Changes In Adiponectin Levels Research Articles

Plasma Adiponectin, clinical factors, and patient outcomes during the acute respiratory distress syndrome.

ObjectiveAdiponectin (APN) is an anti-inflammatory hormone derived from adipose tissue that attenuates acute lung injury in rodents. In this study, we investigated the association between circulating APN and outcomes among patients with acute respiratory distress syndrome (ARDS).MethodsWe performed a retrospective cohort study using data and plasma samples from participants in the multicenter ARDS Network Fluid and Catheter Treatment Trial.ResultsPlasma APN concentrations were measured in 816 (81.6%) trial participants at baseline and in 568 (56.8%) subjects at both baseline and day 7 after enrollment. Clinical factors associated with baseline APN levels in multivariable-adjusted models included sex, body mass index, past medical history of cirrhosis, and central venous pressure (model R2 = 9.7%). We did not observe an association between baseline APN and either severity of illness (APACHE III) or extent of lung injury (Lung Injury Score). Among patients who received right heart catheterization (n = 384), baseline APN was inversely related to mean pulmonary artery pressure (β = −0.015, R2 1.5%, p = 0.02); however, this association did not persist in multivariable models (β = −0.009, R2 0.5%, p = 0.20). Neither baseline APN levels [HR per quartile1.04 (95% CI 0.91–1.18), p = 0.61], nor change in APN level from baseline to day 7 [HR 1.04 (95% CI 0.89–1.23), p = 0.62)] were associated with 60 day mortality in Cox proportional hazards regression models. However, subgroup analysis identified an association between APN and mortality among patients who developed ARDS from extra-pulmonary etiologies [HR per quartile 1.31 (95% CI 1.08–1.57)]. APN levels did not correlate with mortality among patients developing ARDS in association with direct pulmonary injury [HR 0.96 (95% CI 0.83–1.13)], pinteraction = 0.016.ConclusionsPlasma APN levels did not correlate with disease severity or mortality in a large cohort of patients with ARDS. However, higher APN levels were associated with increased mortality among patients developing ARDS from extra-pulmonary etiologies.

Adiponectin induces breast cancer cell migration and growth factor expression.

Adiponectin, the hormone produced and secreted by adipocytes, has been shown to promote migration of the epithelial cells and angiogenesis in these cells. We sought to determine if adiponectin could induce the cellular migration and growth factor expression in breast cancer cells grown in vitro. The breast cancer cell lines MDA-MB-436 and MFM-223 (estrogen-independent) were treated with adiponectin for different time periods. Supernatants of the cell cultures were obtained by centrifugation and were assayed for growth factor expression by the enzyme-linked immunosorbent assay (ELISA). Becton-Dickinson-Falcon Transwell systems were used to assay adiponectin-induced migration. Adiponectin significantly induced the expression of various growth factors, including vascular endothelial growth factor, transforming growth factor-β1, and basic fibroblast growth factor in MDA-MB-436 and MFM-223 cells. Adiponectin also enhanced the migration of breast cancer cells which were inhibited about 50-70 % by the inhibitors of mitogen-activated protein kinase and phosphatidylinositol 3-kinase (PI3K). Adiponectin treatment of the cancer cell induced an increased expression of different growth factors and migration of the cells. These effects are likely to contribute to the progression of breast cancer, implying that change in adiponectin levels associated with obesity may be considered as a high risk factor in breast cancer patients.

Changes in adiponectin level and fat distribution in patients with type 2 diabetes

The aim of this study was to assess the impact of standard hypoglycaemic treatment strategies on adiponectin levels and fat distribution in patients with newly diagnosed type 2 diabetes mellitus (T2DM). This was a prospective observational study of 50 women with newly diagnosed T2DM, aged 64·6±7·9years and treated for 12months with lifestyle modification alone (n=24) or in combination with metformin (n=26), according to current standards of diabetic care and clinical practice guidelines. None of the patients required insulin therapy during the entire study period. Total (BF), abdominal (android) and hip (gynoid) fat were measured by dual-energy X-ray absorptiometry at the baseline and after 12months of treatment. Total adiponectin, glycated haemoglobin (HbA1c) and fasting glucose were measured in 3-month intervals. Baseline adiponectin level was low (9·37±2·81μg/mL). Lifestyle modifications and metformin produced comparable changes in adiponectin levels, which were not associated with changes in BF, HbA1c, glucose and regional fat depots. Baseline adiponectin was inversely correlated with triglycerides (R=-0·441; P=0·0007) and the android/gynoid ratio (R=-0·272; P=0·042). Treatment with metformin was associated with a significant weight reduction (P=0·033), which resulted from a decrease in BF% (P=0·044) but was not associated with changes in android and gynoid depots. In postmenopausal women with newly diagnosed T2DM, lifestyle modifications alone or combined with metformin produced comparable changes in adiponectin levels. Weight reduction in patients treated with metformin was associated with significant decrease in %BF but not in regional fat depots.

Head-to-head comparison of fibrates versus statins for elevation of circulating adiponectin concentrations: a systematic review and meta-analysis

BackgroundElevation of adiponectin levels is a potential therapeutic tool against cardiovascular and metabolic diseases. Clinical evidence suggests differences between fibrates and statins in improving circulating concentrations of adiponectin. AimTo compare the efficacy of fibrates vs. statins on circulating concentrations of adiponectin by meta-analysis of randomized head-to-head trials. MethodsA systematic literature search of Medline was conducted to identify randomized head-to-head comparative trials investigating the efficacy of fibrates vs. statins on circulating levels of adiponectin. Inverse variance-weighted mean differences (WMDs) and 95% confidence intervals (CIs) were calculated for net changes in adiponectin concentrations using a random-effects model. Random-effects meta-regression was performed to assess the effect of putative moderators on adiponectin levels. ResultsSix trials with a total of 326 subjects (166 in the fibrate and 160 in the statin group) met the eligibility criteria and were selected for this meta-analysis. The estimated effect size for fibrate versus statin therapy was 0.42μg/mL (95% CI: −0.34–1.17). This effect size was robust in the leave-one-out sensitivity analysis and not sensitive to any single study. Meta-regression indicated a borderline significant association between duration of treatment and the effect of fibrates vs. statins on adiponectin concentrations (slope: −0.20; 95% CI: −0.41–0.01; p=0.06). However, baseline body mass index, glucose and lipid levels did not predict the effect of fibrate vs. statin therapy on circulating adiponectin concentrations (p>0.05). ConclusionsMonotherapy with either fibrates or statins has comparable effects on circulating concentrations of adiponectin. Thus, differential effects of statins and fibrates on the occurrence of cardiovascular events may not be attributed to the corresponding changes in adiponectin levels.

Effects of Habitual T'ai Chi Exercise on Adiponectin, Glucose Homeostasis, Lipid Profile, and Atherosclerotic Burden in Individuals with Cardiovascular Risk Factors

A single bout of t'ai chi (TC) exercise was previously found to be associated with a significant increase in post-exercise adiponectin levels in individuals with cardiovascular risk factors. The objective of this study was to examine the long-term effects of 24-month habitual TC exercise on adiponectin levels, glucose homeostasis, lipid profile, and atherosclerotic burden in individuals with cardiovascular risk factors. This was a prospective observational study. The study was conducted at a regional hospital in south Taiwan. Participants of a TC exercise program held by the clinics of cardiology and cardiovascular surgery for individuals with cardiovascular diseases were recruited to the TC group. Individuals who did not join the program were recruited as controls. All study subjects had at least one cardiovascular risk factor. Ninety-minute session of Yang's style TC at least once a week. Measurements on adiponectin, glucose homeostasis, lipid profile, and atherosclerotic burden were made at three time points-baseline, 12 months, and 24 months. Two-way repeated-measures general linear model was used to assess the changes over the study period between the TC and control groups. Thirty-seven patients in both the TC and control groups completed the study. The TC group showed a greater increase in natural logarithmic transformed (Ln) adiponectin values than the control group over the study period (interaction effect p=0.009). Glucose homeostasis, lipid profile, risk of atherosclerosis, and atherosclerotic burden did not showed significant changes with TC compared with the controls over the 24-month period. The results of the present study indicate that for individuals with at least one cardiovascular risk factor, engaging in habitual TC exercise could lead to favorable changes in levels of adiponectin. The association between habitual TC and cardiovascular events and diabetic complications will require further investigations.

Adiponectin in mice with altered GH action: links to insulin sensitivity and longevity?

Adiponectin is positively correlated with longevity and negatively correlated with many obesity-related diseases. While there are several circulating forms of adiponectin, the high-molecular-weight (HMW) version has been suggested to have the predominant bioactivity. Adiponectin gene expression and cognate serum protein levels are of particular interest in mice with altered GH signaling as these mice exhibit extremes in obesity that are positively associated with insulin sensitivity and lifespan as opposed to the typical negative association of these factors. While a few studies have reported total adiponectin levels in young adult mice with altered GH signaling, much remains unresolved, including changes in adiponectin levels with advancing age, proportion of total adiponectin in the HMW form, adipose depot of origin, and differential effects of GH vs IGF1. Therefore, the purpose of this study was to address these issues using assorted mouse lines with altered GH signaling. Our results show that adiponectin is generally negatively associated with GH activity, regardless of age. Further, the amount of HMW adiponectin is consistently linked with the level of total adiponectin and not necessarily with previously reported lifespan or insulin sensitivity of these mice. Interestingly, circulating adiponectin levels correlated strongly with inguinal fat mass, implying that the effects of GH on adiponectin are depot specific. Interestingly, rbGH, but not IGF1, decreased circulating total and HMW adiponectin levels. Taken together, these results fill important gaps in the literature related to GH and adiponectin and question the frequently reported associations of total and HMW adiponectin with insulin sensitivity and longevity.

Serum adiponectin concentration in dogs — absence of diurnal variation and lack of effect of feeding and methylprednisolone administration

The aim of the study was to determine the magnitude of diurnal variability of serum adiponectin in healthy beagle dogs, and the possible roles of feeding and glucocorticoids on adiponectin concentrations. For this, adiponectin was measured at 8:00, 10:00, 12:00, 16:00, 20:00, 24:00 and at 4:00 h in 4 beagle dogs that were fasted on the day of the experiment and in 4 dogs that were fed as usual at 9:00 h. Diurnal variability in serum adiponectin concentrations was negligible in both the fed and the fasted dogs. To study the possible effect of glucocorticoids on adiponectin, beagle dogs (n = 14) were assigned to one of three experimental groups. Dogs of the control group were injected with 0.1 ml/kg 0.9% NaCl subcutaneously, while dogs of Groups 1 and 2 were injected with 1 mg/kg and 5 mg/kg of methylprednisolone, respectively, and adiponectin was measured at 8:00, 10:00, 12:00, 16:00 and 20:00 h. Average serum adiponectin levels were not significantly different before and after methylprednisolone exposure at different time-points in the two treated groups. In conclusion, no evidence of postprandial changes in adiponectin level or effects of single-dose glucocorticoid administration on adiponectin were observed in the present study.

P 25: Effect of metformin on arterial properties, adiponectin, leptin and glucose homeostasis in patients with nonalcoholic fatty liver disease

Insulin resistance (IR) is the major driving force behind development and progression of atherosclerosis in patients with nonalcoholic fatty liver disease (NAFLD). Therefore, correction of IR is a relevant therapeutic target. We performed the current trial to evaluate whether 12- month metformin therapy improves vascular stiffness in patients with NAFLD and to assess if this improvement is associated with change in glucose control, insulin resistance or circulating adiponectin. In randomized, placebo controlled study, 63 patients with NAFLD were assigned to one of two groups: Group 1 received daily metformin; Group 2 received placebo. Central aortic augmentation index (AI) was performed using SphygmoCor (version 7.1, AtCor Medical, Sydney, Australia) at baseline, at 4-and 12-month treatment period. Metabolic parameters, insulin resistance markers and serum adiponectin levels were determined. In placebo group: AI did not improve during the treatment period. Liver function and adiponectin levels did not change during the study. In multiple linear regression analysis, the independent predictors of arterial stiffness improvement were metformin treatment and increase in circulating adiponectin levels. Among metformin treated patients: AI decreased significantly during the study. ALP and ALT decreased during initial 4-month treatment period, however raised to the pretreatment levels after 12 months. Serum adiponectin level tended to increase during treatment period with metformin. Metformin treatment was associated with significant decrease in AI during one year treatment in NAFLD patients. These beneficial vascular effects was associated with exposure to metformin per se as well as change in adiponectin levels suggesting that metformin may mediate its vascular effects via glycemic controlindependent mechanisms.

Fat, fire and muscle – The role of adiponectin in pulmonary vascular inflammation and remodeling

Pulmonary hypertension is a life-threatening condition that results from a heterogeneous group of diseases, many of which demonstrate characteristic pathologic changes of pulmonary vascular inflammation and remodeling. Recent clinical studies indicate obesity to be a risk factor for the development of pulmonary hypertension; however, the mechanisms leading to this association are unknown. Adipocytes secrete multiple bioactive mediators that can influence inflammation and tissue remodeling, suggesting that adipose tissue may directly influence the pathogenesis of pulmonary hypertension. One of these mediators is adiponectin, a protein with a wide range of metabolic, anti-inflammatory, and anti-proliferative activities. Paradoxically, adiponectin is present in high concentration in the serum of lean healthy individuals, but decreases in obesity. Studies suggest that relative adiponectin-deficiency may contribute to the development of inflammatory diseases in obesity, and recent animal studies implicate adiponectin in the pathogenesis of pulmonary hypertension. Most notably, experimental studies show that adiponectin can reduce lung vascular remodeling in response to inflammation and hypoxia. Moreover, mice deficient in adiponectin develop a spontaneous lung vascular phenotype characterized by age-dependent increases in peri-vascular inflammatory cells and elevated pulmonary artery pressures. Emerging evidence indicates adiponectin's effects are mediated through anti-inflammatory and anti-proliferative actions on cells in the lung. This review aims to synthesize the existing data related to adiponectin's effects on the pulmonary vasculature and to discuss how changes in adiponectin levels might contribute to the development of pulmonary hypertension.

Low-fat dairy, but not whole-/high-fat dairy, consumption is related with higher serum adiponectin levels in apparently healthy adults

Although previous studies suggested that higher low-fat dairy consumption lower the risk of type 2 diabetes, the mediating factors are not well understood. Higher baseline adiponectin levels are related with a lower risk of type 2 diabetes. This study evaluated whether low-fat dairy is related with adiponectin in apparently healthy adults. We investigated a cross-sectional (n = 938) and one-year longitudinal (n = 759) relationship between low-fat and whole-/high-fat dairy (both including cow's milk and yogurt) and adiponectin. Dairy consumption was assessed with a validated food frequency questionnaire. Serum adiponectin was measured by using a specific sandwich enzyme-linked immunosorbent assay. In the cross-sectional analysis, the geometric means (95 % confidence intervals [95 % CIs]) of log-transformed adiponectin related with the low-fat dairy categories were 7.27 (6.80-7.77) for the lowest category, 7.67 (7.09-8.31) for the middle category, and 8.40 (7.73-9.13) for the highest category (p < 0.001) after adjustment for potential confounders (including all lifestyle factors). In the longitudinal analysis, repeated-measures ANCOVA adjusted for confounding factors showed a significant time-by-categories (categories of low-fat dairy) interaction in the change of adiponectin. In contrast, no significant relationship was found between the whole-/high-fat dairy categories and adiponectin. This study has shown that higher consumption of low-fat dairy, but not of whole-/high-fat dairy, is related with higher levels of adiponectin and with the change of adiponectin level at the one-year follow-up. These results suggest that the consumption of low-fat dairy may have a beneficial effect on serum adiponectin levels.

Effect of Endoplasmic Reticulum Stress on Inflammation and Adiponectin Regulation in Human Adipocytes

The endoplasmic reticulum (ER) of adipocytes plays a major role in the assembly and secretion of adipokines. The levels of serum adiponectin, secreted by adipocytes, are decreased in insulin resistance, diabetes, and obesity. The role of ER stress in downregulating adiponectin levels has been demonstrated in mouse models of obesity. Studies examining human adipose tissue have indicated that there is an increase in the ER stress transcript HSPA5 with increased body mass index (BMI). However, it is not established whether ER stress results in changes in adiponectin levels or multimerization in human adipocytes. We examined whether the induction of ER stress using tunicamycin, thapsigargin, or palmitate alters the messenger RNA (mRNA) and protein expression of adiponectin and the mRNA expression of chaperones ERP44 and ERO1 in adult-derived human adipocyte stem (ADHAS) cells. ER stress was measured using key indicators of ER stress-HSPA5, ERN1, CHOP, and GADD34, as well as changes in eIF2α phosphorylation. Because ER stress is suggested to be the proximal cause of inflammation in adipocytes, we further examined the change in inflammatory status by quantitating the change in Iκβ-α protein following the induction of ER stress. Our studies indicate that: (1) ER stress markers were increased to a higher degree using tunicamycin or thapsigargin compared to palmitate; (2) ER stress significantly decreased adiponectin mRNA in response to tunicamycin and thapsigargin, but palmitate did not decrease adiponectin mRNA levels. In all three instances, the induction of ER stress was accompanied by a decrease in adiponectin protein as well as adiponectin multimerization. All three inducers of ER stress increased tumor necrosis factor-α (TNF-α) mRNA and decreased Iκβ-α protein in adipocytes. The data suggest that ER stress modifies adiponectin secretion and induces inflammation in ADHAS cells.

Waist Circumference as a Predictor of Adiponectin Levels in Peritoneal Dialysis Patients: A 12-Month Follow-up Study

This prospective study, conducted at the dialysis unit of the Nephrology Division, Federal University of Sao Paulo-Oswaldo Ramos Foundation, Brazil, aimed to evaluate whether waist circumference (WC) can predict adiponectin levels in patients undergoing peritoneal dialysis (PD). Among 115 patients on PD at a single dialysis center who were evaluated at 6 and 12 months, 57% were men, 31% had diabetes, mean age was 52.8 ± 16.1 years, body mass index was 25 ± 4.3 kg/m(2), and dialysis vintage was 13 months (range: 5 - 33 months). We measured WC at the umbilicus level. Adiponectin was determined by an enzyme-linked immunosorbent assay. At baseline, WC was inversely associated with adiponectin (r = -0.48, p < 0.01). After adjustment for sex, age, diabetes, peritoneal clearance, and residual renal function, WC was an independent determinant of serum adiponectin (β = -0.52; 95% confidence interval: -0.73 to -0.31; p < 0.001). In the prospective analysis, after adjustment for confounders, changes in WC predicted changes in adiponectin. For each unit increase in WC, adiponectin declined by 0.39 mg/L (p < 0.001). This study demonstrates that WC is associated with adiponectin and, more importantly, that this simple marker of central adiposity was able to predict changes in adiponectin levels over time.

Relation between augmentation index and adiponectin during one-year metformin treatment for nonalcoholic steatohepatosis: effects beyond glucose lowering?

BackgroundInsulin resistance (IR) is the major driving force behind development and progression of atherosclerosis in patients with nonalcoholic fatty liver disease (NAFLD). Therefore, correction of IR is a relevant therapeutic target.We performed the current trial to evaluate whether 12- month metformin therapy improves vascular stiffness in patients with NAFLD and to assess if this improvement is associated with change in glucose control, insulin resistance or circulating adiponectin.MethodsIn randomized, placebo controlled study, 63 patients with NAFLD were assigned to one of two groups: Group 1 received daily metformin; Group 2 received placebo. Central aortic augmentation index (AI) was performed using SphygmoCor (version 7.1, AtCor Medical, Sydney, Australia) at baseline, at 4-and 12-month treatment period. Metabolic parameters, insulin resistance markers and serum adiponectin levels were determined.ResultsIn placebo group: AI did not improve during the treatment period. Liver function and adiponectin levels did not change during the study.In multiple linear regression analysis, the independent predictors of arterial stiffness improvement were metformin treatment and increase in circulating adiponectin levels.Among metformin treated patients: AI decreased significantly during the study. ALP and ALT decreased during initial 4-month treatment period, however raised to the pretreatment levels after 12 months. Serum adiponectin level tended to increase during treatment period with metformin.ConclusionsMetformin treatment was associated with significant decrease in AI during one year treatment in NAFLD patients. These beneficial vascular effects was associated with exposure to metformin per se as well as change in adiponectin levels suggesting that metformin may mediate its vascular effects via glicemic control-independent mechanisms.Trial registryno: NCT01084486

Differential metabolic effects of rosuvastatin and pravastatin in hypercholesterolemic patients

BackgroundRosuvastatin and pravastatin have differential hydrophilicity and potency to inhibit hydroxymethylglutaryl-CoA reductase that may be relevant to changes in adiponectin levels, insulin resistance, and the rate of new onset diabetes in large clinical studies. Therefore, we hypothesized that rosuvastatin and pravastatin may have differential metabolic effects in hypercholesterolemic patients. MethodsThis was a randomized, single-blind, placebo-controlled, parallel study. Age, gender, and body mass index were matched. Fifty-four patients were given placebo, rosuvastatin 10mg, or pravastatin 40mg, respectively once daily for 2months. ResultsWhen compared with pravastatin therapy, rosuvastatin therapy significantly reduced total, LDL cholesterol, and apolipoprotein B levels (P<0.05 by post-hoc comparison), but comparably improved flow-mediated dilation after 2months. Interestingly, rosuvastatin therapy significantly increased fasting insulin (mean % changes; 28%, P=0.005). and HbA1c (1%, P=0.038) while decreasing plasma adiponectin levels (9%, P=0.010) and insulin sensitivity (assessed by QUICKI; 2%, P=0.007) when compared with baseline. By contrast, pravastatin therapy significantly decreased fasting insulin (8%, P=0.042), and HbA1c levels (1%, P=0.019) while increasing plasma adiponectin levels (36%, P=0.006) and insulin sensitivity (3%, P=0.005) when compared with baseline. Moreover, these differential effects were evident when outcomes of rosuvastatin and pravastatin therapy were directly compared (P=0.002 for insulin levels by ANOVA on Ranks, P=0.003 for adiponectin, P=0.003 for QUICKI, and P=0.010 for HbA1c by ANOVA). ConclusionsWhile significantly reducing lipoprotein profiles, rosuvastatin therapy had unwanted metabolic effects in hypercholesterolemic patients when compared with pravastatin therapy, that may be clinically relevant in patients prone to metabolic diseases.

Pioglitazone-Mediated Changes in Lipoprotein Particle Composition Are Predicted by Changes in Adiponectin Level in Type 2 Diabetes

In animal and observational studies, adiponectin is associated with lipoprotein risk factors for cardiovascular disease. We analyzed data from a randomized clinical trial to evaluate the relationship between changes in adiponectin to changes in lipoprotein risk factors after an intervention that alters adiponectin levels. Adiponectin levels were measured at baseline and follow-up, as were lipoprotein risk factors for cardiovascular disease, at academic medical centers and ambulatory care centers. Participants included 361 men and women with type 2 diabetes. Intervention included randomization to treatment with glimepiride or pioglitazone for 72 wk. The relationship of treatment-related differences in adiponectin level to treatment-related differences in lipoprotein cardiovascular risk factors at 72 wk was evaluated. Pioglitazone led to an increase in adiponectin compared with glimepiride. Compared with baseline, pioglitazone treatment at 72 wk led to an increase in low-density lipoprotein (LDL) and high-density lipoprotein (HDL) particle size and a decrease in very-low-density lipoprotein (VLDL) particle size and LDL particle number. Glimepiride treatment more modestly decreased LDL particle number and increased LDL particle size. At 72 wk, there were significant treatment group differences for HDL, LDL, and VLDL particle size, and triglyceride and HDL cholesterol level. The increase in adiponectin predicted treatment-related improvement for triglyceride and HDL cholesterol level and LDL and HDL particle size. Increased adiponectin contributed to treatment-related benefit in lipoprotein cardiovascular disease risk factors in obese diabetic subjects treated with pioglitazone. These results provide support for a model that mechanistically links changes in adiponectin level to changes in lipoprotein composition in humans.

Impact of Combination Therapy with Amlodipine and Atorvastatin on Plasma Adiponectin Levels in Hypertensive Patients with Coronary Artery Disease: Combination Therapy and Adiponectin

Background: In many countries, combination therapy with amlodipine and atorvastatin is indicated for the treatment of patients with hypertension and hypercholesterolemia. The aim of this study was to investigate the impact of this combination therapy on plasma adiponectin levels. Hypothesis: Combination therapy with amlodipine and atorvastatin would increase plasma adiponectin levels. Methods: A total of 25 patients with coronary artery disease and concomitant hypertension and hypercholesterolemia were evaluated. The combination of amlodipine and atorvastatin in 8 different dosage strengths were flexibly titrated over a period of 14 weeks. Lipid profile and plasma adiponectin were measured. Brachial flow-mediated dilation (FMD) was determined by vascular ultrasound. Results: As compared with baseline, combination therapy with amlodipine and atorvastatin significantly reduced systolic and diastolic blood pressure, total cholesterol, and low-density lipoprotein cholesterol (all P < 0.05). Furthermore, there were significant increases in adiponectin levels (mean [95% confidence interval (CI)], 12.1 [10.7-13.7] vs 8.1 [6.5-10.0] μg/mL; P < 0.001) and brachial FMD (4.4 ± 0.6% vs 5.6 ± 0.5%; P = 0.046) over 14 weeks of treatment. The change in adiponectin levels correlated significantly with the changes in diastolic blood pressure (r = −0.49; P = 0.014) and FMD (r = 0.55; P = 0.007). Conclusion: The results of this study indicate that along with its antihypertensive and cholesterol-lowering effects, combination therapy with amlodipine and atorvastatin appears to increase plasma adiponectin levels and improve endothelial function.

Interdisciplinary therapy improves biomarkers profile and lung function in asthmatic obese adolescents

The simultaneous rise in the prevalence of asthma and obesity in the world, have demonstrated the importance of the development of treatment strategies. The purpose of this study was to evaluate the short- and long-term results of interdisciplinary therapy on inflammatory biomarkers and lung function in asthmatics obese adolescents. Seventy-six post-pubertal obese adolescents were recruited, including 50 non-asthmatics [body mass index (BMI), 36 ± 5 kg/m(2) ) and 26 asthmatics (BMI, 39 ± 4 kg/m(2) ). Body composition was measured by plethysmography, and visceral fat was analyzed by ultrasound. Serum levels of adiponectin, leptin, and C-reactive protein (CRP) were analyzed. Asthma and lung function were evaluated according to the American Thoracic Society criteria. Patients were submitted to 1-year weight loss interdisciplinary intervention consisting of medical, nutritional, exercise, and psychological therapy. After interdisciplinary intervention, the lung function and pro/anti-inflammatory adipokines improved significantly in both groups. Most importantly, there was an increase in adiponectin [4 (1.86-12.9) to 5.1 (2.48-16)], a reduction in CRP [2,073 (385-9,174) to 1,538 (205-7,083)] and leptin concentrations [59 (29-69) to 33 (9-49)] in the asthmatics patients. Furthermore, it was observed a reduction in asthma severity after treatment. In addition, Δ adiponectin was an independent factor to improve lung function after therapy in both groups. Interdisciplinary therapy resulted in beneficial changes in inflammatory biomarkers profile and lung function in asthmatic and non-asthmatic obese adolescents. Additionally, for the first time we showed that change in adiponectin level was an independent predictor to improve lung function in Brazilian obese adolescents.

Randomized controlled trial for an effect of catechin-enriched green tea consumption on adiponectin and cardiovascular disease risk factors

BackgroundPrevious observational studies have indicated that green tea (GT) consumption is associated with reduced mortality from cerebral infarction but not with mortality from cerebral hemorrhage. Therefore, we hypothesized that GT exerts a direct antiatherosclerotic effect without any effect on hypertension. To investigate this hypothesis, we focused on adiponectin that seems to be among the several key players in atherosclerosis.ObjectiveThe objective of this randomized controlled trial (RCT) was to assess whether the consumption of catechin-enriched GT affects serum adiponectin levels and cardiovascular disease (CVD) risk factors among apparently healthy subjects.DesignA total of 51 individuals participated in the study. Eligible participants were randomly assigned into GT consumption groups with either high catechin (400 mg/day) or low catechin (100 mg/day). The study participants were asked to stop GT consumption for 2 weeks (washout period), following which they were to start drinking the provided GT beverages everyday for 9 weeks. The outcome measures were changes in the adiponectin levels and CVD risk factors (body weight, body mass index, waist circumference, blood pressure, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglyceride, fasting plasma glucose, as well as aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl transpeptidase, uric acid, and high-sensitive C-reactive protein).ResultsAfter intervention for 9 weeks, we found no significant difference between the high- and low catechin group with respect to changes in the serum adiponectin level: 0.35 µg/ml (95% confidence interval (CI): −1.03, 1.74). Also, no significant difference was observed between the high- and low catechin groups with respect to changes in any of the measured CVD risk factors.ConclusionThis RCT showed no significant difference between the high- and low catechin groups with respect to changes in the serum adiponectin level and any CVD risk factors.

Effects of fenofibrate therapy on circulating adipocytokines in patients with primary hypertriglyceridemia

BackgroundWe investigated effects of fenofibrate therapy on endothelial dysfunction and adipocytokine profiles. MethodsA randomized, single-blind, placebo-controlled, cross-over study was conducted in 53 patients with primary hypertriglyceridemia. We administered placebo or fenofibrate 160mg daily for 8 weeks. ResultsWhen compared with placebo, fenofibrate therapy substantially lowered plasma levels of TNF-α by 6±3% (P=0.014) and hsCRP from 1.10 to 0.90mg/l (P=0.004). When compared with placebo, fenofibrate therapy increased plasma levels of adiponectin by 17±4% (P=0.001), insulin sensitivity by 4±1% (as assessed by QUICKI, P=0.009), and decreased plasma levels of leptin and resistin by 4±7% (P=0.022) and 10±3% (P=0.001), respectively. There were correlations between percent changes in QUICKI and percent changes in adiponectin levels (r=0.279, P=0.043) or leptin (r=−0.280, P=0.042). ConclusionsFenofibrate therapy significantly reduced pro-inflammatory biomarkers and improved adipocytokines levels and insulin sensitivity in hypertriglyceridemic patients.

Effects of Ezetimibe Add-on to Statin Therapy on Adipokine Production in Patients With Metabolic Syndrome and Stable Vascular Disease

The aim of this study was to determine whether the addition of ezetimibe to ongoing statin therapy in patients with atherosclerosis and metabolic syndrome would favorably affect levels of inflammatory markers and adipokines. Individuals with the metabolic syndrome exhibit higher levels of inflammatory biomarkers and adipokines, which have been implicated in the pathobiology of cardiovascular risk. The impact of the addition of ezetimibe to statin therapy on these proinflammatory mediators is unclear. Fifty patients with metabolic syndrome and concomitant vascular disease receiving stable statin monotherapy, with low-density lipoprotein cholesterol (LDL-C) levels >77.4 mg/dL (>2.0 mM), were treated with ezetimibe 10 mg per day for 12 weeks. The primary study end point was the % change in adiponectin levels from baseline to 12 weeks. Secondary study end points included % changes in the levels of other circulating inflammatory markers, adipokines, and plasma lipids. The addition of ezetimibe to statin therapy resulted in a significant reduction in total cholesterol and LDL-C and the ratio of total cholesterol to high-density lipoprotein cholesterol. However, ezetimibe add-on treatment had no effect on the primary outcome of plasma adiponectin or on any of the secondary outcomes, including leptin, hsCRP, tumor necrosis factor-α, or interleukin-6 concentrations. These observations remained unchanged after adjusting for body mass index and for background statin used. The addition of ezetimibe to stable statin therapy in patients with vascular disease and metabolic syndrome, who were not at guideline recommended LDL-C levels, did not alter adipokine levels after 12 weeks. Short-term add-on with ezetimibe may not be associated with additional inflammatory benefits beyond improvements in cholesterol homeostasis.