Lower Adiponectin Levels Research Articles

Obstructive sleep apnea is associated with lower adiponectin and higher cholesterol levels independently of traditional factors and other sleep disorders in middle-aged adults: the ELSA-Brasil cohort.

Obstructive sleep apnea (OSA) may contribute to metabolic and inflammatory deregulation but previous studies failed to consider sleep duration, sleep fragmentation, insomnia, and daytime sleepiness as potential confounders. Consecutive non-diabetic middle-aged participants from the ELSA-Brasil cohortwere invited to perform a clinical evaluation, home sleep study for 1 night, and wrist actigraphy for 7 days. OSA was defined by an apnea-hypopnea index ≥ 15 events/h. Participants were stratified according to the presence of OSA measuring the following markers: fasting glucose, glucose tolerance test, homeostatic model assessment of insulin resistance (HOMA-IR) index, fasting insulin, insulin after 2 h of glucose load, glycated hemoglobin, total cholesterol and their fractions, triglycerides, C-reactive protein, TNF-alpha, interleukin-6, interleukin-10, leptin, adiponectin, E-selectin, ADMA, MCP-1, TGF, apolipoprotein B, fibrinogen, and lipoprotein(a). Differences between groups were identified by chi-square test and ANOVA. We studied 708 participants (mean age: 46 ± 5 years, men: 44%, BMI 26.1 ± 4.1 kg/m2). Compared to no OSA, participants withOSA presented higher levels while fasting and after 2 h glucoseloadof insulin, HOMA-IR, cholesterol, triglycerides, and C-reactive protein (all p < 0.001). After linear regression analysis adjusting for traditional risk factors plus sleep duration, fragmentation, insomnia, and daytime sleepiness, OSA was negatively associated with adiponectin (β = - 0.271 CI 95% - 0.456 - 0.085) and positively associated with cholesterol (β = 9.707 CI 95% 2.737 16.678). Sex-stratification revealed that these associations were significant for men but not women. In non-diabetic middle-age adults, men with OSA presented with lower adiponectin and higher cholesterol levels independently of sleep duration, sleepfragmentation, insomnia, and daytime sleepiness.

Low levels of spexin and adiponectin may predict insulin resistance in patients with non-alcoholic fatty liver

Adipose tissue is endocrine organ that responds by secreting numerous hormones that regulate metabolism in skeletal muscle and the liver. The aim of this study was to compare the levels of spexin and adiponectin in patients with non-alcoholic fatty liver and evaluate the relationship between circulating adipocytokines and insulin resistance. Two groups of subjects were evaluated: 41 non-alcoholic fatty liver subjects (age 35.17 ​± ​12.29 year, BMI 30.97 ​± ​2.75 ​kg/m2) and 38 normal controls (age 38.47 ​± ​11.63 year, BMI 22.83 ​± ​3.00 ​kg/m2). Plasma concentrations of spexin and adiponectin were determined using immunosorbent assay kits. Insulin resistance was assessed using the homeostasis model assessment (HOMA-IR) formula derived from fasting insulin and glucose levels. Compared to normal controls, plasma concentrations of spexin and adiponectin were significantly lower in patients with non-alcoholic fatty liver (P ​< ​0.001). Spexin did not correlate with BMI but did significantly correlate with HOMA-IR (r ​= ​-0.368; P ​= ​0.018) and adiponectin (r ​= ​0.378; P ​= ​0.043), and this correlation remained significant after adjustment for gender and BMI. In this small group of patients with non-alcoholic fatty liver we demonstrated that insulin resistance correlated strongly with spexin and adiponectin levels.

Inflammatory biomarkers and prediction of insulin resistance in Congolese adults

Several studies have shown that low levels of adiponectin (ADP) and high levels of alpha tumor necrosis factor (NFT) increase the risk or severity of many cardiometabolic diseases associated with insulin resistance. The main objective of this study was to evaluate the association between plasma adipokines and IR measured by HOMA-IR. The secondary objective was to determine the biomarker of the potential inflammation to predict IR in Congolese melanoderm subjects residing in Brazzaville. This cross-sectional study was conducted on 234 apparently healthy participants over the age of 18. Socio-demographic and clinical data were collected. Biological data, including the total ADP and NFT dosage, were measured using the ELISA method. Participants were categorized into two groups according to HOMA-IR ≥ 2.5. Univariate and multivariate logistic regression analyses were conducted to identify risk factors for insulin resistance. An optimized model was obtained after the logistic regression. The analysis of the receptor's operating characteristics (OCR) was performed to determine the optimal threshold value and diagnostic characteristics, as well as the area under the curve (ASC). ADP averages were significantly low (11.49 ± 7.61 ng/mL; P < 0.001) while those of TNF were significantly higher (96.03 ± 44.09 pg/mL) in the HOMA-IR group ≥ 2.5. There was a positive and significant correlation (p < 0.05) between BMI, TT, CRPhs, TNF and HOMA-IR. And a negative and significant correlation was noted between ADP and HOMA-IR (r = - 0.39; P < 0.01). Similarly, a negative and significant correlation (p < 0.01) was noted between BMI, TT, TNF, CRPhs and ADP. The optimal threshold value of the total ADP for predicting IR was 17.52 ng/mL with a sensitivity of 89% [IC 95% (0.83–0.95)], 56% specificity [IC 95% (0.47–0.65)] and a CSA of 0.76 [IC 95% (0.69–0.81)]. After logistic regression, the CSA of the optimized model was 0.84 [IC 95% (0.79–0.89)]. ADP can be used as a highly plausible IR prediction biomarker.

Evaluation of Stress and Associated Biochemical Changes in Patients with Type 2 Diabetes Mellitus and Obesity

PurposeType 2 diabetes mellitus (T2DM), a metabolic disorder, remains associated with a physiological impairment affecting large populations worldwide. Onset of T2DM is multifactorial where obesity and abnormal basal metabolic rate are considered most critical. Of people diagnosed with T2DM, about 80% are also obese. It is also reported that obese individuals have an increased odds of developing depression, whereas T2DM is estimated to increase the incidence by two-fold. The preponderance of research data demonstrates that T2DM alters the serum level of cortisol and adiponectin which are known to be associated with neuronal physiology. The study explored, how a metabolic disorder like T2DM is linked with the altered plasma level of cortisol and adiponectin, the risk factors for stress and depression.Patients and MethodsA cross-sectional population study was conducted in T2DM patients using a bimodal approach. First approach used questionnaires, (1) Patient Health Questionnaire (PHQ-9) and (2) Stress Coping Inventory Questionnaire (SCQ) to assess signs and symptoms of depression and stress, respectively, in T2DM patients. In the second approach, robust biochemical analysis was conducted for serum adiponectin and cortisol levels.ResultsAn association of T2DM in stress and depression was evaluated in 158 subjects (105 T2DM obese patients and 53 healthy controls). A lower PHQ-9 score and adiponectin levels were seen in T2DM obese patients compared to healthy controls (p<0.05). Further, results also depicted a lower adiponectin levels in T2DM obese patients with depression compared to T2DM obese patients without depression (p<0.05). The study did not find a significant difference in cortisol serum levels among the T2DM and control groups. However, a higher level of serum cortisol was reported in T2DM obese patients with depression over those T2DM obese patients who lacked depression (p<0.05).ConclusionThe findings suggest that T2DM obese patients might have a higher risk of developing stress and depression. Further, biochemical parameters, adiponectin and cortisol, might be the potential biomarkers for T2DM and may help in early diagnosis of these comorbid conditions.

Increased epicardial adipose tissue thickness associated with increased metabolic risk and the presence of heart failure in patients with Chronic Chagas disease.

It has been described that Trypanosoma cruzi is capable of promoting metabolic disturbances currently considered as cardiovascular risk factors. Moreover, it has been observed that the protozoa can remain in adipose tissue and alter its immune endocrine functions. The aim of this study was to characterize the thickness of epicardial adipose tissue (EAT) in patients with chronic Chagas disease (CCD) concerning their cardiovascular metabolic risk profile compared with those without CCD. A cross-sectional study was performed including T. cruzi seropositive individuals categorized according to a standard CCD classification and a matched seronegative control group. Complete clinical examination, metabolic laboratory tests and transthoracic echocardiography to assess cardiac function and to quantify EAT were performed. Fifty-five individuals aged 46.7±11.9 y, 34 with CCD and 21 in the control group, were included. The CCD group presented higher EAT thickness in relation to controls (4.54±1.28 vs 3.22±0.99 mm; p=0.001), which was significantly associated with the presence of insulin resistance (OR=3, 95% CI 1.58 to 5.73; p<0.001). This group presented lower levels of plasmatic adiponectin than controls, especially in those patients with EAT ≥4.5 mm (p=0.005) who also presented with heart failure more frequently (p=0.01). In patients with CCD, a higher EAT thickness is observed and is associated with an increased metabolic risk profile indicated mainly by insulin resistance.

Hyperandrogenism, Insulin Resistance, and Acanthosis Nigricans (HAIR-AN) Syndrome Reflects Adipose Tissue Dysfunction (“Adiposopathy” or “Sick Fat”) in Asian Indian Girls

Background: Whether HAIR-AN syndrome and polycystic ovarian syndrome (PCOS) are distinct entities or represent a phenotypic spectrum of the same syndrome is still unclear. HAIR-AN syndrome is characterized by high insulin resistance, obesity, and hyperinsulinemia as compared to PCOS and could represent adipose tissue dysfunction as the primary pathophysiologic trigger. This study was undertaken to study the role of adipose tissue dysfunction in HAIR-AN syndrome and PCOS using adipocytokines as surrogate markers of “adiposopathy.” Materials and Methods: A cross-sectional observational study was conducted at a tertiary care hospital over a period of 1 year. Serum adiponectin, leptin, IL-6, and TNF-α levels were measured in 30 women with HAIR-AN syndrome and in 30 women with PCOS. Correlations between adipocytokines, inflammatory markers, serum testosterone, and serum insulin were determined. Data analysis was performed using the SPSS version 23.0 (IBM SPSS Statistics Inc., Chicago, IL, USA) software program. Results: Women with HAIR-AN syndrome had significantly higher hyperandrogenemia, hyperinsulinemia, and insulin resistance as compared to PCOS women. They also had high leptin levels and lower adiponectin levels (p < 0.001). However, the levels of inflammatory markers (TNF-α and IL-6) were similar in both the groups (p > 0.05). Serum adiponectin showed a negative correlation with HOMA-IR and testosterone levels, while leptin showed a positive correlation with both in HAIR-AN patients while no such correlation was found in the PCOS group. Conclusion: The significantly raised adipocytokines in HAIR-AN syndrome patients as compared to PCOS patients indicates the primary role of adipose tissue dysfunction (“adiposopathy”) in the pathogenesis of HAIR-AN syndrome while only a minor role, if any, in PCOS. Both these syndromes stand as distinct entities pathogenically with an overlapping phenotype.

Hypertrophy and Insulin Resistance of Epicardial Adipose Tissue Adipocytes: Association with the Coronary Artery Disease Severity.

Changes in the structural and functional characteristics of the epicardial adipose tissue (EAT) are recognized as one of the factors in the development of cardiometabolic diseases. However, the generally accepted quantitative assessment of the accumulation of EAT does not reflect the size of adipocyte and presence of adipocyte hypertrophy in this fat depot. Overall contribution of adipocyte hypertrophy to the development and progression of coronary atherosclerosis remains unexplored. Objective: To compare the morphological characteristics of EAT adipocyte and its sensitivity to insulin with the CAD severity, as well as to identify potential factors involved in the realization of this relationship. The present study involved 24 patients (m/f 16/8) aged 53–72 years with stable CAD, who underwent coronary artery bypass graft surgery. Adipocytes were isolated enzymatically from EAT explants obtained during the operation. The severity of CAD was assessed by calculating the Gensini score according to selective coronary angiography. Insulin resistance of EAT adipocytes was evaluated by reactivity to insulin. In patients with an average size of EAT adipocytes equal to or exceeding the median (87 μm) the percentage of hypertrophic adipocytes was twice as high as in patients in whom the average size of adipocytes was less than 87 μm. This group of patients was also characterized by the higher rate of the Gensini score, lower adiponectin levels, and more severe violation of carbohydrate metabolism. We have revealed direct nonparametric correlation between the size of EAT adipocytes and the Gensini score (rs = 0.56, p = 0.00047). The number of hypertrophic EAT adipocytes showed a direct nonparametric correlation with the Gensini score (rs = 0.6, p = 0.002). Inverse nonparametric correlations were found between the serum adiponectin level and size (rs = −0.60, p = 0.001), hypertrophy of adipocytes (rs = −0.67, p = 0.00), and Gensini score (rs = −0.81, p = 0.00007). An inverse nonparametric correlation was found between the Gensini score and sensitivity of EAT adipocytes to insulin, estimated by the intracellular redox response (rs = −0.90, p = 0.037) and decrease in lipolysis rate upon insulin addition (rs = −0.40, p = 0.05). The intracellular redox response of adipocytes to insulin was directly correlated with fasting insulin and inversely with postprandial insulin. Our data indicate that the size and degree of hypertrophy of the epicardial adipocytes are related to the CAD severity. According to our results, insulin resistance of adipocytes may be considered as one of the factors mediating this relationship.

Altered acylated ghrelin response to food intake in congenital generalized lipodystrophy.

BackgroundPatients with congenital generalized lipodystrophy (CGL) have very low levels of leptin and are described as having a voracious appetite. However, a direct comparison between CGL and eutrophic individuals is lacking, regarding both appetite parameters and acylated ghrelin, the hormone form that is active in acute food intake stimulation. The objective of the present study was to address whether and in what extent the subjective appetite parameters and acylated ghrelin response to a meal are affected in CGL individuals, in comparison to eutrophic individuals. Additionally, an obese group was included in the study, to allow the comparison between a leptin-resistant and a leptin-deficient condition on these aspects.MethodsEutrophic controls (EUT, n = 10), obese subjects (OB, n = 10) and CGL (n = 11) were fasted overnight and then received an ad libitum meal. Blood was collected and the visual analogue scale was applied before and 90 minutes after the meal. An additional blood sample was collected at 60 minutes for ghrelin determination.ResultsThe CGL patients showed low fasting levels of leptin and adiponectin, dyslipidemia, and insulin resistance. The caloric intake was similar among the 3 groups. However, both CGL (p = 0.02) and OB (p = 0.04) had shorter satiation times than EUT. The CGL patients also had lower satiety time (p = 0.01) and their sensation of hunger was less attenuated by the meal (p = 0.03). Fasting acylated ghrelin levels were lower in CGL than in EUT (p = 0.003). After the meal, the levels tended to decrease in EUT but not in CGL and OB individuals.ConclusionThe data indicate that, although not hyperphagic, the CGL patients present appetite disturbances in relation to eutrophic individuals. Their low fasting levels of acylated ghrelin and the absence of the physiological drop after meal intake suggest a role of these disturbances in hunger attenuation and satiety but not in acute satiation.

Impact of Adiponectin Resistance on Coronary Artery Disease Severity.

The serum adiponectin level (AD), adiponectin resistance (AD-R) may reflect the degree of metabolic syndrome (MetS). The role parameter AD-R, The Homeostasis Model Assessment-Adiponectin (HOMA-AD) index on the coronary artery disease (CAD) severity is not still understood. To determine adiponectin concentration and HOMA-AD index in patients with CAD with/without MetS and to evaluate their prognostic importance on severity of CAD. This cross-sectional study involved selected 130 examinees which were divided into three groups: CAD+MetS, CAD-MetS, control group (no CAD/MetS). In all examinees values of biochemical and anthropometric parameters were determined. We analyzed the severity of coronary artery lesions from coronary angiography. Total serum adiponectin concentration was measured by ELISA. We calculated atherogenic Gensini scoring system, Duke prognostic index, and HOMA-AD-index. Serum adiponectin level was significantly lower in the group with CAD+MetS (p < 0.001) and in CAD-MetS group (p < 0.01), compared to the control group. The HOMA-AD index showed statistically significant positive correlation with the key parameters of MetS, as well as with the parameters of CAD, number of CAD and modified Gensini score. After applying logistic regression analysis the best predictors for CAD were: adiponectin, blood pressure, HOMA-IR index, and HOMA-AD index. The cut-off values of adiponectin ≤1506.38 pg/mL, HOMA-IR index ≥3.91 and HOMA-AD index ≥0.67 were associated with a higher risk of CAD. Patients with CAD with or without MetS had low adiponectin levels and this hypoadiponectinemia indicates that AD and HOMA-AD index may be a useful marker for identifying patients at risk for CAD.

Maternal plasma adiponectin concentration and its association with risk of gestational diabetes

Background Gestational diabetes mellitus (GDM) is a metabolic disorder characterized by glucose intolerance of variable degree, with onset or first recognition during pregnancy. The global prevalence of hyperglycemia in pregnant women aged 20–49 years is 16.9%, and more than 90% of cases of hyperglycemia in pregnancy are estimated to occur in low-income and middle-income countries. Aim To observe changes in maternal plasma adiponectin concentration during 24–32 weeks of gestation in both healthy pregnant women and women with GDM for early detection of GDM. Patients and methods This case–control study was carried out on 88 pregnant women divided into two groups: group I included 50 pregnant women with GDM, and group II included 38 apparently healthy pregnant women who were selected as a control group, and their age was matched with patients. All participants underwent history taking, clinical examination, and oral glucose tolerance test, and plasma adiponectin was measured in both groups. Their analyses were done at Al Azhar University Center for Virus Research and Studies. Results There was a highly significantly decrease in plasma adiponectin levels (P&lt;0.001) in patients with GDM when compared with the control group. The significant association between adiponectin and GDM suggests that low adiponectin levels may predict the development of GDM. Conclusion Findings of our study have demonstrated that low plasma adiponectin concentration was associated with GDM

Gestational Weight Gain Influences the Adipokine-Oxidative Stress Association during Pregnancy

Introduction and Objective: The weight gained during pregnancy could determine the immediate and future health of the mother-child dyad. Excessive gestational weight gain (EGWG) due to abnormal adipose tissue (AT) accumulation is strongly associated with adverse perinatal outcomes as gestational diabetes, macrosomia, obesity, and hypertension further in life. Dysregulation of adipokine, AT dysfunction, and an imbalance in the prooxidant-antioxidant systems are critical features in altered AT accumulation. This study was aimed to investigate the association between adipokines and oxidative stress markers in pregnant women and the influence of the GWG on this association. Methods: Maternal blood samples were obtained in the third trimester of pregnancy (n = 74) and serum adipokines (adiponectin, leptin, and resistin), oxidative damage markers: 8-oxo-2′-deoxyguanosine (8-oxodG), lipohydroperoxides (LOOH), malondialdehyde (MDA), and carbonylated proteins (CP), and glucose a metabolic marker were measured. Results: Women with EGWG had low adiponectin levels than women with adequate weight gain (AWG) or insufficient weight gain (IWG). Multiple linear regression models revealed a positive association between adiponectin and 8-oxodG in women with AWG (B = 1.09, 95% CI: 164–222, p = 0.027) and IWG (B = 0.860, 95% CI: 0.199–1.52, p = 0.013) but not in women with EGWG. In women with EGWG, leptin was positively associated with LOOH (p = 0.018), MDA (p = 0.005), and CP (p = 0.010) oxidative markers. Conclusion: Our findings suggest that concurrent mechanisms regulate adipokine production and oxidative stress in pregnant women and that this regulation is influenced by GWG, probably due to an excessive AT accumulation.

Adipocytokines in Diabetes Mellitus: A Study from a Rural Setting in Haryana, India

Introduction: Diabetes Mellitus (DM) and Obesity are the biggest public health challenges of 21st century. Both these disorders are associated with several co-morbidities like hypertension, hyperlipidemia, Cardiovascular Diseases (CVD) etc., that may be linked to the underlying insulin resistance, hyperglycaemia, dyslipidemia, hyperinsulinemia and altered levels of adipocyte- derived hormones. Furthermore, clinical studies in humans have suggested the possible correlation of plasma concentration of several adipocytokines and measures of adiposity, insulin resistance and endothelial function in humans. Aim: To estimate and compare the serum levels of leptin and adiponectin in patients with Type 2 Diabetes Mellitus (T2DM) and in non-diabetic subjects with and without obesity. Materials and Methods: In the study, 200 T2DM patients (with and without obesity) and 200 non-diabetic subjects (with and without obesity) aged between 30-70 years of either sex were included. In all the subjects included in the study, serum leptin and adiponectin levels were estimated using Enzyme Linked Immunosorbent Assay (ELISA) method. Results: It was observed that the serum adiponectin levels decreased while leptin levels increased significantly (p&lt;0.001) in obese than non-obese diabetics. Similarly, obese non-diabetics showed higher serum leptin and lower adiponectin levels than their non-obese counterparts (p&lt;0.001). Conclusion: Serum levels of leptin and adiponectin are altered in subjects with T2DM and obesity which may indicate the potential role of adipocytokines as an important link between increased fat mass, insulin resistance, deranged glucose metabolism and endothelial dysfunction especially in diabetic patients.

Association between maternal nutrition and fetal developmental profile: Do leptin and adiponectin have a significant role?.

Background: Leptin and adiponectin, which are primarily produced by adipose tissue, have recently been identified as key mediators in the foetal developmental process. Modulation of these adipokines in early life, therefore, provides potential opportunities to improve or reverse the adverse complications associated with an abnormal foetal developmental profile. Aim: The purpose of this study was to determine the effect of maternal dietary habits on foetal leptin and adiponectin levels on foetal developmental outcomes. Subjects and Methods: Sixty-two mothers between the ages of 18 years and 38 years, as well as their full-term neonates, were enrolled in this study, whether they had a normal delivery or a Cesarean section, with no birth complications. All mothers were subjected to a full pregnancy history in order to determine their gestational age, as well as a full examination that included measuring and recording all of their anthropometric measurements. Clinical examinations were performed on newborns, and the Apgar score was also recorded. Newborns were classified as Small for Gestational Age (SGA), Appropriate for Gestational Age (AGA), or Large for Gestational Age (LGA) based on their birth weight (LGA). ELIZA measured leptin and adiponectin levels in both mother's serum and cord blood serum. Results: Mothers who consumed fish and fats during pregnancy were not at risk of having SGA babies, and SGA babies had significantly lower adiponectin levels than AGA and LGA babies. Leptin levels increased significantly as they passed from SGA to LGA. Leptin distribution was significantly higher in infants of mothers who consumed daily breakfast during pregnancy than in infants of mothers who did not consume breakfast. Infant adiponectin distribution was significantly higher in infants of mothers who ate regular fats than in infants of mothers who ate a low fat diet. Infant adiponectin distribution was significantly higher in infants of mothers who consumed sugary drinks once per day than in infants of mothers who did not consume sugary drinks. Furthermore, there is a significant positive correlation between infant weight, infant length, infant head circumference, infant mid-arm circumference, and levels of both infant leptin and infant adiponectin. A highly significant negative correlation was found between mother adiponectin and infant leptin levels, while a highly significant positive correlation was found between mother leptin and infant leptin levels. Conclusion: This study shed light on the important role of maternal nutrition during pregnancy in foetal body fat composition. This study also provides clear evidence for the influence of leptin and adiponectin on foetal development.

Association of Adiponectin−11377 C/G (rs266729) Gene Polymorphism with Nonalcoholic Fatty Liver Disease and Metabolic Features in Egyptian Women

The present cross-sectional study included 150 unrelated non-alcoholic fatty liver disease (NAFLD) patients and 150 healthy subjects. ADIPOQ (-11377C / G) variant was genotyped with polymerase chain reaction-restriction fragment polymorphism (PCR-RFLP) method for both patients and controls. Anthropometric and biochemistry parameters were measured. The Homeostasis Model Insulin Resistance Assessment (HOMA-IR) was used to assess the insulin resistance. The rs266729 polymorphism was associated with NAFLD with significant increase in CG genotype compared to those with the wild genotype CC (OR = 9.24, 95% CI = 4.96 - 17.21, p<0.001) in co dominant tested inheritance model as well in dominant tested inheritance model with CG/GG genotype (OR = 9.58, 95% CI = 5.32 – 17.28, p< 0.001). The G allele increased the risk of NAFLD (OR = 6.06, 95% CI = 3.65 - 10.05, p< 0.001) in comparison with C allele. Subgroup comparison in NAFLD revealed significant higher levels of waist circumference (WHR), HOMA-IR, systolic blood pressure (SBP), fasting glucose and LDL-C in GG and GC carriers compared to CC genotype and significant lower levels of serum adiponectin. Conclusions: The study suggests that ADIPOQ gene polymorphism can be used as a helpful biomarker for NAFLD and abnormal metabolic parameters. Our study sheds light on its role that might be played in the pathogenesis of NAFLD. Proper evaluation of NAFLD is likely to improve therapy effectiveness and safety management.

Is adiponectin in children with immunoglobulin A vasculitis a suitable biomarker of nephritis in the course of the disease?

Immunoglobulin A vasculitis (IgAV) is the most common form of vasculitis in children. Nephritis in the course of this disease (IgAVN) is observed in 30-50% of patients and might lead to chronic kidney disease (CKD) and end-stage renal disease (ESRD). Finding a non-invasive biomarker to distinguish initially between patients with and without nephritis and to facilitate a therapeutic decision to reduce the risk of long-term renal impairment is currently the target of much research. The aim of this study was to evaluate the adiponectin concentration in children with IgAV and estimate whether it might be used as a marker of IgAVN. The study involved 29 IgAV children and 34 healthy controls. Eleven (38%) patients had renal involvement (IgAV-N) and 18 (62%) did not exhibit nephritis (IgAV-noN). The serum adiponectin level was estimated in children in an acute phase of IgAV and after 2-6 months during a follow-up visit. The relationship between the concentration of adiponectin and anthropometric measurements, epidemiological data and laboratory parameters were evaluated. The concentration of adiponectin in serum was significantly higher in children with acute phase of IgAV as compared to the control group (p < 0.001), and in patients without renal involvement in comparison with IgAV-N children (p < 0.049). In analysis of correlation we found a negative relationship between adiponectin level and serum creatinine concentration (r = -0.437, p = 0.02). The logistic regression evaluation demonstrated that a low adiponectin level increased the risk of nephritis in the course of IgAV. Our study revealed that the serum adiponectin level increased markedly in patients with IgAV. We also documented that higher risk of nephritis in the course of the disease was associated with lower concentration of this hormone.

Obesity Contribution in Synthesis and Degradation of Cartilage Marker Through Inflammation Pathway in Osteoarthritis Patient: Analysis of Adiponectin, Leptin, Ykl-40 and Cartilage Oligomeric Matrix Proteinase (Comp) Synovial Fluid

Background: To determine the role of obesity in osteoarthritis (OA) through inflammation pathway byanalyzing articular cartilage synthesis and degradation markers in synovial fluid.Methods: We performed observational study with cross sectional approach. Obesity was determinedbased on WC. OA genu diagnosed based on American College of Rheumatology (ACR) 1986 criteria. Weexamined leptin as inflammation marker, adiponectin as anti-inflammation marker, YKL-40 as cartilagesynthesis marker and COMP as cartilage degradation marker in synovial joint using ELISA.Results: From 70 OA genu patients, 61 subjects with central obesity and 9 subjects with non-central obesity.In OA patient with central obesity group, WC does not correlate directly with COMP and YKL-40, butthrough level of adiponectin and leptin. WC correlates with adiponectin and leptin level, and then adiponectinlevel correlate with YKL-40 level, and leptin level correlate with COMP level, the greater the WC, the loweradiponectin level and the higher leptin level. The lower the adiponectin level, the lower the YKL-40 leveland the higher the leptin level, the higher the COMP level. Whereas in OA patient with non-central obesitygroup, WC is directly correlated with COMP level (not through adiponectin or leptin); the greater WC, thehigher COMP level. WC does not correlate directly with YKL-40, but through adiponectin due to increasingage, not because of changes in WC. In non-central obesity, the older a person is, the lower adiponectin level;and the lower adiponectin level, the lower YKL-40 level.Conclusions: Obesity contributed in central obese OA, group on destruction of articular cartilage wasdirectly correlated with WC without involving inflammation pathway.

Pretilost i rak

For the past several decades, we have witnessed the emergence of the obesity pandemic worldwide and, simultaneously, the increase of incidence of malignant diseases. The effects of obesity and overweight on cancer incidence, morbidity, and mortality started to be meticulously researched only recently. According to the epidemiological data analysis, the connection between obesity and increased risk of numerous cancers has been established. Estimations are that a change in lifestyle and diet can prevent 30-50% of malignant diseases. After smoking, obesity is the second largest preventable cause of cancer. Obesity affects the quality of life and increases the risk of cancer recurrence and cancer-related mortality. By reducing body mass and avoiding gaining weight during adulthood, the risk of getting cancer is lowered. Numerous studies have shown the beneficial effects of physical activity during and after cancer treatment. Obesity influences cancer development; however, the mechanisms responsible for it are still unclear. It is considered that chronic inflammation, caused by the overabundance of nutrients, increases the levels of inflammatory cytokines and immune cells. It has been discovered that adipocytes have an important endocrine role; they synthesize numerous hormones and adipocytokines, such as leptin and adiponectin. High levels of leptons and low levels of adiponectin can activate intracellular signaling pathways involving malignant cells’ development. An important part of cancer development can be attributed to insulin metabolism, insulin-like growth factors, and sex hormones.

Adipokines and Arterial Stiffness in the Elderly.

IntroductionThe aim of this study was to evaluate the relationship between adipokines and arterial stiffness in a group of 85 elderly subjects and the role of leptin and adiponectin on subclinical vascular damage, defined by a PWV>10 m/s.MethodsIn each subject, we evaluated anthropometry, body composition by DXA (fat mass, fat mass%, lean mass), metabolic variables, leptin, adiponectin, systolic, diastolic, mean arterial pressure and pulse pressure (SBP, DBP, MAP, PP), carotid-femoral pulse wave velocity (cfPWV) and carotid-radial pulse wave velocity (crPWV).ResultsIn the study population, significant associations were observed between cfPWV and crPWV, age, SBP, MAP, waist circumference, fat body mass and leptin. The study population was subdivided in 2 subgroups according to adipokine patterns: group 1 included patients with high adiponectin and low leptin, and group 2 patients had high leptin and low adiponectin. SBP, PP, cfPWV were significantly higher in subjects with high leptin and low adiponectin (group 2). Even after adjustment for gender, fat mass%, MAP, HDL cholesterol and triglycerides, cfPWV was higher in group 2 than group 1. In a logistic binary regression on the entire population, considering subclinical vascular damage as a dependent variable and age, gender, MAP, fat mass%, triglycerides, HDL cholesterol and category of subjects with high leptin and low adiponectin as independent variables, MAP and category of subjects with high leptin and low adiponectin were significant predictors (OR, respectively, 1.09 and 3.61).ConclusionIn conclusion, in the elderly, the presence at the same time of high leptin levels and low adiponectin levels seems to have synergic effects on arterial stiffness.

Relationship between Plasma Adiponectin Level and Corrected QT Interval in Smoker and Non-smoker Adult Male Subjects.

ObjectiveThis study determined the relationship between plasma adiponectin level and corrected QT interval (QTc) in smokers and non-smokers.MethodologyThis cross-sectional analytical study was undertaken in 30 smokers and 30 non-smokers. Plasma adiponectin level was determined by enzyme-linked immunosorbent assay (ELISA). The QT interval was measured by routine 12-lead ECG with Lead II rhythm and QTc was calculated.ResultsMean plasma adiponectin level was significantly lower in smokers (27.89±15 μg/ml) than that of non-smokers (52.13±21.57pg/ml) (p<0.001). Mean QTc interval was significantly longer in smokers than that of non-smokers (415.37±29.9 versus 395.63±26.13 ms, p<0.01). Higher risk of low adiponectin level (odds ratio [OR],8.1; 95% confidence interval [CI],1.61-40.77) and QTc interval prolongation (OR,6; 95%CI,1.17-30.73) were observed in smokers. There was weak significant negative correlation between plasma adiponectin level and QTc interval in the study population (n=60, r=-0.407, p=0.001). Moreover, low plasma adiponectin level was significantly associated with prolonged QTc interval in the study population (n=60, Fisher’s exact p value<0.05). Risk of QTc interval prolongation was 4.3 times higher in subjects with low plasma adiponectin level (OR,4.27; 95% CI,1.05-17.46).ConclusionSmokers have greater risk for low plasma adiponectin level and prolonged QTc interval. There is a relationship between plasma adiponectin level and QTc interval.

Abstract 13039: Loss of Visceral Adipose Tissue Macrophage Subsets Induces Myocardial Infarction Induced Insulin Resistance: Role of Adiponectin

Introduction: Myocardial infarction (MI) is the major cause of morbidity and mortality in the western world. Insulin resistance is a major complication in patients with MI. Hypothesis: Loss of visceral adipose tissue (VAT) resident macrophages in MI results in diminished adiponectin production causing systemic insulin resistance. Methods: To understand if MI results in insulin resistance, we analyzed UPMC patient records and identified patients who had normal fasting blood glucose levels on average 15 days before ST elevation myocardial infarction (STEMI) and checked their fasting blood glucose levels 30 days after STEMI. To understand the mechanisms of MI-induced insulin resistance, we used a mouse model of coronary ligation in C57BL/6 mice and analyzed the features of insulin resistance by measuring serum insulin, serum adiponectin, AKT activation status in the liver and muscle. Results: We found that 50% of non-diabetic patients (fasting blood glucose levels 99±2.5 mg/ dl) developed hyperglycemia (141±13 mg/dl) after MI, suggesting that MI causes insulin resistance. Consistently, mice with MI had higher fasting blood insulin, and reduced p-Akt levels in the liver and skeletal muscles confirming insulin resistance. Concomitantly, mice and patients with MI had reduced number of visceral adipose tissue (VAT) resident macrophages. In line with this, MI resulted in marked reduction in the level of macrophage colony stimulating factor (M-CSF), a cytokine required for tissue resident macrophage survival. M-CSF supplementation in mice with MI improved insulin sensitivity and decreased inflammatory phenotype of VAT macrophages. Furthermore, the systemic level of adiponectin, which is reported to augment insulin sensitivity, was profoundly reduced in mice after MI. Specific depletion of VAT resident macrophages resulted in lower levels of adiponectin in the serum, indicating that this macrophage subset is necessary for adiponectin production by adipocytes. Conclusions: Our data demonstrate that diminished M-CSF levels after MI triggers apoptosis of VAT resident macrophages, resulting in reduced adiponectin secretion and systemic insulin resistance.