Serum Adiponectin Research Articles

Evaluation of the production of oppositional cytokines IL-6 and IL-10 in the culture of mononuclear blood leukocytes in rats with metabolic syndrome

Aim: to evaluate the secretory activity of mononuclear blood leukocytes by the level of in vitro production of oppositional cytokines (pro-inflammatory IL-6 and anti-inflammatory IL-10) in rats in a model of diet-induced metabolic syndrome (MS) against the background of changes in the concentration of adipokines leptin and adiponectin.
 Materials and methods. In male Wistar rats, MS was modeled by keeping for 12 weeks on a high-fat and high-carbohydrate diet; control group animals received a normal diet. Mononuclear leukocytes isolated by gradient centrifugation from heparinized blood were cultured in a medium based on RPMI-1640 (concentration of 2×106 cells in 1 ml of medium) for 24 hours in sterile tubes in a CO2-incubator in two variants – without the addition of an inducer and with the addition of bacterial lipopolysaccharide (LPS). The concentration of cytokines in the culture fluid, hormones leptin and adiponectin in the blood serum was determined by enzyme immunoassay. Statistical data processing was carried out in the SPSS Statistics 23.
 Results. In animals exposed to a 12-week high-fat and high-carbohydrate diet, against the background of an increase in body weight, the specific mass of visceral adipose tissue, metabolic disorders (hyperglycemia, impaired glucose tolerance, dyslipidemia), high concentrations of leptin and low concentrations of adiponectin, the ability of mononuclear blood leukocytes to produce IL-6 and IL-10 in vitro at the basal level and when stimulated by bacterial LPS does not change.
 Conclusion. Probably, the morphofunctional status and secretory profile of monocyte-macrophage system cells depends on the severity and duration of the metabolic and hormonal imbalance associated with obesity and systemic chronic inflammation.

The Polymorphism rs17300539 in the Adiponectin Promoter Gene Is Related to Metabolic Syndrome, Insulin Resistance, and Adiponectin Levels in Caucasian Patients with Obesity.

Background and Aims: The present study was designed to investigate SNP rs17300539 in the ADIPOQ gene and its relationships with obesity, metabolic syndrome (MS), and serum circulating adiponectin. Methods: The present design involved a Caucasian population of 329 subjects with obesity. Anthropometric and adiposity parameters, blood pressure, biochemical parameters, and the percentage of patients with metabolic syndrome were recorded. The ADIPOQ gene variant (rs17300539) genotype was evaluated. Results: The percentage of patients with different genotypes of the rs17300539 polymorphism in this sample was 86.0% (n = 283) (GG), 11.2% (n = 37) (GA), and 2.7% (n = 9) (AA). The allele frequency was G (0.76) and A (0.24). Applying the dominant genetic model (GG vs. GA + AA), we reported differences between genotype GG and genotype GA + AA for serum adiponectin levels (Delta: 7.5 ± 1.4 ng/mL; p = 0.03), triglycerides (Delta: 41.1 ± 3.4 mg/dL; p = 0.01), fastingcirculating insulin (Delta: 4.9 ± 1.1 mUI/L; p = 0.02), and insulin resistance as HOMA-IR (Delta: 1.4 ± 0.1 units; p = 0.02). The remaining biochemical parameters were not related to the genotype of obese patients. The percentages of individuals with MS (OR = 2.07, 95% CI = 1.3-3.88; p = 0.01), hypertriglyceridaemia (OR = 2.66, 95% CI = 1.43-5.01; p = 0.01), and hyperglycaemia (OR = 3.31, 95% CI = 1.26-8.69; p = 0.02) were higher in GG subjects than patients with A allele. Logistic regression analysis reported an important risk of the presence of metabolic syndrome in GG subjects (OR = 1.99, 95% CI = 1.21-4.11; p = 0.02) after adjusting for adiponectin, dietary energy intakes, gender, weight, and age. Conclusions: The GG genotype of rs17300539 is associated with hypertriglyceridaemia, insulin resistance, low adiponectin levels, and a high risk of metabolic syndrome and its components.

Taurine supplementation alters gene expression profiles in white adipose tissue of obese C57BL/6J mice: Inflammation and lipid synthesis perspectives

This work aimed to identify the mechanisms by which taurine exerts its anti-obesity effects in the C57BL/6J ob/ob mice model and determine if taurine supplementation increases the amelioration of inflammation and lipogenesis linked genes in the adipose and liver tissues. Three groups of C57BL/6J mice were fed a standard chow diet for a period of 10 weeks the C57BL/6J normal group, the C57BL/6J ob/ob negative control group with no taurine intake and C57BL/6J ob/ob taurine group with taurine intake. Real time PCR was used to examine the gene expression profile in the experimental groups intrascapular brown adipose tissue (BAT), inguinal white adipose tissue (WAT) and liver. TNF-alpha, Ccl2, Adgre and illb genes that are associated with inflammation were found to have varying level of expression in the three tissues. In comparison to BAT and liver these genes were expressed at a much lower level in WAT, with enhanced serum adiponectin levels.

Effect of Chiglitazar and Sitagliptin on Bone Mineral Density and Body Composition in Untreated Patients with Type 2 Diabetes.

To evaluate the changes in bone mineral density (BMD) and body composition in untreated patients with type 2 diabetes mellitus (T2DM) before and after chiglitazar or sitagliptin treatment. A total of 81 patients with T2DM were randomly divided to receive chiglitazar or sitagliptin treatment for 24 weeks (54 in the chiglitazar group and 27 in the sitagliptin group). We measured the spine lumbar BMD, hip BMD, fat mass (FM), fat-free mass (FFM), percent body fat (%BF), android FM, gynoid FM and skeleton muscle mass (SMM) using dual-energy X-ray absorptiometry (DEXA) and examined serum adiponectin (ADP) levels at baseline and the end of the study. There were no significant changes in the BMD of the L2-4, femoral neck, trochanter or total hip as well as in the BMC after 24 weeks of treatment with chiglitazar or sitagliptin. After chiglitazar administration, the FM, gynoid FM and gynoid to total FM ratio were higher, while the android to total FM ratio and the android to gynoid FM ratio (AOI) were significantly lower. Sitagliptin intervention did not result in statistically significant differences in total fat loss, but it did cause significant decreases in %BF and AOI as well as increases in the FFM, gynoid to total FM ratio and SMM. The ADP levels had significantly negative associations with AOI in all eligible patients. The chiglitazar had no deleterious effects on BMD and resulted in body fat redistribution in untreated patients with T2DM. The trial is registered at ClinicalTrials.gov (CT.gov identifier: NCT02173457).

Adiponectin/resistin evaluation is a gold biomarker for monitoring CVD in patients with metabolic syndrome

Abstract Introduction/Objective Introduction: Various studies have tried correlating specific inflammatory markers with metabolic syndrome. Serum adiponectin levels can serve as a biomarker that predicts metabolic syndrome development. Resistin is another adipose-tissue-derived hormone capable of promoting insulin resistance because it increases the reserve of triglycerides in the muscle and the liver rather than the adipose tissue. Methods/Case Report Objectives: To investigate the role of the adiponectin/resistin ratio in monitoring CVD in Jordanian adults with metabolic syndrome. Methods Eighty subjects were randomly selected from individuals who attended two clinical laboratories for routine checks during the period between January 2021 and March 2021. Forty-two participants had metabolic syndrome, while the other 38 represented the healthy group. Resistin and adiponectin were evaluated using the ELISA method, while the adiponectin/resistin ratio was calculated. Lipid profile, glucose and body mass index (BMI) were measured for all metabolic syndrome patients and healthy control ones. Results (if a Case Study enter NA) Results: Plasma resistin levels were significantly higher in metabolic syndrome patients than in healthy controls (p = 0.04), while no significance was found regarding adiponectin (p = 0.07). In contrast, the adiponectin/resistin ratio was highly significant (p < 0.001). Resistin had shown a negative correlation with HDL (r= -0.33), whereas adiponectin was inversely correlated with LDL (r= -0.33) and LDL/HDL ratio (r= -0.34). Adiponectin/resistin ratio positively correlated with HDL (r= 0.45). The multiple linear regression analysis results revealed the predictive potential of adiponectin and resistin when used in different models for CVD risks using HDL as a risk factor. However, the results revealed that only the third model, which included the adiponectin/resistin ratio, was expected to have a higher CVD risk after controlling for the other predictors in the same model. Conclusion The studied metabolic syndrome markers might have an essential role in detecting cardiovascular events. It can be concluded that resistin can be used to evaluate the CVD risks. Furthermore, we found that the adiponectin/resistin ratio is the best marker in predicting CVD events in metabolic syndrome patients compared to other markers, including adiponectin and resistin alone.

The effect of curcumin supplementation on circulating adiponectin and leptin concentration in adults: a GRADE-assessed systematic review and meta-analysis of randomised controlled trials.

Curcumin is a phytocompound found in the root of turmeric, a common herbal ingredient in many Asian cuisines. The compound contains anti-inflammatory activity, which is mediated through an upregulation of adiponectin and reduction of leptin. Results of randomised controlled trials (RCT) have shown that the effects of curcumin on adipokines are conflicting. Therefore, the current systematic review and meta-analysis of RCT were conducted with the aim of elucidating the role of curcumin supplementation on serum adiponectin and leptin. The search included PubMed, Embase, Cochrane Library, Scopus, Web of Science and Google Scholar from inception to August 2023. For net changes in adipokines, standardised mean differences (SMD) were calculated using random effects models. Thirteen RCT with fourteen treatment arms were eligible for inclusion in this meta-analysis. Curcumin supplementation was effective in increasing serum adiponectin (SMD = 0·86, 95 % CI (0·33, 1·39), P < 0·001; I2 = 93·1 %, P < 0·001) and reducing serum leptin (SMD = -1·42, 95 % CI (-2·29, -0·54), P < 0·001; I2 = 94·7 %, P < 0·001). In conclusion, curcumin supplementation significantly increased circulating adiponectin and decreased leptin levels in adults.

Adiponectin serum levels and ADIPOQ (rs2241766) polymorphism in alopecia areata Egyptian patients

BackgroundAlopecia Areata (AA) is an acquired autoimmune form of non-scarring hair loss. Adiponectin and its gene polymorphism were related to many autoimmune disorders. ObjectiveAssessment of adiponectin serum levels and adiponectin gene (ADIPOQ) (rs2241766) Single Nucleoid Polymorphism (SNP) in AA patients and correlating the results with the disease severity in those patients. MethodsThis study included 75 AA patients and 75 age and gender-matched healthy subjects (controls). The severity of Alopecia Tool (SALT) score assessment to evaluate AA severity was done. Adiponectin serum levels by ELISA and ADIPOQ (rs2241766) SNP using PCR were performed. ResultsAdiponectin serum levels were significantly lower in AA patients than controls (p = 0.001). ADIPOQ (rs2241766) TG genotype and G allele were significantly predominant in AA patients increasing its risk by 5 and 4 folds (OR = 5.17, p = 0.001), (OR = 3.82, p = 0.001) respectively. Serum adiponectin levels were negatively correlated with SALT score (r = -0.435, p = 0.001) and associated with alopecia totalis (p = 0.016). ADIPOQ (rs2241766) TG genotype was significantly associated with low serum adiponectin levels and higher SALT score (p = 0.001). Study limitationsThe small sample size. ConclusionsADIPOQ (rs2241766) gene polymorphism (TG genotype and G allele) may modulate AA risk and contribute to the development of AA in Egyptian populations. Decreased circulating adiponectin levels may have a dynamic role in AA etiopathogenesis. Adiponectin serum concentration can be considered a severity marker of hair loss in AA.

Impact of pemafibrate on lipid profile and insulin resistance in patients with statin-treated coronary artery disease with metabolic syndrome

Abstract Background Pemafibrate is a highly selective agonist for peroxisome proliferator-activated receptor α, a vital modulator of lipid and glucose metabolism. We examined the effects of this drug on lipid markers and insulin resistance in patients with metabolic syndrome (MetS). Methods In the randomized, crossover PEBE study, 60 patients with hypertriglyceridemia (fasting triglyceride [TG] ≥ 150 mg/dL) were treated with pemafibrate of 0.2 mg/day or bezafibrate of 400 mg/day for 24 weeks, followed by crossover of another 24-weeks. Forty-six of 60 patients (77%) enrolled in the PEBE study were founded to have MetS. In the present subanalysis, we compared patients with MetS (MetS group, n = 46) and those without MetS (Non-MetS group, n =14). The primary endpoints were changes from baseline in serum TG, high-density lipoprotein cholesterol (HDL-C), and apolipoprotein A-I (Apo A-I) levels, while the secondary endpoint was change in the homeostasis model assessment of insulin resistance (HOMA-IR). Results There was a significant decrease in serum TG levels (from 266.6 mg/dL to 148.0 mg/dL in MetS group, p &amp;lt; 0.001; from 203.9 mg/dL to 97.6 mg/dL in Non-MetS group, p &amp;lt; 0.001), but %Change was not significantly different between the two groups (−44.1% vs. −51.6%, p = 0.099). Serum HDL-C and Apo A-I levels significantly increased in both groups, but no significant differences in %Change were found between the two groups (p = 0.591 in HDL-C; p = 0.432 in Apo A-I). HOMA-IR significantly decreased in MetS group (from 4.3 ± 4.0 to 3.1 ± 2.2, p = 0.011) but not in Non-MetS group (from 1.7 ± 1.0 to 1.5 ± 1.0, p = 0.553). %Change in liver enzyme levels was markedly decreased in MetS group than in Non-MetS group (alanine aminotransferase, −25.1% vs. −11.3%, p = 0.027; gamma-glutamyl transferase, −45.8% vs. −36.2%, p = 0.020). Although serum adiponectin levels did not change significantly in both groups, leptin levels significantly decreased in MetS group (from 18.5 ng/mL to 16.6 ng/mL, p = 0.004), but not in Non-MetS group (from 9.2 ng/mL to 9.0 ng/mL, p = 0.917). Conclusion Pemafibrate is as efficient in patients with MetS as in patients without MetS in improving the lipid and glucose metabolism. In addition, the use in MetS patients may be more effective in improving liver function and insulin resistance.

Correlation of Plasma Adiponectin Levels and Adiponectin Gene Polymorphisms with Idiopathic Atrial Fibrillation

Introduction: Adiponectin is a cellular protein secreted by adipocytes, which is closely related to a variety of diseases, including atrial fibrillation (AF). Idiopathic atrial fibrillation (IAF) is defined as AF without hypertension, diabetes, and other underlying diseases. Genetic polymorphism of adiponectin affects serum adiponectin concentration. However, the association of serum adiponectin concentration and its genetic polymorphism with IAF has not been studied. This study investigated the relationship between serum levels of adiponectin, adiponectin gene polymorphisms, and the risk of developing IAF in a Chinese Han population. Methods: Patients with IAF (n = 172, IAF group) and healthy individuals (n = 150, control group) were consecutively and randomly recruited and fasting peripheral blood samples were collected. All participants were examined for serum adiponectin concentrations and the polymorphisms SNP45T>G (SmaI locus, rs2241766) and SNP276G>T (BsmI locus, rs1501299) of the adiponectin gene were genotyped using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Related clinical data from the two groups were also collected. Results: Plasma adiponectin levels in the IAF group were significantly lower than those in the control group (9.9 ± 2.6 mg/L vs. 16.1 ± 7.0 mg/L, p = 0.006). There were no significant differences among the three genotypes (wild type, mutant heterozygote, and homozygote) of SNP45T>G or SNP276G>T in the prediction value of IAF. The frequency of the T allele of SNP45 T>G was 70.3% in the IAF group and significantly different from that of the control group (71.3%; p = 0.02). In the case of SNP276G>T, the frequency of the G allele was 68.61% in patients with IAF compared to 73.34% in the control group (p = 0.35). Furthermore, a comparison of the clinical data of individuals in the two groups revealed that the left atrial diameter (LAD) in patients in the IAF group was obviously higher than that in the control group (43.3 ± 6.7 mm vs. 37.9 ± 5.1 mm, respectively; p < 0.001). The left ventricular ejection fraction (LVEF) in the IAF group was obviously reduced than that in the control group (54.7 ± 11.9% vs. 60.2 ± 5.6%, respectively; p < 0.001). Conclusions: Low plasma adiponectin levels were significantly associated with IAF. Hypoadiponectinemia can thus serve as an important factor for the incidence of IAF. The genotypes of SNP45T>G and SNP276G>T in the adiponectin gene may not correlate with the occurrence of IAF. However, our results demonstrate that the T allele of SNP45T>G may be responsible for IAF development in the Chinese Han population.

Abstract 11649: Serum Adiponectin Levels Correlate With Atrial PPARγ and TGFβ1 mRNA Expression in Patients Receiving Cardiac Surgery: Involvement of PPARγ on Atrial Fibrotic Remodeling

Introduction: The peroxisome proliferator-activated receptor gamma (PPAR γ) plays important roles in regulating processes related to fibrogenesis. On the other hand, adiponectin, a marker for PPARγ activity, is a hormone involved in maintaining energy homeostasis, and exerts anti-profibrotic effects in various organs. However, the roles of PPARγ and adiponectin on atrial fibrotic remodeling are still unknown. Hypothesis: We investigated the association of serum adiponectin levels and atrial gene expression of adiponectin, PPARγ and fibrosis-related genes in cardiovascular surgery patients including heart valve disease. Methods: Atrial mRNA expression levels including adiponectin and PPARγ were analyzed by real-time reverse transcription polymerase chain reaction (RT-PCR) in 59 cases (sinus rhythm (SR) 24 patients, atrial fibrillation (AF) 35 patients) in which left atrium (LA) tissues were removed from the appendage during surgery. The immunohistochemical studies were used to identify the protein expression. The serum levels of adiponectin were measured by ELISA. Results: The immunohistochemical staining showed the expression of adiponectin, PPARγ and PPARα. The significant correlations were observed among the mRNA expression levels of extracellular matrix (ECM) (COL1A1, COL3A1, fibronectin) and the fibrosis-related genes such as TGFβ1, TIMP1, MMP2, NOX2, CTGF and PDGFD attributed to the fibrosis of myocardium. The mRNA expression level of PPARγ, but not PPARα, positively correlated with that of the ECM and the fibrosis-related gene expression level. The mRNA expression level of adiponectin also positively correlated with that of ECM. Patients with AF had higher atrial expression level of adiponectin, PPARγ, COL1A1 and TGFβ than those with SR. Serum adiponectin levels significantly correlated with atrial mRNA expression level of PPARγ and TGFβ1. Patients with AF had serum higher levels of adiponectin than those with SR. Conclusions: Atrial PPARγ and adiponectin associate with atrial fibrotic remodeling in cardiovascular surgery patients. Serum adiponectin levels correlate with atrial PPARγ and TGFβ1 mRNA expression, and might have potential utility as a biomarker in atrial fibrotic remodeling.

Serum Tsukushi Level Is Associated With the Severity of Liver Fibrosis Independent of Type 2 Diabetes.

Tsukushi (TSK) is a recently identified hepatokine, and we aimed to investigate the association between systemic TSK and the severity of nonalcoholic fatty liver disease (NAFLD) in subjects with and without type 2 diabetes mellitus (DM). Three hundred ninety-three DM and 289 without DM individuals were recruited for transient elastography assessment to determine liver steatosis and fibrosis. Serum TSK was measured by ELISA. The presence of NAFLD was defined as controlled attenuation parameter ≥ 248 dB/m. NAFLD was present in 276 (70.2%) and 129 (44.6%) subjects with and without DM respectively, and they had higher serum TSK levels than those without NAFLD [DM group: 91.0 ng/mL (61.7-133.8) vs 82.5 (60.9-118.5), P < .01 respectively; without DM group: 97.1 ng/mL (69.3-148.6) vs 80.8 (53.4-111.6) respectively, P < .01]. Univariate analysis showed that serum TSK significantly correlated with the degree of steatosis and fibrosis both in subjects with and without DM. On multivariable regression analysis, only liver stiffness and estimated glomerular filtration rate were significant determinants of TSK level, and the relationship was independent of diabetes and serum adiponectin. Out of 405 subjects with NAFLD, 49 had either advanced fibrosis or cirrhosis. The area under receiver operating characteristic curve of serum TSK to indicate advanced fibrosis or cirrhosis was 0.70 (95% CI .62-.77), which was significantly better than that of fibrosis-4 index, 0.64 (95% CI .55-.72), P < .05. Serum TSK levels were increased in subjects with NAFLD and reflected the severity of liver fibrosis.

Adiponectin restores the obesity-induced impaired immunomodulatory function of mesenchymal stromal cells via glycolytic reprogramming

Obesity has been known to negatively modulate the life-span and immunosuppressive potential of mesenchymal stromal cells (MSC). However, it remains unclear what drives the compromised potency of obese MSC. In this study, we examined the involvement of adiponectin, an adipose tissue-derived hormone, in obesity-induced impaired therapeutic function of MSC. Diet-induced obesity leads to a decrease in serum adiponectin, accompanied by impairment of survival and immunomodulatory effects of adipose-derived MSC (ADSC). Interestingly, priming with globular adiponectin (gAcrp) improved the immunomodulatory potential of obese ADSC. Similar effects were also observed in lean ADSC. In addition, gAcrp potentiated the therapeutic effectiveness of ADSC in a mouse model of DSS-induced colitis. Mechanistically, while obesity inhibited the glycolytic capacity of MSC, gAcrp treatment induced a metabolic shift toward glycolysis through activation of adiponectin receptor type 1/p38 MAPK/hypoxia inducible factor-1α axis. These findings suggest that activation of adiponectin signaling is a promising strategy for enhancing the therapeutic efficacy of MSC against immune-mediated disorders.

Associations between nutritional intake, stress and hunger biomarkers, and anxiety and depression during the treatment of anorexia nervosa in adolescents and young adults

Adolescents and young adults (AYA) with anorexia nervosa (AN) frequently have co-occurring anxiety and depression, which can negatively impact prognosis. To inform treatment of co-occurring anxiety and depression, we assessed the association of nutritional intake and hunger/stress hormones on anxiety and depression using a six-month longitudinal study of 50 AYA females receiving care for AN. At baseline and six months, we measured anxiety (Spielberger State/Trait Anxiety Inventory [STAI]), depression (Beck Depression Inventory [BDI]), body mass index (BMI), 3-day dietary intake (total calories and proportion of fat, carbohydrate, protein), and serum cortisol, leptin, and adiponectin. We performed mixed effects linear regression analyses, adjusting for age, duration of AN, and percentage of median BMI (%mBMI). At baseline, median age was 16.3 (interquartile range [IQR] = 2.5) years, duration of AN was 6 (IQR = 8.8) months and %mBMI was 87.2 (IQR = 10.5)%. Fifty-six percent had clinically significant anxiety; 30 % had depression. Over 6 months, participants had significant improvements in %mBMI (+2.2[IQR = 9.2]%, p < .01), STAI (−9.0[IQR = 25.0], p < .01), and BDI (−5.0[IQR = 13.8], p < .01) scores. Participants with larger improvements in caloric intake had greater improvements in STAI (p = .03) and BDI scores (p = .04). Larger improvement in BDI was significantly associated with increased fat intake (p < .01), but not carbohydrate or protein intake. Change in STAI was not associated with changes in fat, carbohydrate, or protein intake. Changes in STAI or BDI scores were not associated with changes in cortisol, leptin, or adiponectin. Increased caloric intake may augment treatment of co-occurring anxiety and depression, and increased fat intake may improve depression for AYA with AN.

LRRK2 negatively regulates glucose tolerance via regulation of membrane translocation of GLUT4 in adipocytes.

Epidemiological studies have shown that abnormalities of glucose metabolism are involved in leucine-rich repeat kinase 2 (LRRK2)-associated Parkinson's disease (PD). However, the physiological significance of this association is unclear. In the present study, we investigated the effect of LRRK2 on high-fat diet (HFD)-induced glucose intolerance using Lrrk2-knockout (KO) mice. We found for the first time that HFD-fed KO mice display improved glucose tolerance compared with their wild-type (WT) counterparts. In addition, high serum insulin and leptin, as well as low serum adiponectin resulting from HFD in WT mice were improved in KO mice. Using western blotting, we found that Lrrk2 is highly expressed in adipose tissues compared with other insulin-related tissues that are thought to be important in glucose tolerance, including skeletal muscle, liver, and pancreas. Lrrk2 expression and phosphorylation of its kinase substrates Rab8a and Rab10 were significantly elevated after HFD treatment in WT mice. In cell culture experiments, treatment with a LRRK2 kinase inhibitor stimulated insulin-dependent membrane translocation of glucose transporter 4 (Glut4) and glucose uptake in mouse 3T3-L1 adipocytes. We conclude that increased LRRK2 kinase activity in adipose tissue exacerbates glucose tolerance by suppressing Rab8- and Rab10-mediated GLUT4 membrane translocation.

The Association among Urinary Lead and Cadmium, Serum Adiponectin, and Serum Apoptotic Microparticles in a Young Taiwanese Population.

Previous studies reported that lead (Pb) and cadmium (Cd) exposure are linked to changes in serum adiponectin; an adipokine that promotes glycolysis and inhibits gluconeogenesis to regulate glucose metabolism. However, no study has ever explored the relationship between exposure to these two heavy metals and adiponectin in adolescents and young adults. Additionally, the role of adiponectin in the relationship between Pb and Cd exposure and vascular endothelial cell apoptosis has never been investigated. In this study, 724 Taiwanese participants, aged 12 to 30 years, were enrolled to investigate the association among urinary lead and cadmium, serum adiponectin, and apoptotic microparticles (CD31+/CD42a-, CD31+/CD42a+, and CD14). The results of the current study revealed a statistically significant inverse association between urine Pb and Cd levels and adiponectin levels, as well as a positive association with apoptotic microparticles (CD31+/CD42a-, CD31+/CD42a+, and CD14). Adiponectin was also inversely correlated with CD31+/CD42a- and CD31+/CD42a+. Moreover, when subjects with both Pb and Cd levels above the 50th percentile were compared to those below it, the former group exhibited the lowest average adiponectin value. Additionally, a more pronounced positive association between heavy metals and apoptotic microparticles (CD31+/CD42a- and CD31+/CD42a+) was observed when adiponectin levels were lower. Furthermore, an interaction between adiponectin and heavy metals was identified in the relationship between these metals and CD31+/CD42a-. In conclusion, these findings suggest that Pb and Cd exposure may have an adverse effect on adiponectin, and it may play a role in the link between heavy metal exposure and the dysfunction of vascular endothelial cells. Future studies are needed to establish whether a causal relationship exists.

Association of Adipocytokines and Vitamin D Status in Tuberculosis

Leptin and Adiponectin are considered principal indicators of tuberculosis (TB). They are critical parts of the pathophysiological processes to which treatment can be applied. Thus, this research aimed at finding out the role of Adipocytokines and 25-dihydroxy vitamin D in the aetiology of tuberculosis. The research sample included (90) participants divided into (50) tuberculosis patients and (40) healthy subjects representing the control group who were age and sex-matched. Circulating levels of adipocytokines and 25- dihydroxy vitamin D were analysed by using ELISA techniques. Compared to the subjects of control group, tuberculosis subjects had significantly (P&lt;0.0001) lower levels of serum leptin (5.84±1.83 pg/mL) and vitamin D (2.77±0.52 ng/mL). However, compared to their control counterparts, tuberculosis patients had significantly (P&lt;0.0001) higher levels of adiponectin (16.30±1.23 ng/mL). The ROC curve analysis of Leptin, Adiponectin, and 25-dihydroxy vitamin D indicated a high diagnostic value in predicting the risk of tuberculosis. The present study findings revealed that elevated serum adiponectin with decreased serum leptin levels and hypovitaminosis D are strongly correlated with the pathogenesis and state of tuberculosis.

Correlation analysis of obesity phenotypes with leptin and adiponectin

Obesity can be categorized as metabolically healthy obesity (MHO) and metabolically unhealthy obesity (MUO). However, individuals with MHO are characterized by the absence of metabolic syndrome (MS) and appear to have lower inflammation levels compared to MUO. This study aimed to investigate the association of obesity phenotypes with leptin (LEP) and adiponectin (ADP). According to the inclusion and exclusion criteria, we selected 178 subjects from the previous cross-sectional survey. Based on the body mass index (BMI) and diagnostic criteria of MS, we divided the individuals into three groups, including healthy control group (HC group), metabolically healthy obesity group (MHO group) and metabolically unhealthy obesity group (MUO group). The concentrations of LEP and ADP in serum were measured, and the association of these two cytokines with different obesity phenotypes were subsequently analyzed. Compared to both the HC and MHO groups, the MUO group showed significantly higher BMI, waist circumference (WC), waist-hip ratio (WHR), triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), fasting plasma glucose (FPG), homeostasis model assessment of insulin resistance (Homa-IR) and blood pressure (P < 0.05). In contrast, serum high-density lipoprotein cholesterol (HDL-C) was notably lower in the MUO group (P < 0.05). ADP was found to have a positive correlation with systolic blood pressure (SBP) and a negative correlation with FPG in the MHO group. In the MUO group, LEP demonstrated a positive correlation with fasting insulin (FINS) and Homa-IR, while ADP showed a positive correlation with TC and SBP. Linear regression analysis further indicated that SBP (β = 0.234, P = 0.043), TG (β = − 0.292, P = 0.001) and LDL-C (β = 0.626, P = 0.000) were independently correlated with ADP, and BMI (β = 0.398, P = 0.002) was independently correlated with LEP in obese individuals. In conclusion, ADP and LEP were closely related with glucose and lipid metabolism in obese individuals, these two cytokines might play critical roles in obesity-associated metabolic disorders.

Involvement of the vagus nerve and hepatic gene expression in serum adiponectin concentrations in mice.

Several humoral factors, such as adiponectin and urate, have been suggested to affect metabolic syndromes. Previously, we reported a reduction in blood adiponectin concentrations after a high-fructose diet partially via the vagus nerve in rats. Although a lithogenic diet (LD), i.e., supplementation of a normal control diet (CT) with 0.6% cholesterol and 0.2% sodium cholate, reduced blood adiponectin concentrations, the involvement of the vagus nerve in this mechanism remains unclear. To estimate the involvement of the vagus nerve in the regulation of blood adiponectin concentrations using an LD, male imprinting control region mice that had been vagotomized (HVx) or only laparotomized (Sham) were administered a CT or an LD for 10weeks. Serum adiponectin concentrations in the Sham-LD, HVx-CT, and HVx-LD groups were reduced by half compared with the Sham-CT group. The hepatic mRNA levels of fibroblast growth factor 21 (Fgf21), which reportedly stimulates adiponectin secretion from white adipose tissue, were lower in the LD groups compared with the CT groups. HepG2 hepatoma cells showed that various bile acids reduced the mRNA expression of FGF21. Moreover, the LD increased serum urate concentrations and reduced hepatic expressions of the acyl-CoA oxidase 1 (Acox1) mRNA and glucokinase, suggesting insufficient regeneration of ATP from AMP. In conclusion, serum adiponectin concentration may be regulated via the vagus nerve in normal mice, whereas a reduction of hepatic Fgf21 mRNA by bile acids may also lower serum adiponectin levels. Moreover, the LD may promote hepatic AMP accumulation and subsequently increase the serum urate concentration in mice.

Adipokines in rheumatoid arthritis patients suffering glomerulonephritis

Background: Beside their eminent role in metabolic syndrome, white adipose tissue (WAT) derived adipokines might have a distinguished role in autoimmune and rheumatic diseases. In addition, increased level of many adipokines is observed in patients suffering glomerulonephritis. The status of adipokines was not studied in rheumatoid arthritis patients (RA) suffering glomerulonephritis (GN). Objective: To study serum level of adiponectin, leptin, and Visfatin in RA patients suffering GN in a trial to elucidate if they play a role on metabolic or endothelial function. Cases and methods: In this cross-sectional case control observational study, we compared serum level of adiponectin, leptin, and Visfatin in fifty RA patients (group I) in coparison to fifty RA cases suffering chronic GN (group II) and fifty normal control subjects. In addition, we looked for kidney function tests and 24 urine protein (UP), serum calcium, phosphorus, alkaline phosphatase (AP), 25 hydroxy vitamin D (25 OH vit. D), parathyroid hormone (PTH), C-reactive protein (CRP), interleukin 6(IL6), lipid profile, and Homa insulin resistanc (Homa IR). RA cases were further investigated for rheumatoid factor (RF), anti-cyclic citrullinated peptide (anti-CCP) carotid arteries intima media thickness (IMT), brachial artery flow mediated Dilation (BA-FMD), health assessment questionnaire (HAQ), disease activity score calculator (DASC), simple disease activity index (SDAI), and clinical disease activity index (CDAI). Percutaneous kidney biopsies were obtained in group II patients. Results: Serum adiponectin and Visfatin are significantly higher and serum leptin is significantly lower in Group II compared to group I and the control group (20.3 vs. 18.6 and 12.3, 24,5 vs. 20.9 and 9.8, and 3.6 vs. 4.6 and 7.8 ng/mL for median serum adiponectin, visfatin, and leptin in group II vs group I and control group respectively, P&lt;0.001 in all). Serum level of 25 (OH) vit D is significantly lower, while serum AP, PTH and Homa IR are significantly higher in group I compared to control subjects (18 vs. 37 ng/mL, 140.5 vs, 57 u/L, 63 vs 47.8 ng/mL, and 13.2 vs 4 respectively, P&lt;0.001 in all) whilst there is no significant difference in these parameters between the RA groups. BA-FMD is significantly lower in group II vs group I (3% vs 4%, P=0.02) but there are no significant differences between these two groups in IMT of carotid arteries, HAQ, DASC, SDAI or CDAI. Moreover, there is no difference in any of the studied parameters within patients of group II according to renal histopathology. Conclusion: Studied adipokines have no relation to metabolic or vascular complications of RA. Changes of serum adipokines in GN patients are unrelated to inflammation. This pilot study would stimulate further research looking for the possible role of different adipokines in GN complicating RA.

Serum and salivary adiponectin levels as predictive markers for diabetes mellitus in children with a family history of diabetes.

Diabetes mellitus (DM) is a chronic, metabolic condition marked by defects in insulin production, action, or both. Environmental and genetic factors can contribute to the onset of diabetes mellitus. Adiponectin, a hormone affecting pancreatic beta cell proliferation, has emerged as a potential indicator of diabetes risk. This cross-sectional study aimed to evaluate serum and salivary adiponectin levels as predictors of diabetes mellitus in children with/without a family history of diabetes mellitus. The study was conducted at Al-Zahra Hospital in Najaf city and included 125 children aged 5 to 16. Data on demographics, including name, age, and gender, were collected, and body mass index (BMI) was assessed. Serum and salivary adiponectin levels were measured and analyzed in relation to family history and BMI. Children with a family history of DM had high serum adiponectin (ADP) levels. Serum adiponectin levels were significantly higher in children with first-degree relatives having a history of diabetes mellitus, except for cases involving mothers and other relatives with diabetes mellitus history (p<0.05). Furthermore, serum adiponectin levels were higher in obese children. Salivary adiponectin levels were significantly elevated in children with a maternal family history of diabetes (p=0.01), while no significant correlation was found with BMI. A significant negative correlation (r=-0.180, p=0.05) between salivary and serum adiponectin concentrations was observed. Compared to children with a normal, healthy weight, children with obesity had decreased salivary adiponectin levels and increased serum adiponectin levels.