracellular signal regulated kinase 1/2 pathway and induction of endoplasmic reticulum stress response, specifically C/EBP homologous protein expression, may contribute to the inhibitory effect exerted by homocysteine. Conclusion: Chronic alcohol feeding caused abnormal accumulation of homocysteine in adipocytes, which contributes to decreased adiponectin production in ALD. (HEPATOLOGY 2008.) [source]


    Low adiponectin levels are associated with renal cell carcinoma: A case-control study

    INTERNATIONAL JOURNAL OF CANCER, Issue 7 2007
    Themistoklis N. Spyridopoulos
    Abstract Adiponectin is a novel endogenous insulin sensitizer, secreted by mature adipocytes. Circulating levels of adiponectin are inversely associated with obesity and insulin resistance. Because obesity is a risk factor for renal cell carcinoma (RCC), we hypothesized that low adiponectin levels are associated with RCC. To evaluate this hypothesis, we conducted a case- control study of 70 patients with histologically confirmed RCC and 280 healthy controls matched by gender, age and county of residence. Study subjects were interviewed and blood samples were collected during a 32-month period in Athens, Greece. Serum adiponectin levels were statistically, significantly and inversely associated with RCC when compared with controls (OR = 0.76, p = 0.05) and this association remained practically unchanged after controlling for BMI; the introduction of waist to hip ratio along with adiponectin in the multiple logistic regression analysis model rendered the association between adiponectin and RCC risk insignificant, indicating that altered levels of adiponectin may mediate the effect of central or intra-abdominal obesity on RCC. Prospective studies as well as studies exploring underlying mechanisms are needed to fully explore the role of adiponectin in predicting future risk of RCC in humans. © 2006 Wiley-Liss, Inc. [source]


    Improved myocardial perfusion in chronic diabetic mice by the up-regulation of pLKB1 and AMPK signaling

    JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 5 2010
    Claudia Kusmic
    Abstract Previous studies related impaired myocardial microcirculation in diabetes to oxidative stress and endothelial dysfunction. Thus, this study was aimed to determine the effect of up-regulating pAMPK-pAKT signaling on coronary microvascular reactivity in the isolated heart of diabetic mice. We measured coronary resistance in wild-type and streptozotocin (STZ)-treated mice, during perfusion pressure changes. Glucose, insulin, and adiponectin levels in plasma and superoxide formation, NOx levels and heme oxygenase (HO) activity in myocardial tissue were determined. In addition, the expression of HO-1, 3-nitrotyrosine, pLKB1, pAMPK, pAKT, and peNOS proteins in control and diabetic hearts were measured. Coronary response to changes in perfusion pressure diverged from control in a time-dependent manner following STZ administration. The responses observed at 28 weeks of diabetes (the maximum time examined) were mimicked by L-NAME administration to control animals and were associated with a decrease in serum adiponectin and myocardial pLKB1, pAMPK, pAKT, and pGSK-3 expression. Cobalt protoporphyrin treatment to induce HO-1 expression reversed the microvascular reactivity seen in diabetes towards that of controls. Up-regulation of HO-1 was associated with an increase in adiponectin, pLKB1, pAKT, pAMPK, pGSK-3, and peNOS levels and a decrease in myocardial superoxide and 3-nitrotyrosine levels. In the present study we describe the time course of microvascular functional changes during the development of diabetes and the existence of a unique relationship between the levels of serum adiponectin, pLKB1, pAKT, and pAMPK activation in diabetic hearts. The restoration of microvascular function suggests a new therapeutic approach to even advanced cardiac microvascular derangement in diabetes. J. Cell. Biochem. 109: 1033,1044, 2010. © 2010 Wiley-Liss, Inc. [source]


    Adiponectin Is a Link Among Inflammation, Insulin Resistance, and High-Density Lipoprotein Cholesterol But Is Not Associated With Paraoxonase Activity in Premenopausal Women

    JOURNAL OF CLINICAL HYPERTENSION, Issue 11 2009
    Pinar Cetinalp-Demircan PhD
    The aim of this study was to evaluate whether insulin sensitivity, inflammatory response, and plasma lipid profile are associated with circulating adiponectin levels in nondiabetic healthy women. The authors also assessed whether adiponectin has any effect on high-density lipoprotein cholesterol,linked paraoxonase 1 (PON-1) activity and on the susceptibility of low-density lipoproteins to oxidation. Plasma adiponectin was measured in 91 nondiabetic premenopausal women, and the patients were then divided into quartiles. Circulating adiponectin was found to be associated with body mass index (r=.55, P<.001). After adjustment for body mass index, adiponectin showed an inverse correlation with the homeostasis model assessment of insulin resistance (HOMA-IR) (r=,.41, P<.001) and a positive correlation with high-density lipoprotein cholesterol (r=.43, P<.001). In linear regression analysis, HOMA-IR, tumor necrosis factor ,, and high-density lipoprotein cholesterol levels were found to be independently associated with adiponectin. However, high-density lipoprotein cholesterol,linked PON-1 activity and the susceptibility of low-density lipoproteins to in vitro oxidation did not seem to be related to plasma adiponectin concentrations. [source]


    Low plasma adiponectin concentration is associated with myocardial infarction in young individuals

    JOURNAL OF INTERNAL MEDICINE, Issue 2 2010
    J. Persson
    Abstract., Persson J, Lindberg K, Gustafsson TP, Eriksson P, Paulsson-Berne G, Lundman P. (Danderyd University Hospital; Karolinska Institutet, Novum; Karolinska University Hospital, Karolinska Institutet; Atherosclerosis Research Unit; Karolinska Institutet, Stockholm, Sweden). Low plasma adiponectin concentration is associated with myocardial infarction in young individuals. J Intern Med 2010; 268: 194,205. Objective., The importance of adiponectin in coronary heart disease remains to be elucidated. Therefore, the associations between plasma adiponectin levels and i) myocardial infarction and ii) genetic variation within the adiponectin gene were investigated. Methods., The study included young survivors (age <60 years) of a first myocardial infarction and gender- and age-matched controls (244 pairs). Adiponectin concentrations were analysed by radioimmunoassay. Two polymorphisms, rs266729 and rs1501299, of the adiponectin gene ADIPOQ were genotyped. Results., Adiponectin levels were inversely associated with myocardial infarction [odds ratio (OR) 9.3, 95% confidence interval (CI) 4.7,18.2, for the lowest quartile compared to the highest quartile]. This persisted after adjustment for history of hypertension, HDL cholesterol, smoking and body mass index (BMI) (OR 3.1, 95% CI 1.3,7.6). The rs266729 polymorphism was associated with adiponectin levels. Plasma adiponectin concentrations were lower in individuals with the rare G/G genotype [median 4.3 mg mL,1, interquartile range (IQR) 2.8,6.2] compared to the C/G (median 5.8 mg mL,1, IQR 3.9,8.0; P = 0.035) and C/C genotypes (median 5.5 mg mL,1, IQR 4.0,7.5; P = 0.083). Conclusion., Low plasma adiponectin concentrations are associated with myocardial infarction in individuals below the age of 60, and this remains significant after adjustment for history of hypertension, HDL cholesterol, smoking and BMI. In addition, adiponectin levels differ according to rs266729 genotype. [source]


    Low plasma adiponectin is associated with coronary artery disease but not with hypertension in high-risk nondiabetic patients

    JOURNAL OF INTERNAL MEDICINE, Issue 5 2006
    M. CESARI
    Abstract. Objective., To investigate the association of plasma adiponectin levels with coronary artery disease (CAD), arterial hypertension (HT), and insulin resistance (IR) in nondiabetic Caucasian patients. Design., We measured plasma adiponectin levels, IR (HOMA index), and the CAD atherosclerotic burden (angiography-based modified Duke Index score) in 400 nondiabetic patients undergoing coronary angiography. HT was diagnosed by the European Society of Hypertension/European Society of Cardiology (ESH/ESC) guidelines or if patients were on antihypertensive treatment. Results., Coronary artery disease was found in 62% of the patients and ruled out in the rest (non-CAD group). Plasma adiponectin levels were inversely related to the CAD score (, = ,0.12, P = 0.029) and predicted the coronary atherosclerotic burden independent of other cardiovascular risk factors. However, they were similar in NT and HT and showed no correlation with blood pressure values. In non-CAD, but not in CAD patients, they were lower in patients with than without IR (8.3 ± 1.2 vs. 11.3 ± 1.3, respectively; P = 0.007). Conclusions., In nondiabetic high-risk Caucasian patients plasma adiponectin levels are inversely related to CAD severity and IR; however, they are not strongly related to blood pressure values. [source]


    Circulating adiponectin reflects severity of liver disease but not insulin sensitivity in liver cirrhosis

    JOURNAL OF INTERNAL MEDICINE, Issue 3 2005
    S. KASER
    Abstract. Background., The adipocytokine adiponectin has been proposed to play important roles in the regulation of energy homeostasis, insulin sensitivity and shows anti-inflammatory properties. Aim., In this study we investigated the role of circulating adiponectin in different chronic liver diseases, its regulation by systemic anti-tumour necrosis factor (TNF)- , treatment and its hepatic metabolism. Patients and methods., Plasma adiponectin levels were determined in 87 patients with liver cirrhosis of different aetiologies, seven patients with alcoholic steatohepatitis undergoing systemic anti-TNF- , treatment, in 11 patients with liver cirrhosis receiving transjugular intrahepatic portosystemic shunt implantation and in 21 healthy controls. Results., Adiponectin levels were significantly higher in all subjects with liver cirrhosis of different aetiologies when compared with healthy controls and increased dependent on Child-Pugh classification. In subjects with alcoholic steatohepatitis, systemic anti-TNF- , treatment caused a significant decrease in circulating adiponectin. Adiponectin concentrations were similar in portal, hepatic and peripheral veins. No correlation between adiponectin levels and insulin resistance was found in any patient group. Conclusions., Our data suggest that circulating adiponectin is increased in liver cirrhosis independent of the aetiology of liver disease. We suggest that high adiponectin levels in chronic liver disease might reflect one of the body's anti-inflammatory mechanisms in chronic liver diseases. [source]


    Relationship of adiponectin and resistin levels in umbilical and maternal serum with fetal macrosomia

    JOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 3 2010
    Jing Wang
    Abstract Aim:, Adiponectin and resistin are novel hormones secreted by human adipocytes and mononuclear cells, which have been postulated to play roles in the regulation of energy metabolism during pregnancy. However, correlations between adiponectin and resistin levels in umbilical and maternal serum and fetal macrosomia remain poorly understood. The purpose of this study was to clarify the relationship of adiponectin and resistin levels in umbilical and maternal serum with fetal macrosomia. Methods:, Serum adiponectin and resistin levels were prospectively measured by enzyme immunoassay in 70 mothers and their 70 neonates. The study group included 30 neonates with macrosomia and the control group included 40 neonates that were appropriate for gestational age. The correlations of cord serum adiponectin and resistin with maternal serum adiponectin and resistin, birth weight, body mass index (BMI), and placental weight were analyzed. Results:, Serum adiponectin and resistin levels were significantly decreased in macrosomic mothers compared with those in control women. The levels of adiponectin and resistin were diminished in macrosomic babies in comparison with control newborns. Umbilical serum adiponectin levels were inversely correlated with birth weight, newborn BMI, and placental weight, but not with maternal serum adiponectin levels. Umbilical serum resistin levels had a positive correlation with maternal serum resistin and a negative correlation with birth weight, newborn BMI, and placental weight. In addition, maternal serum resistin levels were inversely correlated with newborn birth weight. Conclusion:, It is suggested that adiponectin and resistin play important roles in controlling body weight and may be related to the occurrence of fetal macrosomia. [source]


    Adiponectin changes in HCV-Genotype 4: relation to liver histology and response to treatment

    JOURNAL OF VIRAL HEPATITIS, Issue 10 2009
    M. Derbala
    Summary., Recently, attention has been focussed on adiponectin and its changes in different types of chronic liver disease. Its relation to hepatic fibrosis and insulin resistance in post-hepatitis liver disease is not clear. The aim of this study was to clarify the adiponectin changes in genotype 4 hepatitis C virus (HCV)-infected patient in relation to liver histology and insulin resistance, and its usefulness as a predictor of hepatic fibrosis and response to treatment. Total adiponectin and its high molecular weight (HMW) form as well as insulin levels were studied in 92 chronic HCV, genotype 4 and 66 healthy control volunteers. Neither total adiponectin (r = 0.101, P = 0.220) nor HMW adiponectin (r = 0.081, P = 0.328) correlated with viral load. Total and not HMW adiponectin was significantly correlated with hepatic fibrosis and inflammation (r = 0.267, P = 0.002, r = 0.278, P < 0.001, respectively). In addition, total adiponectin (r = 0.224, P = 0.002) and HMW adiponectin (r = 0.266, P < 0.0006) significantly correlated with insulin resistance. As fibrosis did not correlate with insulin resistance (r = 0.081, P = 0.204), the correlation between total adiponectin and fibrosis was not mediated by insulin resistance. Multivariable regression analysis, (including pretreatment cases and controls) revealed that total adiponectin was significantly associated with gender, being lower among male subjects (X2 = 13.04, P = 0.0001). The multivariable regression model supported the lack of association between insulin resistance and total adiponectin levels (X2 = 1.88, P = 0.171), while non cirrhotics had significantly lower total adiponectin levels than cirrhotics (X2 = 10.90, P = 0.004) and lower level of inflammation significantly lower total adiponectin levels than more severe inflammation (X2 = 8.95, P = 0.003). Total or HMW adiponectin did not yield receiver operating characteristic (ROC) curves with area under the curve (AUC) >75%, thus the cutoff points have poor sensitivity/specificity as predictors of fibrosis. However, as a predictor of end-of-treatment response, the ROC curve of adiponectin index gave yield an AUC = 81.4%. We can conclude that total adiponectin level, in HCV genotype 4 patients, increases with progression of hepatic fibrosis regardless of insulin resistance. Its high molecular form does not have such correlation. The adiponectin changes are not related to viral load, insulin resistance or other demographic data suggesting that this change is histologically related. In spite of this, no adiponectin cutoff level had reasonable sensitivity/specificity for predicting hepatic fibrosis stage, while this may be used as a predictor for antiviral response possibly reflecting improvement in hepatic inflammation post treatment. [source]


    Adiponectin levels among patients with chronic hepatitis B and C infections and in response to IFN-, therapy

    LIVER INTERNATIONAL, Issue 4 2005
    Jin-Ying Lu
    Abstract: Aims: The study was designed to survey the change of adiponectin levels before and after interferon-, (IFN-,) therapy in patients with chronic hepatitis B and C infections. Methods: Twenty-one biopsy-proved patients with chronic hepatitis B (10 cases) and hepatitis C (11 cases) were given IFN-, for a total of 24 weeks. Fasting plasma glucose, insulin and adiponectin levels were obtained before and 12 weeks after completion of IFN-, therapy. Insulin suppression test was conducted before and within 1 week after IFN-, therapy. Results: The change of adiponectin levels differed significantly between responders (eight cases) and non-responders (13 cases) to IFN-, treatment (,4.8±2.2 vs. 0.5±1.0 ,g/ml, P=0.03). After adjusting for age, gender and change in body mass index, the study found the change of adiponectin levels still significantly related to the response to IFN-, (P=0.04). When hepatitis B virus (HBV) and hepatitis C virus (HCV)-infected patients were separately analyzed, the adiponectin levels reported a trend to decrease in HCV responders (11.9±3.2 vs. 10.8±3.0 ,g/ml, P=0.02, n=4) and HBV responders (17.7±4.1 vs. 9.2±1.0 ,g/ml, P=0.10, n=4). In addition, a significant decrease of steady-state plasma glucose in insulin suppression test was noted in responders (13.6±1.8,11.7±1.2 mmol/l, P=0.03), but not in non-responders (12.3±1.1,11.0±1.0 mmol/l, P=0.20), after IFN-, therapy. Conclusions: IFN-, resulted in a decrease of serum adiponectin levels but an improvement of insulin resistance in responders to the treatment. The result contradicts previous concept of the relationship between insulin resistance and adiponectin levels. Whether and how the augmented immune response, which was supposed to result from the disappearance or the profound down-regulation of the virus or viral antigens in responders to IFN-, treatment, contributes to the lowering of adiponectin levels needs to be further investigated. [source]


    Increased arterial stiffness in children and adolescents with type 1 diabetes: no association between arterial stiffness and serum levels of adiponectin

    PEDIATRIC DIABETES, Issue 1 2010
    Angela Galler
    Galler A, Heitmann A, Siekmeyer W, Gelbrich G, Kapellen T, Kratzsch J, Kiess W. Increased arterial stiffness in children and adolescents with type 1 diabetes: no association between arterial stiffness and serum levels of adiponectin. Objective: Type 1 diabetes is associated with an increased risk of atherosclerosis. Adiponectin serum levels correlate inversely with cardiovascular disease in adults. The aim of this study was to examine associations between arterial stiffness indices and serum adiponectin concentrations in children and adolescents with type 1 diabetes and to study the impact of metabolic control. Subjects and methods: We evaluated arterial stiffness, distensibility, and compliance in 93 children and adolescents with type 1 diabetes and correlated the data with clinical parameters and HbA1c levels. The control group comprised 85 matched healthy children. Serum levels of adiponectin in children with diabetes were measured by enzyme-linked immunoassay and correlated with arterial stiffness indices. Results: Arterial stiffness was significantly increased in children and adolescents with type 1 diabetes (aged 13.0 ± 3.8 yr) compared with matched healthy children (p = 0.03). Arterial stiffness was elevated in males with type 1 diabetes compared with females (p = 0.023). Arterial distensibility was significantly lower in children with diabetes compared with healthy controls (p = 0.025). Arterial stiffness, distensibility, and compliance did not correlate with diabetes duration, level of HbA1c, or serum cholesterol. Adiponectin concentrations in children and adolescents with diabetes were significantly elevated compared with normal values based on gender, age, and body mass index. We found no significant associations between arterial stiffness indices and adiponectin levels in children with type 1 diabetes. Conclusions: Children and adolescents with type 1 diabetes had increased arterial stiffness and reduced arterial distensibility and arterial compliance. However, no associations between arterial functional alterations and adiponectin concentrations were seen. [source]


    Short communication: A longitudinal study of serum adiponectin during normal pregnancy

    BJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 1 2006
    Jens Fuglsang
    Adiponectin is secreted from adipose tissue. Serum adiponectin levels are inversely correlated with body mass index (BMI) and also insulin resistance, independent of the BMI. A role for adiponectin in the development of insulin resistance has been implied in pregnancy. However, no studies have been performed to describe the individual longitudinal course of adiponectin in normal pregnancies. Therefore, we measured serum adiponectin during and after normal pregnancy in 11 healthy women. Serum levels peaked in midpregnancy and the lowest levels were seen in late pregnancy. An inverse association with maternal BMI was observed. [source]


    Adiponectin, ghrelin, and leptin in cancer cachexia in breast and colon cancer patients

    CANCER, Issue 4 2006
    Ido Wolf M.D.
    Abstract BACKGROUND The hormone ghrelin and the adipocytokines leptin and adiponectin participate in body weight regulation. In response to weight loss, ghrelin and adiponectin levels increase and leptin decreases. Cancer cachexia is a complex metabolic state, characterized by loss of muscle mass and adipose tissue together with anorexia. The authors hypothesized that responses of these hormones may be attenuated in cancer cachexia. METHODS Fasting plasma ghrelin, adiponectin, and leptin levels, as well as weight loss, were determined in 40 cancer patients: 18 of them suffered from cancer-induced cachexia, and 22 served as a comparison group. Hormone levels were measured before administration of cancer therapy. RESULTS A similar distribution of age, gender, and diagnosis was observed in both study groups, but the cachectic patients had higher rates of metastatic disease and lower albumin levels. No significant correlation was observed between plasma adiponectin levels and weight loss. Mean plasma ghrelin levels were higher among cachectic compared with noncachectic patients. Notably, the association between ghrelin levels and weight loss was only modest, and in a third of the cachectic patients, ghrelin levels were equal to or lower than those in the noncachectic group. Plasma leptin levels showed gender-dependent associations, and significantly lower levels were found among cachectic women but not among cachectic men. CONCLUSIONS Results suggested a gender-dependent attenuation of expected physiologic responses to weight loss among cancer cachexia patients. Thus, impaired response of adiponectin, ghrelin, and leptin may play a role in the pathogenesis of cancer cachexia syndrome. Cancer 2006. © 2006 American Cancer Society. [source]


    Pharmacological and Clinical Studies with Temocapril, an Angiotensin Converting Enzyme Inhibitor that is Excreted in the Bile

    CARDIOVASCULAR THERAPEUTICS, Issue 3 2004
    Kenichi Yasunari
    ABSTRACT Temocapril is an angiotensin converting enzyme inhibitor (ACEI), a prodrug with a thiazepine ring. Its active form, temocaprilat, is slightly more potent than enalaprilat in inhibiting ACE isolated from rabbit lung. The inhibitory potency of temocaprilat on isolated rat aorta is 3 times that of enalaprilat. Temocapril is excreted in the bile and urine and can be used in patients with renal insufficiency. It reduces blood pressure without causing any significant change in heart rate or cardiac output. Temocapril has been reported to improve endothelial dysfunction in vitro by suppressing increased oxidative stress. In vivo it improves reactive hyperemia in patients with essential hypertension. It has been reported to prevent coronary vascular remodeling in vivo by suppressing local ACE and increased oxidative stress. In humans temocapril has been found to improve insulin resistance partly by increasing adiponectin levels. Cardiac remodeling was improved by temocapril not only in experiment animals but also in humans. It improves renal function and decreases urinary albumin excretion in diabetics as well as in hypertensive patients. Temocapril is currently marketed only in Japan. Considering its beneficial effects and unique pharmaco-kinetics, temocapril, is likely to be introduced in other countries as well. [source]


    Circulating adiponectin levels during human endotoxaemia

    CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 1 2003
    P. KELLER
    SUMMARY Adiponectin, an adipocytokine secreted by fat tissue, may prevent development of diabetes type II, as high adiponectin levels are linked with insulin sensitivity. In contrast, tumour necrosis factor (TNF)- ,, which is also produced by fat tissue, leads to insulin resistance and furthermore inhibits adiponectin mRNA production and secretion of the protein. However, adiponectin also negatively regulates TNF- , levels. Therefore, we set out to test whether an infusion of endotoxin would influence circulating adiponectin levels in healthy human subjects. Twenty-three healthy human subjects were injected with endotoxin (2 ng/kg body weight); eight of these subjects were also injected with saline and served as controls. Plasma levels of adiponectin, TNF- , and interleukin-6 were measured at 0, 1·5, 2, 4, 8 and 24 h. TNF- , and interleukin-6 levels peaked at 1·5 h and 2 h, respectively. Control subjects injected with saline showed a decrease in adiponectin plasma levels with time (P < 0·05) presumably owing to the effect of fasting or physical inactivity. However, there was no change in adiponectin plasma levels in endotoxin injected subjects, thus the effect of fasting was opposed. In conclusion, circulating adiponectin levels are reduced during a resting and fasting state, an effect reversed by endotoxin injection. [source]