Serum Adiponectin Levels Research Articles

Adipocytokines and Inflammation in Patients and a Gerbil Model: Implications for Obesity-Related and Nonobese Diabetes.

Background: Obesity is a predisposing risk factor for type 2 diabetes mellitus (T2DM). Actually, not only obese/overweight but also nonobese/lean individuals may be prone to T2DM. This study is aimed at identifying the contribution of adipose tissue to the development of nonobese diabetes (NOD) and obese diabetes (OD). Methods: Serum samples from the nonobese nondiabetes (NOND, n = 47, age = 46.8 ± 8.4, BMI ≤ 23.9 kg/m2) controls, NOD (n = 48, age = 50.7 ± 6.5, BMI ≤ 23.9 kg/m2) and OD (n = 65, age = 49.8 ± 10.2, BMI ≥ 28 kg/m2) patients were utilized to measure the expression of metabolic indicators, adipocytokines, inflammatory factors. Different adipose depots from offspring with corresponding blood glucose and obesity levels of a spontaneously diabetic gerbil line with various degrees of diabetic penetrance and body weights were examined for adipocytokines and inflammation factors detected by ELISA and western blot. Adipose tissue volume and fat cell size of the gerbils were evaluated by magnetic resonance imaging and immunohistochemistry, respectively. Results: The study yielded four key findings. Firstly, in comparison to the NOD group, the OD group exhibited more severe insulin resistance (IR) and metabolic dysfunction in both patients and gerbils, attributed to higher visceral adipose tissue mass and larger fat cell sizes. Secondly, in gerbils, gonadal fat deposition was linked to obesity development, whereas kidney fat deposition correlated with obesity and diabetes occurrence. Thirdly, in both patients and gerbils, the interplay between adiponectin and leptin levels in serum may significantly influence the development of obesity and diabetes. Lastly, heightened expression of MCP3 in gerbils' kidney adipose tissue may serve as a pivotal factor in initiating obesity-associated diabetes. Conclusions: Our study, which may be considered a pilot investigation, suggests that the interaction of adipocytokines and inflammation factors in different adipose depots could play diverse roles in the development of diabetes or obesity.

Adiponectin Resistance in Obesity: Adiponectin Leptin/Insulin Interaction.

The adiponectin (APN) levels in obesity are negatively correlated with chronic subclinical inflammation markers. The hypertrophic adipocytes cause obesity-linked insulin resistance and metabolic syndrome. Furthermore, macrophage polarization is a key determinant regulating adiponectin receptor (AdipoR1/R2) expression and differential adiponectin-mediated macrophage inflammatory responses in obese individuals. In addition to decrease in adiponectin concentrations, the decline in AdipoR1/R2 messenger ribonucleic acid (mRNA) expression leads to a decrement in adiponectin binding to cell membrane, and this turns into attenuation in the adiponectin effects. This is defined as APN resistance, and it is linked with insulin resistance in high-fat diet-fed subjects. The insulin-resistant group has a significantly higher leptin-to-APN ratio. The leptin-to-APN ratio is more than twofold higher in obese individuals. An increase in expression of AdipoRs restores insulin sensitivity and β-oxidation of fatty acids via triggering intracellular signal cascades. The ratio of high molecular weight to total APN is defined as the APN sensitivity index (ASI). This index is correlated to insulin sensitivity. Homeostasis model of assessment (HOMA)-APN and HOMA-estimated insulin resistance (HOMA-IR) are the most suitable methods to estimate the metabolic risk in metabolic syndrome. While morbidly obese patients display a significantly higher plasma leptin and soluble (s)E-selectin concentrations, leptin-to-APN ratio, there is a significant negative correlation between leptin-to-APN ratio and sP-selectin in obese patients. When comparing the metabolic dysregulated obese group with the metabolically healthy obese group, postprandial triglyceride clearance, insulin resistance, and leptin resistance are significantly delayed following the oral fat tolerance test in the first group. A neuropeptide, Spexin (SPX), is positively correlated with the quantitative insulin sensitivity check index (QUICKI) and APN. APN resistance together with insulin resistance forms a vicious cycle. Despite normal or high APN levels, an impaired post-receptor signaling due to adaptor protein-containing pleckstrin homology domain, phosphotyrosine-binding domain, and leucine zipper motif 1 (APPL1)/APPL2 may alter APN efficiency and activity. However, APPL2 blocks adiponectin signaling through AdipoR1 and AdipoR2 because of the competitive inhibition of APPL1. APPL1, the intracellular binding partner of AdipoRs, is also an important mediator of adiponectin-dependent insulin sensitization. The elevated adiponectin levels with adiponectin resistance are compensatory responses in the condition of an unusual discordance between insulin resistance and APN unresponsiveness. Hypothalamic recombinant adeno-associated virus (rAAV)-leptin (Lep) gene therapy reduces serum APN levels, and it is a more efficient strategy for long-term weight maintenance.

Non-alcoholic fatty liver disease in obese subjects as related to increasing insulin resistance and deteriorating glucose control: Three years of follow-up from a longitudinal survey

PurposeThis observational trial was performed to evaluate liver parameters in overweight or obese subjects in the context of insulin resistance and glucose control over time.Subjects/MethodsInsulin resistance, glucose control and several parameters for liver integrity were monitored in 177 overweight (BMI > 28 kg/m2) subjects over a mean of 30 months. Volunteers were categorized according to insulin resistance (HOMAIR score) and glucose control in subjects with normal glucose control (NGT), impaired glucose control (IGT), or diabetes mellitus type 2 (T2DM). Liver fat and fibrosis were evaluated by sonographic elastography (FibroScan®) and clinical scores, such as the AST/ALT ratio, fatty liver index (FLI), and NAFLD fibrosis score (NFS).ResultsLiver fat fraction as estimated by the controlled attenuation parameter (CAP), and the FLI were significantly higher in subjects with T2DM compared to IGT and NGT. While fasting insulin levels and the HOMAIR score continuously increased over time, no change in CAP or FLI occurred during follow up. CAP was correlated with FLI (r = 0.50; p < 0.0001) and the HOMAIR score (r = 0.32; p < 0.0001). An inverse correlation was observed between serum adiponectin levels and FLI (r = -0.37; p < 0.0001), the HOMAIR score (r = -0.19; p < 0.001, and CAP (r = -0.15; p < 0.01).ConclusionsIn subjects with a BMI ≥ 28 kg/m2, liver fat fraction is significantly elevated in those with T2DM compared to IGT or NGT. Liver fat fraction is associated with deteriorating insulin sensitivity and loss of glucose control. Despite a continuous increase in insulin resistance, no change in liver fat content or stiffness occurred over 30 months.

Comparative Evaluation of Adipokine Metrics for the Diagnosis of Gestational Diabetes Mellitus.

Gestational diabetes mellitus (GDM) is one of the most common medical disorders in pregnancy. Adipokines, predominantly secreted by adipose tissue, are involved in numerous metabolic processes. The exact role of adipokines in the pathogenesis of GDM is still not well known, and numerous adipokines have been analysed throughout pregnancy and proposed as biomarkers of GDM. This study aimed to evaluate serum adiponectin, chemerin, lipocalin and apelin levels in GDM and non-GDM women, to assess them as clinically useful biomarkers of the occurrence of GDM and to demonstrate the correlation between the levels of the above adipokines in the blood serum and the increased risk of the development of GDM. The role of these adipokines in the pathogenesis of GDM was also analysed. The statistically significant differences between the levels of adiponectin (7234.6 vs. 9837.5 ng/mL, p < 0.0001), chemerin (264.0 vs. 206.7 ng/mL, p < 0.0001) and lipocalin (39.5 vs. 19.4 ng/mL, p < 0.0001) were observed between pregnant women with GDM and healthy ones. The diagnostic usefulness of the tested adipokines in detecting GDM was also assessed. The research results confirm the hypothesis on the significance of adiponectin, chemerin, lipocalin and apelin in the pathophysiological mechanisms of GDM. We speculate that these adipokines could potentially be established as novel biomarkers for the prediction and early diagnosis of GDM.

Experimental periodontitis induced hypoadiponectinemia by IRE1α-mediated endoplasmic reticulum stress in adipocytes

BackgroudHypoadiponectinemia is the important cause of insulin resistance. Recent studies have shown that periodontitis is associated with hypoadiponectinemia. The purpose of this study was to investigate the effect of periodontitis-induced endoplasmic reticulum stress (ERS) in visceral adipocytes on hypoadiponectinemia.MethodsRat periodontitis models were established by local ligation with silk around the bilateral maxillary second molars. Porphyromonas gingivalis-lipopolysaccharid (P.g-LPS) was also used to stimulate the visceral adipocytes in vitro. The protein expression levels of glucose regulated protein 78 (GRP78), inositol-requiring protein 1α (IRE1α), protein kinase RNA-like ER kinase (PERK), activating transcription factor 6 (ATF6) and adiponectin were detected. IRE1α lentiviruses were transfected into visceral adipocytes in vitro, and an IRE1α inhibitor (KIRA6) was injected in epididymal adipose tissue of rats to detect and verify the effect of ERS on adiponectin expression in visceral adipocytes in vivo.ResultsHypoadiponectinemia was observed in periodontitis rat, and the expression levels of ERS key proteins GRP78 and the phosphorylation levels of IRE1α (p-IRE1α)/IRE1α in visceral adipocytes were increased, while the expression levels of adiponectin protein were decreased. After KIRA6 injection into epididymal adipose tissue of rats with periodontitis, adiponectin levels in visceral adipocytes increased, and serum adiponectin levels recovered to a certain extent. The protein expression levels of GRP78 and p-IRE1α/IRE1α were increased and adiponectin protein expression was decreased in P.g-LPS-induced visceral adipocytes. Overexpression of IRE1α further inhibited adiponectin expression in P.g-LPS-stimulated visceral adipocytes, and conversely, IRE1α inhibition restored adiponectin expression.ConclusionsOur findings suggest that periodontitis induces ERS in visceral adipocytes leading to hypoadiponectinemia. IRE1α is a key protein regulating adiponectin expression in visceral adipocytes.

Anti-obesity activity of lactic acid bacteria-starter-based kimchi in high-fat diet-induced obese mice

Previously, lactic acid bacteria (LAB) and selected LAB-inoculated kimchi (SK) have anti-obesity activity in vitro. Herein, anti-obesity activity of SK was investigated in vivo. LAB-uninoculated kimchi (NK) and SK were orally administered (70 mg/kg) for 8 weeks to high-fat diet (HFD)-fed mice. The body weight, food efficiency rate (FER), and body composition were measured. Serum glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), adipocytokine, and lipid profiles and lipid accumulation levels were assessed. The effects of SK on microbiome changes were investigated. In kimchi groups, body weight, body fat, and organ weight and lipid profiles in low GOT and GPT levels significantly decreased (p < 0.05); serum adiponectin and leptin levels increased and decreased, respectively. Kimchi significantly decreased obesity-related gene expression and lipid accumulation (p < 0.05). Kimchi corrected HFD-induced gut microbiome imbalance, notably with more reliable recovery in the SK group. Its in vivo confirmed anti-obesity activity supports using kimchi's health functionalities.

Association of adiponectin gene expression with atrial fibrillation in a Pakistani populace

Adiponectin, an adipocytokine produced and secreted by adipose tissue, has anti-diabetic, anti-atherogenic, and anti-inflammatory properties. This case-control study was aimed to assess the expression and serum levels of adiponectin in subject suffereing from atrial fibrillation (AF). The study's subjects (n = 690) were enrolled from the Punjab Institute of Cardiology, Lahore and were grouped into control, AF without Metabolic syndrome (MetS), and AF with MetS groups. Along with the collection of demographic data, an analysis of adiponectin and biochemical parameters were performed. A highly significant difference in serum levels of adiponectin was observed among the control, AF without MetS, and AF with MetS groups (61.61 ± 45.30 ng/ml, 37.20 ± 19.46 ng/ml, 63.78 ± 61.69 ng/ml). The expression analysis of adiponectin was decreased (n-fold = ̴ 0.30) in AF without MetS group as compared to control group (n-fold = ~ 1.16) but increased in AF with MetS group (n-fold = ̴ 6.26). The correlation analysis revealed a highly significant positive relationship between the expression of the adiponectin gene with waist-to-hip ratio (WHR) in AF without MetS group. Whereas, serum adiponectin was negatively related to serum triglycerides (TG) in AF with MetS group. In multiple regression analysis using adiponectin expression as the dependent variable, WHR was a determinant in AF without MetS. Whereas, when serum adiponectin was used as the dependent variable, serum TG was the determinant in group AF with MetS. The present study implicates that decreased expression and serum levels of adiponectin were associated with the development of AF in which WHR and serum TG also contributed towards the onset of atrial fibrillation.

The effect of physical activity on cardiometabolic parameters in women with a history of hypertension during pregnancy

Background. The effect of physical activity (PA) on the state of the cardiovascular system and quality of life in patients with hypertension (HTN) remains insufficiently studied, while there is no data on the effect of PA and rehabilitation programs on cardiometabolic parameters, according to duration and recurrence of their effect in women with a history of HTN during pregnancy. Objective. To compare cardiometabolic parameters in women with a history of HTN during pregnancy versus women without HTN during pregnancy and measure the effects of an exercise program on their dynamics changes. Design and methods. The study included 66 women divided into two groups: group 1 — 33 women with a history of HTN during pregnancy. The distribution of different HTN disorders of pregnancy was the following: 75% — gestational HTN; 12,5% — chronic HTN; 12,5% — preeclampsia. Group 2 — 33 women with a history of normotension during pregnancy. Walking for at least 150 min per week (30 min a day, 5 times a week) for 9 months was a mandatory component of the physical training program in group 2. Women in group 2 continued clinical follow-up without physical training program. All participants filled in a specially designed questionnaire. Anthropometric, clinical, and biochemical parameters were evaluated, including PA level, quality of life (short questionnaire SF‑36), and serum leptin and adiponectin concentrations. Results. A PA training program for 9 months in women with a history of HTN during pregnancy led to a decrease in waist circumference and body mass index, a decrease in serum leptin levels and an increase in serum adiponectin levels, an increase in PA levels and an improvement in quality of life for account of the general physical and spiritual components.

A scientifically validated combination of garcinol, curcuminoids, and piperine for mild to moderate nonalcoholic steatohepatitis patients-results from a randomized, double-blind, placebo-controlled study.

Garcinol is a naturally occurring compound from the fruit rind of the Garcinia indica, with antioxidant, anti-inflammatory, and anticancer properties. Curcuminoids are the active molecule from the rhizome of Curcuma longa, studied extensively for its health benefits as an anti-inflammatory and antioxidant activities. Non-alcoholic steatohepatitis (NASH) is the progressive form of nonalcoholic steatohepatitis characterized by liver fat and inflammation. To evaluate the clinical efficacy and safety of Garcinol, Curcuminoids and piperine (GCP) combination in patients with mild to moderate NASH in a randomized, double-blind, placebo-controlled study. The patients received one tablet (450 mg) of GCP containing garcinol-50 mg, curcuminoids -250 mg and piperine 5 mg or a placebo (450 mg of microcrystalline cellulose) twice daily for 90 days. Changes in circulating aspartate aminotransferase (AST), alanine transaminase (ALT) levels, liver stiffness measurement (LSM), and controlled attenuation parameter (CAP) using Fibroscan were compared from baseline to day 90. Anthropometric parameters, serum levels of lipids, Interleukin (IL-6), hsCRP, and adiponectin were estimated. Safety was evaluated by laboratory parameters and by monitoring adverse events. Seventy-two patients were randomized and 63 (GCP = 32, Placebo = 31) completed the study. The mean age of the patients was 48.3 ± 8.7 years (36 males and 27 females). The mean reduction in AST (U/L) was 9.53 in GCP and 3.16 in placebo (p < 0.001) and that of ALT (U/L) was 13.47 in GCP and 7.43 in Placebo (p = 0.002). The liver stiffness and CAP scores showed a better reduction in GCP (0.56 kPa and 12.38 db/m) compared to placebo (0.064 kPa and 10.42 db/m) p < 0.05. Consequently, the noninvasive Fibroscan-AST (FAST) score reduction was also found to be significant in GCP compared to placebo. Additionally, body weight, lipid levels, hsCRP, and IL-6 in serum decreased, while adiponectin levels increased in GCP-supplemented participants compared to placebo. The combination of garcinol and curcuminoids was well tolerated with no significant changes in hematological and clinical laboratory parameters during the 90-day supplementation. Our results suggest that GCP could be a possible supplement for the management of NASH.Clinical trial registration: https://clinicaltrials.gov/, identifier CTRI/2019/11/022147.

Weight loss and vitamin D improve hyporesponsiveness to corticosteroids in obese asthma.

Obesity negatively impacts on asthma response to inhaled corticosteroids by unknown mechanisms. Objective: To demonstrate that the poor response to inhaled corticosteroids in obese asthma is associated with an impaired anti-inflammatory activity of corticosteroids and vitamin D deficiency, both improved by weight loss. 23 obese asthmatics (OA) [18 females; median age (interquartile range) 56 (51-59) years], 14 non-obese asthmatics (NOA) [11 females; 53 (43-60) years], 15 obese (O) [13 females; 47 (45-60) years], and 19 healthy controls (HC) [14 females; 43 (34-56) years] were enrolled. 10 OA and 11 O patients were evaluated at baseline (V1) and six months after (V2) bariatric surgery. Corticosteroid response was measured by dexamethasone inhibition of peripheral blood mononuclear cell (PBMC) proliferation. Lung function, serum levels of leptin, adiponectin, and vitamin D were measured at V1 and V2. We found a reduced response to dexamethasone in PBMCs of O and OA patients with respect to NOA and HC subjects, that inversely correlated with the diponectin/leptin ratio and vitamin D levels. Bariatric surgery improved corticosteroid responses in O and OA patients and normalized adiponectin/leptin ratio and vitamin D levels. Exposure of PBMCs to vitamin D potentiated the antiproliferative effects of corticosteroids. Dexamethasone and vitamin D induced similar MKP-1 expression in O and OA patients. We found a reduced response to dexamethasone in PBMCs of O and OA patients with respect to NOA and HC subjects, that inversely correlated with the adiponectin/leptin ratio and vitamin D levels. Bariatric surgery improved corticosteroid responses in O and OA patients and normalized adiponectin/leptin ratio and vitamin D levels. Exposure of PBMCs to vitamin D potentiated the antiproliferative effects of corticosteroids. Dexamethasone and vitamin D induced similar MKP-1 expression in O and OA patients.

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 &amp;lt; 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.

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.

CCN3/NOV serum levels in coronary artery disease (CAD) patients and its correlation with TNF-α and IL-6

IntroductionDysregulation in the secretion of adipokines or adipocytokines plays a significant role in triggering a pro-inflammatory state, leading to endothelial dysfunction and insulin resistance, and ultimately elevating the risk of atherosclerosis and coronary artery disease (CAD). Previous studies have shown a link between NOV/CCN3 (an adipokine) and obesity, insulin resistance, and inflammation. However, no research has explored the relationship between CCN3 serum levels and CAD. Therefore, we conducted the first investigation to examine the correlation between CCN3 and CAD risk factors in patients.MethodsIn a case-control study, we measured the serum levels of CCN3, IL-6, adiponectin, and TNF-α in 88 angiography-confirmed CAD patients and 88 control individuals using ELISA kits. Additionally, we used an auto analyzer and commercial kits to measure the biochemical parameters.ResultsIn patients with CAD, the serum levels of CCN3, TNF-α, and IL-6 were significantly higher compared to the control group, whereas lower levels of adiponectin were observed in the CAD group (P < 0.0001). A positive correlation was found between CCN3 and IL-6 and TNF-α in the CAD group ([r = 0.38, P < 0.0001], [r = 0.39, P < 0.0001], respectively). A binary logistic regression analysis showed the risk of CAD in the model adjusted (OR [95% CI] = 1.29 [1.19 − 1.41]), (P < 0.0001). We determined a cut-off value of CCN3 (3169.6 pg/mL) to distinguish CAD patients from the control group, with good sensitivity and specificity obtained for this finding (83.8% and 87.5%, respectively).ConclusionThis study provides evidence of a positive association between CCN3 serum levels and CAD, as well as inflammation markers such as IL-6 and TNF-α. These findings suggest that CCN3 may serve as a potential biomarker for CAD, and further investigations are necessary to validate this association and explore its potential use in clinical settings.

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.