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BackgroundWeight and waist gain are significant concerns in adulthood. Both weight and waist gain are particularly important among South Asians, known to have an increased risk of developing chronic cardiometabolic complications at any body mass index compared to other racial and ethnic groups. The aim of this study was to investigate factors predicting weight and waist gain in a longitudinal cohort of South Asians living in the US (United States).MethodsThis was a prospective analysis using data from exam 1 (2010-2013) and exam 2 (2015-2018) of the Mediators of Atherosclerosis in South Asians Living in America (MASALA) study, a prospective cohort study of South Asians (recruited from San Francisco and Chicago), with a mean 4.8 years of follow-up.ResultsOf 634 participants studied (42.7 % women, mean age 55 years, BMI 25.7 kg/m2, weight 70.4 kg at exam 1), 34.7 % had gained ≥5 % weight and 32.3 % gained ≥5 % waist at exam 2. In the adjusted models, older age, higher number of years of US residence, and having diabetes were associated with lower odds of weight gain; being female and having higher adiponectin were associated with higher odds of weight gain. Being female and being employed full/part time or being retired predicted lower likelihood of waist gain. Being single, separated/divorced, having a higher leptin and a higher C-reactive protein level predicted higher likelihood of waist gain.ConclusionsThe current study identified several social, demographic, and clinical factors that can serve as targets for obesity interventions among US South Asians. In addition, this study also raises hypotheses about associations of adipokine levels with weight and waist gain.

Mutations in the adiponectin receptor 1 gene (AdipoR1) lead to retinitis pigmentosa and are associated with age-related macular degeneration. This study explores the effects of AdipoR1 gene deficiency in mice, revealing a striking decline in ω3 polyunsaturated fatty acids (PUFA), an increase in ω6 fatty acids, and elevated ceramides in the retina. The AdipoR1 deficiency impairs peroxisome proliferator-activated receptor α signaling, which is crucial for FA metabolism, particularly affecting proteins associated with FA transport and oxidation in the retina and retinal pigmented epithelium. Our lipidomic and proteomic analyses indicate changes that could affect membrane composition and viscosity through altered ω3 PUFA transport and synthesis, suggesting a potential influence of AdipoR1 on these properties. Furthermore, we noted a reduction in the Bardet-Biedl syndrome proteins, which are crucial for forming and maintaining photoreceptor outer segments that are PUFA-enriched ciliary structures. Diminution in Bardet-Biedl syndrome-proteins content combined with our electron microscopic observations raises the possibility that AdipoR1 deficiency might impair ciliary function. Treatment with inhibitors of ceramide synthesis led to substantial elevation of ω3 LC-PUFAs, alleviating photoreceptor degeneration and improving retinal function. These results serve as the proof of concept for a ceramide-targeted strategy to treat retinopathies linked to PUFA deficiency, including age-related macular degeneration.

1. This study evaluated the effects and mechanisms of action of the peptide gADP3 on hepatic inflammatory injury induced by lipopolysaccharide (LPS).2. Hepatic inflammatory injury was induced in geese by intraperitoneal injection of LPS and gADP3, and the adiponectin receptor agonist AdipoRon (positive control) was used for potential amelioration. Serum inflammatory factor levels, liver function-related biochemical indicators and oxidative stress-related biochemical parameters in the liver tissues were determined. The expression levels of adiponectin and its receptors, inflammation and oxidative stress-related genes and key signalling molecules involved in adiponectin, inflammation and oxidative stress signalling pathways in liver tissues were detected.3. The peptide gADP3 alleviated inflammatory cell infiltration and hepatic inflammatory changes, reversed the decrease in serum albumin (ALB), total protein (TP), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) content or activity induced by LPS and increased the activity of the antioxidant enzymes CAT (catalase), SOD (superoxide dismutase) and GSH-Px (glutathione peroxidase).4. The peptide gADP3 upregulated the expression of antioxidant enzyme-related genes GCLC, HO-1 and NQO1 in liver tissues, decreased the levels of inflammatory factors like TNF-α, IL-1β, IL-6, IFN-γ and TGF-β and reduced mRNA expression levels of inflammatory-related genes TNF-α, IL-1β, iNOS and TGF-β. Additionally, it increased the mRNA and protein expression levels of adiponectin and its receptors, as well as key molecules in the adiponectin signalling pathway like AMPK and PPARα. In addition, gADP3 reversed the changes in mRNA or protein expression of inflammatory and oxidative stress signalling pathway-related genes P38MAPK, NF-κBP65, TLR4 and Nrf2 in liver tissues caused by LPS treatment.5. In conclusion, goose-derived adiponectin peptide gADP3, similar to the adiponectin receptor agonist AdipoRon, attenuated LPS-induced hepatic inflammatory injury in geese. [ABSTRACT FROM AUTHOR]

Asthma is an autoimmune disorder characterized by chronic inflammation within the bronchial tubes of the respiratory system. Many cells and cellular elements contribute to the development of asthma, this causes the return of inflammatory cells that attack the respiratory system and cause wheezing, shortness of breath, chest tightness, coughing, and difficulty sleeping. This study was conducted to evaluate adiponectin and leptin levels and body mass index in asthma patients. The samples consisted of 120 volunteers divided into a patient group of 80 men and women with asthma (40 for each group) and a healthy group of 40 men and women as control groups (20 for each group). They were collected at Al-Zahra Center for Allergy and Asthma / Baghdad / Al-Karkh during the period from December 2022 to April 2023, and their ages ranged between (18 - 76) years after their clinical features were confirmed by a specialist doctor. The current results showed a significant increase in levels of both adiponectin and leptin and in body mass index (BMI) at (P ≤ 0.05) in the patient group compared to the healthy. [ABSTRACT FROM AUTHOR]

Objective: To determine the effect of Vitamin-D-supplementation on glycemic parameters: glucose levels in blood, insulin, HbA1c, HOMA-IR, and adiponectin in women with gestational diabetes. Methods: An experimental study was executed at PGMI/LGH of Lahore from June 2020 to June 2021, with 34 VitaminD-deficient women who had gestational diabetes (20–26 weeks). All were aged between 21–32 years, randomly and equally divided into controls and cases. Cases received 200,000 IU Vitamin-D-dose. Fasting blood was collected before as well as after treatment from each participant. Spectrophotometry and peroxidase method were used to estimate HbA1c and glucose concentrations respectively. Insulin, adiponectin, and Vitamin-D were assessed by ELISA. To verify data normality, the Shapiro-Wilk test was applied and to prove group comparison Mann-Whitney U, Wilcoxon signedrank, and Sample-t tests were used via IBM-SPSS version-21. Results: No difference in blood glucose was found between controls and cases before treatment (p=0.858), while post-treatment, significant reduction found in cases (p=0.019). Before treatment, no difference was noticed in insulin levels of both groups (p=0.44), however, post-treatment, a significant decline was expressed in cases (p=0.001). No difference was found in HOMA-IR between controls and cases before treatment (p=0.14) but post-treatment, significant reduction was observed in cases (p=0.001). Non-significant difference was noted in HbA1c before (p=0.664) and after (p=0.169) treatment in both groups. Non-significant upsurge in adiponectin was observed in cases before (p=0.544) and after (p=0.194) treatment. Conclusion: Vitamin-D supplementation significantly improves glycemic control in gestational diabetic women, however, its effect on adiponectin was non-significant. [ABSTRACT FROM AUTHOR]

Purpose: Niacin (nicotinic acid), known for its lipid-modifying effects, has been explored for its potential anti-inflammatory properties and potential to affect adipokines secretion from adipose tissue. The aim of this systematic review and meta-analysis was to assess the effects of niacin on inflammatory markers and adipokines. Methods: A comprehensive search was conducted across five databases: PubMed, Scopus, Cochrane Library, Embase, and ISI Web of Science. Randomized controlled trials exploring the effects of niacin on inflammatory markers (CRP, IL-6, TNF-α) and adipokines (Adiponectin, Leptin) were included. Pooled effect sizes were analysed using a random-effects model, and additional procedures including subgroup analyses, sensitivity analysis and dose-response analysis were also performed. Results: From an initial 1279 articles, fifteen randomized controlled trials (RCTs) were included. Niacin administration demonstrated a notable reduction in CRP levels (SMD: -0.88, 95% CI: -1.46 to -0.30, p = 0.003). Subgroup analyses confirmed CRP reductions in trials with intervention durations ≤ 24 weeks, doses ≤ 1000 mg/day, and elevated baseline CRP levels (> 3 mg/l). The meta-analysis of IL-6 and TNF-α revealed significant TNF-α reductions, while IL-6 reduction did not reach statistical significance. Niacin administration also substantially elevated Adiponectin (SMD: 3.52, 95% CI: 0.95 to 6.1, p = 0.007) and Leptin (SMD: 1.90, 95% CI: 0.03 to 3.77, p = 0.04) levels. Conclusion: Niacin treatment is associated with significant reductions in CRP and TNF-α levels, suggesting potential anti-inflammatory effects. Additionally, niacin positively influences adipokines, increasing Adiponectin and Leptin levels. These findings provide insights for future research and clinical applications targeting inflammation and metabolic dysregulation. [ABSTRACT FROM AUTHOR]

Introduction: Adiponectin is a factor secreted by adipocytes and has been shown to play an important role in many physiological and pathological processes. Previous studies have shown that adiponectin levels are closely related to the occurrence and prognosis of ischemic stroke, but the results of different studies are conflicting. Therefore, this study aimed to update the data in this area to explore the relationship between adiponectin levels and the occurrence and prognosis of ischemic stroke. Results: After searching 762 records, 14 studies were finally included, including 10 studies on the incidence of ischemic stroke and 4 studies on the prognosis of patients with ischemic stroke. The results of Meta-analysis showed that the correlation between the level of adiponectin and the occurrence and prognosis of ischemic stroke was not significant. The risk of ischemic stroke was not significantly changed in the population with high adiponectin levels (pooled RR=1.00, 95% CI=0.86-1.16, P=1.00). Similarly, there was no significant difference in all-cause mortality among those with high adiponectin levels compared with ischemic stroke patients with low adiponectin levels (pooled RR 0.61, 95% CI 0.47-0.80). However, significant heterogeneity was found during the meta-analysis, P<0.0001; I2=72% and P<0.0001; I2=88%, respectively. Subgroup analysis showed that factors such as study design, follow-up time and publication time could partly explain this heterogeneity. Conclusions: In conclusion, adiponectin level is not significantly correlated with the occurrence and prognosis of ischemic stroke, suggesting that adiponectin level may not be used as a potential biomarker for ischemic stroke risk assessment and patient prognosis prediction. [ABSTRACT FROM AUTHOR]

Diabetes is a chronic metabolic disease which has affected approximately 10,5% of the global population (1).The most common forms of diabetes are: type I diabetes, insulin dependent, or youth type, and type II diabetes, or non-insulin dependant, also adulthood diabetes.Fructose effect on carbohydrate, adiponectin, insulin and other metabolic parameters metabolism. The role of interleukin 6 (IL-6) in mechanism of insulin resistency and diabetes and the role of tumor necrosis factor (TNF- α) in mechanisms of obesity, insulin resistance and pre-diabetes.128 Adult rats (3 months of age), Wistar species of both genders, weighting 160-180g and 65 white young rats (10-25 days) weighting 45-60g were taken for purposes of this study. The number of experimental animals in individual groups is between 5-8 while the details are added in the results section. The application of palm oil was conducted through special probe using oral administration straight into gastro-intestinal system. Figure 1 shows the differences of TNF-α after palm oil administration. There are statistically significant raised levels of this cytokines in blood of both young and adult rats compared to control cases. In Figure 2 it is emphasized the effect of palm oil (30 and 60 days) in IL-6 blood levels of young and adult male rats. Figure 3 shows the impact of palm oil, applied 30 and 60 days respectively against GTT of adult rats of male gender. The results of GTT studies on young rats are shown in Figure 4. They show the differences in GTT, which are statistically significant in day 60 compared to 30 days of palm oil treatment. Elongated administration 60 days of palm oil in experimental rats of adult and young rats, raise the blood levels of TNF-α and IL-6, thus changing metabolism of carbohydrates with data supporting pre-diabetic conditions. [ABSTRACT FROM AUTHOR]

The list of standard abbreviations for JDS is available at adsa.org/jds-abbreviations-24. Nonstandard abbreviations are available in the Notes. Reduced feed intake in early lactation prompts increased fat mobilization to meet dairy cow energy needs for milk production. The increased lipolysis in cows presents significant health risks with unclear mechanisms. The objectives of our study were to compare the longitudinal profiles of metabolites and lipids of serum from high- and low-lipolysis cows. Forty multiparous Holstein dairy cows were enrolled in the retrospective study. Serum samples were collected on d 7 before expected calving, as well as on d 5, 7, 14, and 21 postpartum. Dairy cows were grouped according to mean serum nonesterified fatty acids on d 5 and 7 after parturition as low (<0.600 mmol/L; n = 8; LFM) and high (>0.750 mmol/L; n = 8; HFM), indicating fat mobilization during early lactation. Lactational performance and serum metabolic parameters related to glucose and lipid metabolism, liver functions, oxidative status, and inflammatory responses were determined. Serum samples were subjected to liquid chromatography-MS-based metabolomics and lipidomics. Despite differences in postpartum BW change, there were no observed variations in milk yield and composition between the 2 groups. Serum β-hydroxybutyric acid, glucose, leptin, aspartate aminotransferase, IL-6, and tumor necrosis factor alpha were greater in cows with HFM than in cows with LFM. Serum adiponectin, revised quantitative insulin sensitivity check index, and albumin were lower in cows with HFM than in cows with LFM. Intensified fat mobilization in the HFM cows came along with reduced estimated insulin sensitivity, impaired liver functions, and increased oxidative stress and inflammatory responses. Differences in metabolic patterns were observed across the transition period when comparing serum blood matrixes (e.g., in different amino acids, acylcarnitines, and sphingolipids). The serum metabolome of the HFM cows was characterized by higher concentrations of glycine, acylcarnitines, carnosine, Cer(d20:0/18:0), Cer(d18:1/16:0), and Cer(t18:0/24:0) compared with LFM cows. The differential serum metabolites and lipids at different sampling times during the peripartum period were enriched in the sphingolipid metabolism. Differences in serum metabolic status parameters suggest that cows adopt varied metabolic adaptation strategies to cope with energy deficits postpartum. Our investigation found a comprehensive remodeling of the serum metabolic profiles in transition dairy cattle, highlighting the significance of alterations in sphingolipid species, as they play a crucial role in insulin resistance and metabolic disorders. [ABSTRACT FROM AUTHOR]

AdipoRon is an adiponectin receptor 1, 2 (ADIPOR1 and ADIPOR2) agonist with potential antifibrotic effects. Whether AdipoRon can mitigate joint stiffness in a rabbit model of arthrofibrosis is unknown. We examined the efficacy of intravenous (IV) AdipoRon at mitigating contracture in a rabbit model of knee arthrofibrosis. Fifty‐six female New Zealand White rabbits were divided into three dosing groups: vehicle (dimethyl sulfoxide, DMSO), 2.5 mg/kg AdipoRon, and 5 mg/kg AdipoRon. AdipoRon, in DMSO, was administered IV preoperatively and for 5 days postoperatively (30 rabbits, Aim 1). AdipoRon was again dosed similarly after Kirschner wire (K‐wire) removal at 8 weeks (26 rabbits; Aim 2). The primary outcome of joint passive extension angle (PEA,°) was measured at 8, 10, 12, 16, and 24 weeks following index surgery. At 24 weeks, rabbits were euthanized and limbs were harvested to measure posterior capsular stiffness (N cm/°). In Aim 1, the 5 mg/kg treated rabbits had a significant increase in PEA when compared to controls at 16‐week (p < 0.05). In Aim 2, the 5 mg/kg treated rabbits had a significant increase in PEA when compared to controls at 10‐week (p < 0.05). In both aims, no significant differences were observed at later time points. Capsular stiffness was no different in any group. We are the first to report the efficacy of IV AdipoRon in a rabbit model of arthrofibrosis. We identified a significant dose‐dependent decrease in joint PEA at early time points; however, no differences were observed between groups at later time points. Clinical Significance: The present investigation provided the first assessment of AdipoRon's efficacy in mitigating knee stiffness in the current gold standard rabbit model of arthrofibrosis. Results of this investigation provided further evidence as to the potential role of AdipoRon as a preventative for arthrofibrosis in large mammals. [ABSTRACT FROM AUTHOR]

Adipose tissues produce a variety of biologically active compounds, including cytokines, growth factors and adipokines. Adipokines are important as they function as endocrine hormones that are related to various metabolic and reproductive diseases. The goal of this review was to summarise the role of asprosin, a recently discovered adipokine, and compare its role in ovarian steroidogenesis with that of other adipokines including adiponectin, leptin, resistin, apelin, visfatin, chemerin, irisin, and gremlin 1. The summary of concentrations of these adipokines in humans, rats and other animals will help researchers identify appropriate doses to test in future studies. Review of the literature indicated that asprosin increases androstenedione production in theca cells (Tc), and when cotreated with FSH increases oestradiol production in granulosa cells (Gc). In comparison, other adipokines (1) stimulate Gc oestradiol production but inhibit Tc androgen production (adiponectin), (2) inhibit Gc oestradiol production and Tc androstenedione production (leptin and chemerin), (3) inhibit Gc steroidogenesis with no effect on Tc (resistin), (4) inhibit Gc oestradiol production but stimulate Tc androgen production (gremlin 1), and (5) increase steroid secretion by Gc, with unknown effects on Tc steroidogenesis (apelin and visfatin). Irisin has direct effects on Gc but its precise role (inhibitory or stimulatory) may be species dependent and its effects on Tc will require additional research. Thus, most adipokines have direct effects (either positive or negative) on steroid production in ovarian cells, but how they all work together to create a cumulative effect or disease will require further research. Adipose tissues produce a variety of biologically active compounds including adipokines, which function as endocrine hormones that are linked to various metabolic and reproductive diseases. The goal of this review was to provide an up-to-date summary of the role of some of these adipokines in mammalian reproduction and how they regulate ovarian steroid production. Understanding the effects of these adipokines on ovarian function will help formulate solutions for improved reproductive efficiency. Image by Leon Spicer. [ABSTRACT FROM AUTHOR]

• What is the primary question addressed by this study? In the largest study on the topic to date, we examined preoperative adipokine concentrations in circulation and the risks of postoperative delirium (POD) and cognitive dysfunction (POCD). • What is the main finding of this study? Lower free leptin was associated with an increased risk of POD during the hospital stay, although due to a large number of statistical analyses, we cannot rule out an influence of type I error. • What is the meaning of the finding? We present preliminary evidence for low leptin as a potential risk factor for POD. Perioperative neurocognitive disorders (NCD) are poorly characterized in terms of their risk factor profiles. Leptin and adiponectin are adipose-tissue-derived hormones with a role in inflammation and atherosclerosis whose function in perioperative NCD is unclear. Here, we used a cohort of older adults to examine the association of preoperative plasma concentrations of these biomarkers with the risk of perioperative NCD. Prospective analysis of 768 participants aged ≥ 65 years of the BioCog study. Blood was collected before surgery for measurement of plasma total and high-molecular-weight (hmw) adiponectin, leptin, and soluble leptin receptor (sOB-R). The free leptin index (FLI, leptin:sOB-R) was calculated. Postoperative delirium (POD) was assessed twice daily until postoperative day 7/discharge. Five hundred twenty-six patients (68.5%) returned for 3-month follow-up and provided data on postoperative cognitive dysfunction (POCD). POCD was defined as a decline on six neuropsychological tests that exceeded that of a nonsurgical control group. Logistic regression analyses examined the associations of each exposure with POD and POCD risk, in separate models adjusted for age, sex, fasting, surgery type, and body mass index (BMI). Of 768 patients, 152 (19.8%) developed POD. Of 526 attendants of the follow-up, 54 (10.3%) had developed POCD. Leptin, sOB-R, and total and hmw adiponectin were each not associated with POD. For POCD, we observed reduced risk in patients in FLI quartile 4 compared with quartile 1 (odds ratio, 0.26; 95% CI 0.08, 0.89). Sensitivity analyses for the outcome POD revealed statistically significant interaction terms of sOB-R and total adiponectin with obesity (BMI≥30kg/m2 versus BMI<30kg/m2). For the outcome POCD, a higher sOB-R was associated with an increased risk in the obese subgroup (odds ratio, 4.00; 95% CI 1.01, 15.86). We did not find consistent evidence for the role of leptin, its receptor, and total and hmw adiponectin in POD and POCD risk. Future research should be used to support or refute our findings and to fully characterize any differences in the associations of these hormones with POD/POCD between obese and nonobese individuals. [ABSTRACT FROM AUTHOR]

Purpose: Obesity may promote kidney damage through hemodynamic and hormonal effects. We investigated the association between body mass index (BMI), total body fat (TBF) and chronic kidney disease (CKD) and whether hypertension, diabetes, leptin and adiponectin mediated these associations. Methods: In this cross-sectional analysis of the Netherlands Epidemiology of Obesity study, 6671 participants (45–65 y) were included. We defined CKD as eGFR <60 ml/min/1.73 m2 and/or moderately increased albuminuria. The percentage of mediation was calculated using general structural equation modeling, adjusted for potential confounding factors age, sex, smoking, ethnicity, physical activity and Dutch healthy diet index. Results: At baseline mean (SD) age was 56 (6), BMI 26.3 (4.4), 44% men, and 4% had CKD. Higher BMI and TBF were associated with 1.08 (95%CI 1.05; 1.11) and 1.05-fold (95%CI 1.02; 1.08) increased odds of CKD, respectively. As adiponectin was not associated with any of the outcomes, it was not studied further as a mediating factor. The association between BMI and CKD was 8.5% (95%CI 0.5; 16.5) mediated by diabetes and 22.3% (95%CI 7.5; 37.2) by hypertension. In addition, the association between TBF and CKD was 9.6% (95%CI −0.4; 19.6) mediated by diabetes and 22.4% (95%CI 4.2; 40.6) by hypertension. We could not confirm mediation by leptin in the association between BMI and CKD (35.6% [95%CI −18.8; 90.3]), nor between TBF and CKD (59.7% [95%CI −7.1; 126.6]). Conclusion: Our results suggest that the relations between BMI, TBF and CKD are in part mediated by diabetes and hypertension. [ABSTRACT FROM AUTHOR]

Introduction: Children and young adults with congenital adrenal hyperplasia (CAH) are at increased risk of obesity and insulin resistance. There is evidence that children with CAH have increased visceral adiposity, which has been linked to metabolic syndrome and cardiovascular disease (CVD). The adipokine adiponectin has been shown to correlate with reduced metabolic risk, whereas the adipokines visfatin and leptin have been linked to visceral fat and adipocyte inflammation and can serve as biomarkers of increased metabolic risk. Few studies to date have characterized adipokine levels in children and young adults with congenital adrenal hyperplasia. We sought to investigate the relationship between adiponectin, leptin and visfatin levels to metabolic risk factors and androgen levels in children and young adults with CAH. Methods: Fasting blood was obtained for visfatin, leptin, adiponectin, glucose, insulin, CRP, lipid panel, total cholesterol (TC), triglycerides (TG) and HbA1c, as well as standard laboratory tests to assess adrenal control, from children with CAH due to 21-hydroxylase deficiency. HOMA-IR was calculated based on fasting glucose and insulin. Anthropomorphic measurements of BMI and waist-to-hip ratio were also obtained. Results: Adiponectin and androstenedione were inversely correlated (R = -0.57, p =0.016). There was a positive correlation between leptin and BMI percentile (R = 0.63, p <0.001) as well as leptin and HOMA-IR (R = 0.63, p <0.01). Glucocorticoid dose had a positive correlation with HOMA-IR (R=0.56, p = 0.021). Visfatin was inversely correlated with HDL cholesterol (R = -0.54, p = 0.026) and total cholesterol (R = -0.49, p <0.05). Overweight children and young adults had a significantly higher leptin (p = 0.02) and HOMA-IR (p=0.001) than non-overweight children and young adults. Conclusion: The inverse relationship between adiponectin and androstenedione suggests that better CAH control can reduce the risk of insulin resistance and metabolic syndrome. However, a high glucocorticoid dose appears to increase the risk of insulin resistance, underscoring the delicate balance required when treating CAH. [ABSTRACT FROM AUTHOR]

Biochemical recurrence is a process that progresses to castration-resistant prostate cancer (CRPC) and prediction of biochemical recurrence is useful in determining early therapeutic intervention and disease treatment. Prostate cancer is surrounded by adipose tissue, which secretes adipokines, affecting cancer progression. This study aimed to investigate the correlation between blood adipokines and CRPC biochemical recurrence. We retrospectively analyzed the clinical data, including preoperative serum adipokine levels, of 99 patients with pT3a pN0 prostate cancer who underwent proctectomy between 2011 and 2019. The primary outcome was biochemical recurrence (prostate-specific antigen: PSA > 0.2). We identified 65 non-recurrences and 34 biochemical recurrences (one progressed to CRPC). The initial PSA level was significantly higher (p = 0.006), but serum adiponectin (p = 0.328) and leptin (p = 0.647) levels and their ratio (p = 0.323) were not significantly different in the biochemical recurrence group compared with the non-recurrence group. In contrast, significantly more biochemical recurrences were observed in the group with adiponectin < 6 μg/mL and Leptin < 4 ng/mL (p = 0.046), initial PSA > 15 ng/mL, clinical Gleason pattern ≥ 4, and positive resection margin. A significant difference was also observed in the multivariate analysis (hazard ratio: 4.04, 95% confidence interval: 1.21–13.5, p = 0.0232). Thus, low preoperative serum adiponectin and high leptin levels were significantly associated with biochemical recurrence in adipose tissue-invasive prostate cancer, suggesting that they may be useful predictors of biochemical recurrence. Further studies with larger cases are needed to increase the validity of this study. [ABSTRACT FROM AUTHOR]

Women typically have less muscle mass and more fat mass than men, while at the same time possessing similar or even greater whole‐body insulin sensitivity. Our study aimed to investigate the molecular factors in primarily adipose tissue, but also in skeletal muscle, contributing to this sex difference. In healthy, moderately active premenopausal women and men with normal weight (28 ± 5 and 23 ± 3 years old; BMI 22.2 ± 1.9 and 23.7 ± 1.7) and in healthy, recreationally active women and men with overweight (32.2 ± 6 and 31.0 ± 5 years old; BMI 29.8 ± 4.3 & 30.9 ± 3.7) matched at age, BMI, and fitness level, we assessed insulin sensitivity and glucose tolerance with a hyperinsulinemic–euglycemic clamp or oral glucose tolerance test and studied subcutaneous adipose tissue and skeletal muscle samples with western blotting. Additionally, we traced glucose‐stimulated glucose disposal in adipose tissues of female and male C57BL/6J littermate mice aged 16 weeks and measured glucose metabolic proteins. Our findings revealed greater protein expression related to glucose disposal in the subcutaneous adipose tissue (AKT2, insulin receptor, glucose transport 4) and skeletal muscle (hexokinase II, pyruvate dehydrogenase) in women compared to matched men with normal weight and with overweight. This increased protein capacity for glucose uptake extended to white adipose tissues of mice accompanied with ~2‐fold greater glucose uptake compared to male mice. Furthermore, even in the obese state, women displayed better glucose tolerance than matched men, despite having 46% body fat and 20 kg less lean mass. In conclusion, our findings suggest that the superior potential for glucose disposal in female subcutaneous adipose tissue and skeletal muscle, driven by greater expression of various glucose metabolic proteins, compensates for their lower muscle mass. This likely explains women's superior glucose tolerance and tissue insulin sensitivity compared to men. [ABSTRACT FROM AUTHOR]

Human milk (HM) composition, including metabolic hormones and lipids, is influenced by various factors, including lactation stage and, potentially, infant sex, which may affect infant body composition (BC) development. We aimed to: (a) characterize the longitudinal concentration and intake profiles of HM leptin, adiponectin, insulin, and total lipids; (b) determine if their concentrations and intakes differ by infant sex; and (c) explore the intakes relationships with the development of infant BC. Milk samples (n = 501) were collected from 82 mother–infant dyads during the first 6 months postpartum. Infant 24 h HM intake was measured, and the average cumulative HM component intakes were calculated. The statistical analysis used linear mixed modeling. Intakes of HM leptin, adiponectin, insulin, and total lipids increased to 1 month postpartum and then remained stable. HM intake and total lipids intake but not hormone intakes were positively associated with infant BC (fat-free mass, fat-free mass index, fat mass, fat mass index, percentage fat mass, and fat mass to fat-free mass ratio). HM component concentrations and intakes did not differ by sex. These findings advance our understanding of the temporal nature of HM components, emphasizing the role of infant 24 h HM and total lipids intake in development of infant lean and adipose tissue. [ABSTRACT FROM AUTHOR]

Introduction: Filipino Americans (FAs) are at high risk for developing type 2 diabetes despite other Asian phenotypes. Evidence suggests that pro-inflammatory interleukin-18 (IL-18) and anti-inflammatory adiponectin biomarkers associated with visceral adipose tissue (VAT) may explain this risk. Objectives: This study aimed to quantify the biomarkers in relation to standard ranges of VAT or typical circulating concentration ranges reported in the literature of IL-18 and adiponectin, examine relationships of these markers, and determine if they were different among those participants without diabetes, prediabetes, and diabetes. Methods: A cross-sectional study was used to enroll FAs without diabetes, prediabetes, or diabetes. VAT was measured using the InBody 570© Body Composition Analyzer. Blood samples were obtained to assess plasma concentrations of IL-18 and adiponectin using enzyme-linked immunosorbent assay. All analyses were conducted using a 5% type I error rate. Mean ±SD and percentages were used to describe the sample and data where appropriate. Pearson's correlations (R) were calculated to determine the relationships between VAT and IL-18 in each group. Analysis of variance was used to determine differences in VAT, IL-18, and adiponectin among groups. Further, nonparametric procedures examined the differences in adiponectin among those within groups. Results: Seventy-five participants were enrolled. Biomarkers above the typical concentration range were observed for VAT, IL-18, and adiponectin. Adiponectin significantly differed among groups with lower values in the diabetes group vs. the nondiabetes group. Conclusions: The findings indicate that while inflammation-related biomarkers, such as adiponectin, correlate with VAT and may serve as indicators of increased risk of type 2 diabetes in FAs, correlation alone does not establish causality. [ABSTRACT FROM AUTHOR]

Aims Methods Results Conclusion Endothelin‐1 (ET‐1) is elevated in patients with obesity and adipose tissue of obese mice fed high‐fat diet (HFD); however, its contribution to the pathophysiology of obesity is not fully understood. Genetic loss of endothelin type B receptors (ETB) improves insulin sensitivity in rats and leads to increased circulating adiponectin, suggesting that ETB activation on adipocytes may contribute to obesity pathophysiology. We hypothesized that elevated ET‐1 in obesity promotes insulin resistance by reducing the secretion of insulin sensitizing adipokines, via ETB receptor.Male adipocyte‐specific ETB receptor knockout (adETBKO), overexpression (adETBOX), or control littermates were fed either normal diet (NMD) or high‐fat diet (HFD) for 8 weeks.RNA‐sequencing of epididymal adipose (eWAT) indicated differential expression of over 5500 genes (p < 0.05) in HFD compared to NMD controls, and changes in 1077 of these genes were attenuated in HFD adETBKO mice. KEGG analysis indicated significant increase in metabolic signaling pathway. HFD adETBKO mice had significantly improved glucose and insulin tolerance compared to HFD control. In addition, adETBKO attenuated changes in plasma adiponectin, insulin, and leptin that is observed in HFD versus NMD control mice. Treatment of primary adipocytes with ET‐1 caused a reduction in adiponectin production that was attenuated in cells pretreated with an ETB antagonist.These data indicate elevated ET‐1 in adipose tissue of mice fed HFD inhibits adiponectin production and causes insulin resistance through activation of the ETB receptor on adipocytes. [ABSTRACT FROM AUTHOR]

Adipocytokines are substances with endocrine functions produced by adipose tissue, playing crucial roles in regulating metabolic functions and inflammatory processes. Dysregulation of fatty tissue's endocrine functions and dysregulation of the production of adipocytokines such as adiponectin, leptin, fibroblast-stimulating factor, and others can lead to a low-grade systemic inflammation and an insulin resistance in patients. These conditions contribute to the pathophysiology of type 2 diabetes mellitus, atherosclerosis, arterial hypertension, metabolic syndrome, and other disorders. Conversely, these metabolic disorders exert feedback-regulatory effects on adipocytokines and their functions. Glomerulonephritis encompasses a group of immune-mediated diseases characterized by inflammation of the glomeruli. Diagnosis can involve examining urine sediment, detecting autoantibodies, and identifying immune complexes in the blood. However, a kidney biopsy is required for definitive confirmation of glomerulonephritis and is considered the gold standard and a necessity in diagnosis. Affecting the level of adipocytokines could be one of the new strategies for the pharmacological treatment of many diseases. Given a better understanding of their functions and molecular targets, adipocytokines may herald the emergence of new diagnostic approaches (1, 2). Monitoring the level of adipocytokines could contribute to a better patient management and thus become an auxiliary tool for predicting and diagnosing diseases. [ABSTRACT FROM AUTHOR]

Simple Summary: We studied a population of overweight and obese Chinese university students. Obesity, which was previously limited to the Western world, has emerged in Asia and China in recent years. Owing to the massive population of the Asian region, even effects on a small percentage of this population correspond to substantial problems. University students are an at-risk group for obesity due to the sedentary lifestyle imposed by their heavy study schedule. We measured the physical capacities, as well as several biochemical and behavioral variables, of Chinese students. We measured the blood levels of two multifunctional hormones, namely leptin (LEP) and adiponectin (ADPN), and levels of physical activity. We found that in obese students, physical capacities are linked with the hormone ADPN, which has been hypothesized to be linked with muscle development. We also found that sleep was associated with the blood levels of LEP and ADPN. To the best of our knowledge, our study is the first work to provide data on the association of LEP and ADPN with behavioral, physical, and biochemical variability in overweight and obese Asian populations. Such an association has potential for use as a comparison tool. The aim of this study is to assess the relationship of leptin (LEP) and adiponectin (ADPN) with other circulating fat markers, physical capacity, behaviors, and anthropometric indices in a population of overweight and obese Chinese university students. LEP and ADPN levels, as well as behavioral, anthropometric, biochemical, and performance characteristics, were measured. Method: A total of 17 anthropometric parameters, 8 questionnaires (investigating quality of life, sleep, eating, perceived functioning, stress, and depression), 9 biochemical parameters, and 12 functional parameters were investigated. Results: In contrast to previous studies, our work found an unusually strong relationship between LEP and ADPN (r = 0.961, p = 0.000) that can be related to ethnicity. We also found that LEP and ADPN were associated with stress and bodily pain. A total of 12 anthropometric measures were also associated with LEP/ADNP levels. Moreover, LEP and ADPN were found to be related to lower limb, hand, and abdominal strength; blood pressure; and basic metabolism. However, we did not find associations with sleep; eating habits; or cardiovascular fitness, which was measured in the form of resting heart rate and VO2max. Conclusion: This study reveals new relationships of LEP and ADPN with selected anthropometric and behavioral parameters in obese Chinese college students. [ABSTRACT FROM AUTHOR]

Despite some reported benefits, there is a low quality of evidence for resistance training (RT) improving metabolic health of individuals with overweight or obesity. We evaluated the impact of RT on body composition, cardiorespiratory fitness (CRF) and physical performance, lipid–lipoprotein profile, inflammation, and glucose–insulin homeostasis in 51 postmenopausal women versus 29 controls matched for age, obesity, and physical activity. Exercised women were further subdivided for comparison of RT effects into those presenting metabolically healthy obesity (MHO) and those with metabolically unhealthy obesity (MUHO) classified according to Karelis and Rabasa-Lhoret or an approach based on adipose tissue secretory dysfunction using the plasma adiponectin(A)/leptin (L) ratio. Participants followed a 4-month weekly RT program targeting major muscle groups (3 × 10 repetitions at 80% one repetition maximum (1-RM)). Percent fat marginally decreased and lean body mass increased (0.01 < p < 0.05) while CRF and muscular strength improved in all women, after RT (effect size (ES): 0.11–1.21 (trivial to large effects), p ˂ 0.01). Fasting plasma triacylglycerol and high-density lipoprotein-cholesterol levels slightly increased and decreased, respectively, in participants with MHO using the A/L ratio approach (ES: −0.47 to 1.07 (small to large effects), p ˂ 0.05). Circulating interleukin-6 soluble receptor decreased in both groups and soluble tumor necrosis factor receptor-1/soluble tumor necrosis factor receptor-2 in women with MUHO only, irrespective of definition (ES: −0.42 to −0.84 (small to large effects), p ˂ 0.05). Glucose–insulin homeostasis was unchanged regardless of group or definition. RT improved physical performance and body composition but had a lesser impact on cardiometabolic risk in women with obesity, irrespective of their metabolic phenotype. [ABSTRACT FROM AUTHOR]

Aim: To investigate systemic regulators of the cancer‐associated cachexia syndrome (CACS) in a pre‐clinical model for lung cancer with the goal to identify therapeutic targets for tissue wasting. Methods: Using the Kras/Lkb1 (KL) mouse model, we found that CACS is associated with white adipose tissue (WAT) dysfunction that directly affects skeletal muscle homeostasis. WAT transcriptomes showed evidence of reduced adipogenesis, and, in agreement, we found low levels of circulating adiponectin. To preserve adipogenesis and restore adiponectin levels, we treated mice with the PPAR‐γ agonist, rosiglitazone. Results: Rosiglitazone treatment increased serum adiponectin levels, delayed weight loss, and preserved skeletal muscle and adipose tissue mass, as compared to vehicle‐treated mice. The preservation of muscle mass with rosiglitazone was associated with increases in AMPK and AKT activity. Similarly, activation of the adiponectin receptors in muscle cells increased AMPK activity, anabolic signaling, and protein synthesis. Conclusion: Our data suggest that PPAR‐γ agonists may be a useful adjuvant therapy to preserve tissue mass in lung cancer. [ABSTRACT FROM AUTHOR]

In all vertebrates, reproductive strategies are achieved by modulation of the neuroendocrine system in a similar manner and with minor variations among the different classes. Most of the available information on amphibian testicular cycles derive from anurans, and among these, water frogs have been extensively studied in terms of reproductive mechanisms and sex steroid correlation. Adiponectin (AdipoQ) and its receptors—AdipoR1 and AdipoR2—are essential for most of the normal testicular and sperm functions. In this study, the identification of AdipoQ and its two receptors was carried out by immunohistochemistry in the testis of adult males of Pelophylax bergeri. The AdipoQ system was observed in the frog spermatogenic cysts, in both germinal and Sertoli cells, as well as in the rete testis. AdipoQ and AdipoR1 were localized in germ-line cells, from spermatogonia to round spermatids, while AdipoR2 was detected in the elongated spermatids, spermatozoa, and Sertoli cells. AdipoR1 was also observed in the intratesticular canals of the rete testis. This preliminary study shows the AdipoQ system's presence in the anurans' testis. The results obtained could be a starting point for future functional studies aimed at defining the physiological role of the AdipoQ system in frog testicular functions. [ABSTRACT FROM AUTHOR]

• Increased pregnancy adiponectin was associated with lower infant negative affect. • Pregnancy Adiponectin mediated the effect of pregnancy adiposity on infant negative affect. • Greater cord blood leptin was associated with increased negative affect. • Pregnancy adipokines may be novel biomarkers of offspring risk for psychopathology. Increased adiposity during pregnancy may be related to offspring risk for mental health disorders, although the biological mechanisms are poorly understood. One promising hypothesis is that factors secreted from adipocytes such as leptin and adiponectin may explain this association. The current study examined whether pregnancy or umbilical cord blood concentrations of leptin and/or adiponectin a) predict elevated infant negative affect at 6 months (an early life marker of risk for psychopathology); and b) help explain the association between pregnancy adiposity and increased infant negative affect. Data came from a prospective cohort (N = 305) of pregnant individuals and their offspring. Second trimester adiposity was assessed using air displacement plethysmography. Concentrations of leptin and adiponectin were measured in second trimester plasma and umbilical cord plasma. Infant negative affect was assessed by standardized observation at 6 months. Second trimester inflammation was assessed using a comprehensive panel of cytokines. Lower second trimester adiponectin was associated with elevated infant negative affect, and mediated the effect of pregnancy adiposity on infant negative affect. This association was independent of the effect of second trimester inflammation. Umbilical cord leptin also predicted higher infant negative affect and mediated the association between pregnancy adiposity and infant negative affect. This is the first study to link pregnancy adiponectin or cord blood leptin to infant markers of risk for psychopathology, and the first to demonstrate that these adipokines mediate the association between pregnancy adiposity and offspring behavioral outcomes, suggesting novel markers of risk and potential mechanisms of effect. [ABSTRACT FROM AUTHOR]

Simple Summary: NSCLC is one of the most life-threatening forms of oncological diseases. Although targeted and immunotherapy treatments have improved NSCLC prognosis, the chance of surviving is still limited for many patients. Therefore, further efforts are required to improve NSCLC care. AdipoRon is emerging as an antineoplastic molecule in the treatment of different cancers, but its potential in NSCLC is yet to be explored. Herein, we demonstrated that AdipoRon strongly impairs viability, growth and stemness in NSCLC cells. We also recorded higher glucose consumption and lactate accumulation as a result of AdipoRon treatment. Remarkably, the employment of glycolytic-interfering agents enhanced its antiproliferative features. A signaling pathways analysis revealed a marked AMPK phosphorylation, while, in contrast, its abrogation by Compound-C significantly counteracted AdipoRon effectiveness. Altogether, these findings emphasize AdipoRon's anticancer feature even in NSCLC, supporting its endorsement as a future candidate in cancer and NSCLC therapy. Despite the countless therapeutic advances achieved over the years, non-small-cell lung cancer (NSCLC) is the leading cause of cancer-related death worldwide. To this primacy contribute both non-oncogene addicted and advanced NSCLCs, in which conventional therapies are only partially effective. The adiponectin receptor agonist AdipoRon has revealed antiproliferative action in different cancers, including osteosarcoma and pancreatic cancer. Herein, we investigated its potential anticancer role in NSCLC for the first time. We proved that AdipoRon strongly inhibits viability, growth and colony formation in H1299 and A549 NSCLC cells, mainly through a slowdown in cell cycle progression. Along with the biological behaviors, a metabolic switching was observed after AdipoRon administration in NSCLC cells, consisting of higher glucose consumption and lactate accumulation. Remarkably, both 2-Deoxy Glucose and Oxamate glycolytic-interfering agents greatly enhanced AdipoRon's antiproliferative features. As a master regulator of cell metabolism, AMP-activated protein kinase (AMPK) was activated by AdipoRon. Notably, the ablation of AdipoRon-induced AMPK phosphorylation by Compound-C significantly counteracted its effectiveness. However, the engagement of other pathways should be investigated afterwards. With a focus on NSCLC, our findings further support the ability of AdipoRon in acting as an anticancer molecule, driving its endorsement as a future candidate in NSCLC therapy. [ABSTRACT FROM AUTHOR]

The modulation of cellular phenotypes within adipose tissue provides a potential means for therapeutic intervention for diabetes. Endogenous interleukin-10 (IL-10) protects against diet-induced insulin resistance. We examined the effects and mechanisms of action of IL-10-treated adipose-derived stromal cells on diabetes-induced insulin resistance and liver gluconeogenesis. We harvested stromal vascular fractions (SVFs) from the adipose tissue of diabetic (Leprdb/db) mice and treated them with IL-10 in vitro. SVFs treated with 10 or 100 ng of IL-10 were injected into the inguinal adipose tissue of Leprdb/db mice. IL-10 treatment suppressed the mRNA expression of IL-6, IL-33, CCL2, TNF-α, and IL-1β. Additionally, it suppressed the protein expression of IL-6, pmTOR, pJNK, and pNF-κB but enhanced Foxp3 mRNA expression in SVFs from diabetic mice. Meanwhile, IL-10 treatment repressed CCL2 and PDGFRα expression in adipose tissue macrophages (ATMs) and IL-6 expression in non-ATMs but increased the Foxp3 and IL-10 mRNA expression of ATMs from diabetic mice. Injection of IL-10-treated SVFs decreased the IL-6, IL-33, CCL2, IL-1β, and CCL2 but enhanced the Foxp3 and IL-10 mRNA expression of adipose tissue from Leprdb/db mice. Furthermore, injection of IL-10-treated SVFs increased CD4+ regulatory T cells (Tregs) in SVFs and adipose IL-10 levels and suppressed plasma adiponectin levels and DPP4 activity in diabetic mice. Injection of IL-10-treated SVFs decreased hepatic G6PC and PCK1 mRNA expression and increased Akt activation, STAT3 phosphorylation in the liver, and glucose tolerance in diabetic mice. Our data suggest that IL-10 treatment decreases inflammation in adipose SVFs of diabetic mice. Injection of IL-10-treated SVFs into the adipose tissue decreased diabetes-induced gluconeogenesis gene expression, DPP4 activity, and insulin resistance by enhancing Treg cells in diabetic mice. These data suggest that IL-10-treated adipose stromal vascular cells could be a promising therapeutic strategy for diabetes mellitus. [ABSTRACT FROM AUTHOR]

Background: Alzheimer's disease (AD) is a neurodegenerative condition featuring by gradual degradation of the cortical and hippocampal neurons, which results in impaired cognitive and memory functions. Objectives: To assess the effect of chronic moderate and high intensity pattern of exercise on brain functions regarding memory and implication changes of adiponectin (APN) and brain derived neurotropic factor (BDNF) gene expression. Subjects and methods: Sixty adult male albino rats were subdivided randomly into two main groups (n=30), control group and AD group. Each main group was suballocated into three subgroups (n=10) according to intensity of exercise. Finally we had 6 groups: Subgroup Ia: vehicle only. Subgroup Ib: vehicle + Moderate intensity exercise. Subgroup Ic: vehicle + High intensity exercise. Subgroup IIa: AlCl3. Subgroup IIb: AlCl3 + Moderate intensity exercise. Subgroup IIc:AlCl3+ High intensity exercise. APN and BDNF gene expression were assessed and histopathological examination of cerebral cortex and hippocampus was done. Evaluation of behavioral parameters was done using modified T-maze to evaluate short term and working memory. Results: Gene expressions of APN and BDNF were substantially decreased in the all AD subgroups compared to their corresponding control subgroups. However, they were remarkably elevated in moderately exercised subgroups compared to the sedentary subgroups. Moreover, in high intensity exercised subgroups, they were significantly higher than that of the sedentary and moderately exercised subgroups. Conclusion: APN & BDNF gene expression can be employed as a biomarker for early diagnosis of AD. Also regular exercise with increased intensity should be recommended for all patients with AD. [ABSTRACT FROM AUTHOR]

Adiponectin has previously been investigated for exerting its protective effect against myocardial injury through anti-apoptotic and anti-oxidative actions. Therefore, the present study aimed to investigate the nature and mechanism of adiponectin inhibition of H2O2-induced apoptosis in chicken skeletal myoblasts. Skeletal muscle satellite cells were differentiated and assigned into three groups. Group C was on the blank control group, group H was stimulated with the H2O2 (500 μmol/L, 4 h) alone group, group A + H was pre-treated with adiponectin (10 μg/mL, 24 h) and stimulated with the H2O2 (500 μmol/L, 4 h) group. Cytotoxicity inhibited by adiponectin was evaluated by the CCK-8 assay. The degree of apoptosis and oxidative damage was investigated by the TdT-mediated dUTP nick end labeling (TUNEL) and reactive oxygen species (ROS) staining assays. Oxidative stress was assessed by evaluating lipid peroxidation, superoxide dismutase, and reduced glutathione. Acridine orange (AO) staining detected lysosomal membrane permeability. The changes in mitochondrial membrane potential (MMP) were analyzed using 5,5,6,6′-tetrachloro-1,1,3,3-tetraethylimidacarbocyanine iodide (JC-1) dye under a fluorescence microscope. The lysosomal function, mitochondrial function, and apoptosis-related mRNA and protein expression levels were quantified by real-time quantitative PCR and western blot, respectively. The results suggested that adiponectin treatment attenuated H2O2-induced cytotoxicity and oxidative stress in skeletal myoblasts. Compared with H2O2 treatment, TUNEL and ROS staining demonstrated lower apoptosis upon adiponectin treatment. AO staining confirmed the amelioration of lysosomal membrane damage, and JC-1 staining revealed an increase in mitochondrial membrane potential after adiponectin treatment. At the molecular level, adiponectin treatment inhibited the expression of the lysosomal apoptotic factors cathepsin B, chymotrypsin B, and the mitochondrial apoptotic pathway cytochrome-c (cyt-c) and caspase-8; decreased the apoptotic marker gene Bax; and increased the expression of the anti-apoptotic marker gene Bcl-2. Adiponectin treatment attenuated H2O2-induced apoptosis in skeletal myoblasts, possibly by inhibiting oxidative stress and apoptosis through the lysosomal-mitochondrial axis. [ABSTRACT FROM AUTHOR]

There is increasing evidence that selenium (Se) and its major transport protein, selenoprotein-P (SePP), may be associated with polycystic ovary syndrome (PCOS). However, the association of serum Se and SePP levels with circulating adipokines in this population has not received sufficient attention. In the present study, we aimed to investigate the associations of serum Se and SePP with circulating adipokine levels in patients with PCOS. In this cross-sectional study, 115 patients aged 18–45 years with PCOS diagnosed according to the Rotterdam Consensus Criteria were recruited. The general characteristics of the participants were collected using a general questionnaire and anthropometric measurements were taken. Blood samples were obtained and serum levels of leptin, adiponectin, visfatin, resistin, and omentin-1, as well as markers of glucose metabolism, were measured. Serum levels of Se and SePP were inversely correlated with fasting blood glucose (FBS), serum insulin, and homeostatic model assessment for insulin resistance (HOMA-IR). In addition, serum levels of Se and SePP were positively correlated with serum levels of adiponectin and visfatin. Although there was no significant correlation between serum Se and serum omentin-1 levels, a significant positive correlation was found between serum SePP levels and this adipokine. The present study found that serum Se and SePP levels were positively correlated with serum adiponectin and visfatin levels. Further studies are needed to confirm these findings. [ABSTRACT FROM AUTHOR]

Adipose tissue (AT), composed mainly of adipocytes, plays a critical role in lipid control, metabolism, and energy storage. Once considered metabolically inert, AT is now recognized as a dynamic endocrine organ that regulates food intake, energy homeostasis, insulin sensitivity, thermoregulation, and immune responses. This review examines the multifaceted role of adiponectin, a predominant adipokine released by AT, in glucose and fatty acid metabolism. We explore the regulatory mechanisms of adiponectin, its physiological effects and its potential as a therapeutic target for metabolic diseases such as type 2 diabetes, cardiovascular disease and fatty liver disease. Furthermore, we analyze the impact of various dietary patterns, specific nutrients, and physical activities on adiponectin levels, highlighting strategies to improve metabolic health. Our comprehensive review provides insights into the critical functions of adiponectin and its importance in maintaining systemic metabolic homeostasis. [ABSTRACT FROM AUTHOR]

Stroke is a leading cause of death and severe disability worldwide. Rapid diagnosis is critical to ensure the timely administration of medical treatment. Given that in some cases CT scans fail to show the classic clinical signs of stroke, we aimed to evaluate the diagnostic capacity of adiponectin levels and their association with the clinical parameters of patients with acute ischemic stroke (AIS). Adiponectin was measured within 24 h (T1) and 48 h (T2) of AIS onset in 70 patients. A total of 68 control cases were included in the study. Adiponectin levels were significantly higher in the AIS patients than in the controls (16.64 (3.79; 16.69) vs. 3.78 (3.79; 16.69); p < 0.001), with an accuracy of 0.98 (AUC = 0.99). Lower levels were seen in males and in AIS patients with obesity. Higher levels of adiponectin at T1 were associated with a moderate/severe NIHSS score at patient discharge. Moreover, higher levels of borderline significance were seen in patients who died within 12 months of their AIS episode (p = 0.054). Adiponectin may be a useful biomarker for the identification of AIS patients who do not present classic CT signs and could be used to stratify severe cases. Further studies are needed to validate these results. [ABSTRACT FROM AUTHOR]

Physical activity promotes metabolic health and prevents lifestyle-related diseases. Adiponectin is specifically produced by adipose tissue and comes in three forms, differing in terms of weight: trimers (LMW), hexamers (MMW), and high-molecular-weight (HMW) oligomers. The oligomers are associated with the beneficial effects of adiponectin. In this study, we aimed to investigate the impact of a single bout of exhaustive exercise on adiponectin expression in 25 male amateur athletes, divided into two groups, one comprising young adults (YAs) (n = 15), and the other comprising middle-aged adults (MAs) (n = 10). Body fat was estimated through skinfold thickness. Adiponectin levels were assessed at baseline and at 15 min and 24 h post-exercise, while HMW oligomer levels were evaluated at baseline and at 24 h post-exercise. We observed a significant increase in total adiponectin at both 15 min and 24 h after exercise, with there being a more evident effect among the YA subjects. HMW oligomers also increased significantly after exercise both in the total sample and among the YA subjects, but this was not the case in the MA subjects. The increase in adiponectin levels was significantly associated with Powerpeak. Furthermore, a significant inverse correlation was found between basal adiponectin and VO2peak and Powerpeak. In conclusion, a single bout of exhaustive exercise can rapidly and significantly enhance the basal circulating adiponectin concentration, which seems to be negatively associated with maximal aerobic capacity. [ABSTRACT FROM AUTHOR]

Fragile X syndrome (FXS) is the most common inherited cause of intellectual disability and is the leading known single-gene cause of autism spectrum disorder. Patients with FXS display varied behavioural deficits that include mild to severe cognitive impairments in addition to mood disorders. Currently, there is no cure for this condition; however, there is an emerging focus on therapies that inhibit mechanistic target of rapamycin (mTOR)-dependent protein synthesis owing to the clinical effectiveness of metformin for alleviating some behavioural symptoms in FXS. Adiponectin (APN) is a neurohormone that is released by adipocytes and provides an alternative means to inhibit mTOR activation in the brain. In these studies, we show that Fmr1 knockout mice, like patients with FXS, show reduced levels of circulating APN and that both long-term potentiation (LTP) and long-term depression (LTD) in the dentate gyrus (DG) are impaired. Brief (20 min) incubation of hippocampal slices in APN (50 nM) was able to rescue both LTP and LTD in the DG and increased both the surface expression and phosphorylation of GluA1 receptors. These results provide evidence for reduced APN levels in FXS playing a role in decreasing bidirectional synaptic plasticity and show that therapies which enhance APN levels may have therapeutic potential for this and related conditions. This article is part of a discussion meeting issue 'Long-term potentiation: 50 years on'. [ABSTRACT FROM AUTHOR]

Background: Apart from the well-established skeletal effects, vitamin D has been explored as a secretagogue influencing various adipokines, including adiponectin and irisin. Recent evidence suggests that specific forms of 25-Hydroxyvitamin D (25(OHD), such as free and bioavailable 25(OH)D, may provide more accurate measurements of vitamin D status. The relationship between vitamin D status and serum irisin and adiponectin concentrations remains largely unexplored, particularly during pregnancy. Methods: We analyzed data from 67 healthy maternal-neonatal pairs from Northern Greece at birth. Biochemical and hormonal tests were conducted on each maternal-neonatal pair. The vitamin D forms were estimated using validated mathematical models. Subsequently, regression analyses were conducted to determine the association between the vitamin D forms and adipokine levels. Results: Bioavailable maternal 25(OH)D was inversely associated with neonatal irisin concentrations [b=-73.46 (-140.573 to -6.341), p=0.034]. No other associations were observed between maternal vitamin D status and neonatal adipokine concentrations. Conclusion: In conclusion, maternal bioavailable vitamin D concentrations are inversely associated with neonatal serum irisin concentrations, warranting further studies to evaluate the underlying mechanisms for this finding. [ABSTRACT FROM AUTHOR]

Objectives: This study aimed to investigate the serum level of adipolin and adiponectin in healthy pregnant women and pregnant women with gestational diabetes mellitus (GDM) during the second trimester, the prepartum period, and in the newborns of these patients. Methods: A total of 55 women diagnosed with GDM and 110 healthy pregnant women were included in this study. Pearson's and Spearman's correlation coefficients were calculated to determine the association of adipolin and adiponectin with anthropometric markers of obesity (body mass index (BMI), mid-upper arm circumference (MUAC), tricipital skinfold thickness (TST)), inflammation markers (neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), C-reactive protein (CRP)), and maternal glucose homeostasis parameters (fasting glucose, insulin, C peptide, glycosylated hemoglobin A1c (HbA1c), Insulin Resistance—Homeostatic Model Assessment (IR HOMA)). Results: There were no statistical differences between the adipolin value in patients with GDM compared to healthy patients (p = 0.65 at diagnosis and p = 0.50 prepartum) and in newborns from mothers with GDM compared to healthy mothers (p = 0.24). Adipolin levels are significantly higher in patients with GDM who gave birth via cesarean section (p = 0.01). In patients with GDM, the adipolin level correlates positively with HgA1c in the prepartum period. We found a positive correlation between the maternal adipolin values at diagnosis and prepartum and neonatal adipolin (respectively: r = 0.556, p = 0.001; r = 0.332, p = 0.013). Adiponectin levels were significantly lower in patients with GDM at diagnosis and prepartum (p = 0.0009 and p = 0.02), but their levels increased prepartum (5267 ± 2114 ng/mL vs. 6312 ± 3150 ng/mL p = 0.0006). Newborns of mothers with GDM had lower adiponectin levels than newborns of healthy mothers (p < 0.0001). The maternal adiponectin value correlates negatively with maternal BMI, MUAC, and IR HOMA in both groups at diagnosis and prepartum. There were no differences between the groups in terms of cesarean rate (p > 0.99). The relative risk of occurrence of adverse events in patients with GDM compared to healthy ones was 2.15 (95% CI 1.416 to 3.182), and the odds ratio for macrosomia was 4.66 (95% CI 1.591 to 12.69). Conclusions: There was no difference in adipolin levels between mothers with GDM and healthy mothers during the second trimester and the prepartum period. Adipolin is known to enhance insulin sensitivity and reduce inflammation, but unlike adiponectin, it does not appear to contribute to the development of GDM. [ABSTRACT FROM AUTHOR]

Adipokines play essential roles in regulating a range of biological processes, but growing evidence indicates that they are also fundamental in immunological mechanisms and, primarily, inflammatory responses. Adipokines mediate their actions through specific receptors. However, although adipokine receptors are widely distributed in many cell and tissue types, limited data are available on their expression in mast cells (MCs) and, consequently, adipokine's significance in the modulation of MC activity within the tissues. In this study, we demonstrate that rat peritoneal MCs constitutively express the leptin receptor (i.e. LEPR), adiponectin receptors (i.e. ADIPOR1 and ADIPOR2) and the chemerin receptor (i.e. CMKLR1). We also found that LEPR, ADIPOR1, ADIPOR2 and CMKLR1 expression in MCs changes in response to stimulation by their specific ligands and some cytokines with potent proinflammatory properties. Furthermore, the involvement of intracellular signaling molecules in leptin‐, adiponectin‐ and chemerin‐induced MC response was analyzed. Overall, our findings suggest that adipokines leptin, adiponectin and chemerin can significantly affect the activity of MCs in various processes, especially during inflammation. These observations may contribute significantly to understanding the relationship between adipokines, immune mechanisms and diseases or conditions with an inflammatory component. [ABSTRACT FROM AUTHOR]

This narrative review explores the pathophysiology of obesity, cellular senescence, and exosome release. When exposed to excessive nutrients, adipocytes develop mitochondrial dysfunction and generate reactive oxygen species with DNA damage. This triggers adipocyte hypertrophy and hypoxia, inhibition of adiponectin secretion and adipogenesis, increased endoplasmic reticulum stress and maladaptive unfolded protein response, metaflammation, and polarization of macrophages. Such feed-forward cycles are not resolved by antioxidant systems, heat shock response pathways, or DNA repair mechanisms, resulting in transmissible cellular senescence via autocrine, paracrine, and endocrine signaling. Senescence can thus affect preadipocytes, mature adipocytes, tissue macrophages and lymphocytes, hepatocytes, vascular endothelium, pancreatic β cells, myocytes, hypothalamic nuclei, and renal podocytes. The senescence-associated secretory phenotype is closely related to visceral adipose tissue expansion and metaflammation; inhibition of SIRT-1, adiponectin, and autophagy; and increased release of exosomes, exosomal micro-RNAs, pro-inflammatory adipokines, and saturated free fatty acids. The resulting hypernefemia, insulin resistance, and diminished fatty acid β-oxidation lead to lipotoxicity and progressive obesity, metabolic syndrome, and physical and cognitive functional decline. Weight cycling is related to continuing immunosenescence and exposure to palmitate. Cellular senescence, exosome release, and the transmissible senescence-associated secretory phenotype contribute to obesity and metabolic syndrome. Targeted therapies have interrelated and synergistic effects on cellular senescence, obesity, and premature aging. [ABSTRACT FROM AUTHOR]

Burns generate every year an important burden of morbidity, being a major global public health problem through prolonged hospitalization, complications, and increased mortality. This study's purpose was to evaluate the serum levels of three adipokines and to establish significant correlations with other circulating molecules and with some clinical parameters. We evaluated 32 children with severe burns (over 25% total burned surface area—TBSA) at 48 h, day 10, and day 21 post burn, and 21 controls. The serum levels of adiponectin, resistin, leptin, tumor necrosis factor-α (TNF-α), plasminogen activator inhibitor-1 (PAI-1), and C-reactive protein (CRP) (among nine other biochemical parameters) were detected by Multiplex technique. Significant statistical differences were obtained for resistin and leptin compared to the control group, in different moments of measurements. Adiponectin serum levels presented statistically significant correlations with hot liquid mechanism of burn, the Revised Baux score, TBSA, resistin, PAI-1, CRP, TNF-α, and triglycerides (TGLs) serum levels. Resistin serum levels presented statistically significant correlations with adiponectin, CRP, PAI-1, leptin, and TNF-α. Additionally, we found statistically significant correlations between leptin serum levels and length of hospitalization, TNF-α, resistin, adiponectin, and PAI-1 serum levels. In severely burned children, adiponectin, resistin, and leptin specifically correlate with clinical parameters and with proteins involved in the systemic inflammatory response and the hypermetabolic response. [ABSTRACT FROM AUTHOR]

Background People with the human immunodeficiency virus (PWH) have microvascular disease. Because perivascular adipose tissue (PVAT) regulates microvascular function and adipose tissue is inflamed in PWH, we tested the hypothesis that PWH have inflamed PVAT that impairs the function of their small vessels. Methods Subcutaneous small arteries were dissected with or without PVAT from a gluteal skin biopsy from 11 women with treated HIV (WWH) aged < 50 years and 10 matched women without HIV, and studied on isometric myographs. Nitric oxide (NO) and reactive oxygen species (ROS) were measured by fluorescence microscopy. Adipokines and markers of inflammation and ROS were assayed in PVAT. Results PVAT surrounding the small arteries in control women significantly (P <.05) enhanced acetylcholine-induced endothelium-dependent relaxation and NO, and reduced contractions to thromboxane and endothelin-1. However, these effects of PVAT were reduced significantly (P <.05) in WWH whose PVAT released less adiponectin but more markers of ROS and inflammation. Moderation of contractions by PVAT were correlated positively with adipose adiponectin. Conclusions PVAT from WWH has oxidative stress, inflammation, and reduced release of adiponectin, which may contribute to enhanced contractions and therefore could promote small-artery dysfunction. [ABSTRACT FROM AUTHOR]

Introduction: Sudden sensorineural hearing loss (SSNHL) is a common emergency symptom in otolaryngology that requires immediate diagnosis and treatment. SSNHL has a multifactorial etiology, and its pathophysiologic mechanisms may be associated with inflammatory and metabolic changes that may affect the cochlear microenvironment or its nervous component, thus triggering the process or hindering hearing recovery. Therefore, the aim of this study was to assess metabolic and inflammatory changes to identify systemic parameters that could serve as prognostic factors for hearing recovery in patients with SSNHL. Materials and methods: Thirty patients with a sudden hearing loss of at least 30 dB in three contiguous frequencies were enrolled in this study. Patients were followed up for 4 months and peripheral blood samples were collected at 7 days (V1), 30 days (V2) and 120 days (V3). Interleukins (IL)-1F7, IL-2, IL-4, IL-5, IL-6, IL-10, interferon γ (IFN-γ), tumor necrosis factor α (TNF-α) and adiponectin were quantified in serum. In addition, lipid and glycemic profiles as well as concentration of creatinine, uric acid, fructosamine, peroxide, total proteins and albumin were analyzed. Patients underwent weekly ear-specific hearing tests with standard pure tone thresholds for frequencies of 250-8,000 Hz, speech recognition threshold and word recognition score. Results: Patients with SSNHL were divided into a group of patients who did not achieve hearing recovery (n = 14) and another group who achieved complete and significant recovery (n = 16). Most serologic parameters showed no significant changes or values indicating clinical changes. However, IFN-γ levels decreased by 36.3% between V1 and V2. The cytokine TNF-α showed a statistically significant decrease from V1 to V3 (from 22.91 to 10.34 pg./mL). Adiponectin showed a decrease from 553.7 ng/mL in V1 to 454.4 ng/mL in V3. Discussion: Our results show that serologic cytokine levels change in the acute phase of manifestation of SSNHL and establish a parallel between systemic changes and improvements in hearing, especially TNF-α, which showed differences in hearing recovery. The use of IFN-γ, TNF-α and adiponectin may elucidate the clinical improvement in these patients. [ABSTRACT FROM AUTHOR]

Background: This study aimed to explore the impact of Diacerein (DIC) on endocrine and cardio-metabolic changes in polycystic ovarian syndrome (PCOS) mouse model. Methods: A total of 18 adult female mice (Parkes strain), aged 4–5 weeks, were randomly assigned to three groups, each comprising 6 animals, as follows: Group I (control), received normal diet and normal saline as vehicle for 51 days; Group II received Letrozole (LET; 6 mg/kg bw) for 21 days to induce PCOS; Group III received LET, followed by daily oral gavage administration of DIC (35 mg/kg bw) for 30 days. Results: This study indicates that treatment with LET resulted in PCOS with characteristics such as polycystic ovaries, elevated testosterone, weight gain, visceral adiposity, high levels of insulin as well as fasting blood glucose in addition to insulin resistance, improper handling of ovarian lipids, atherogenic dyslipidemia, impaired Na + /K + -ATPase activity and serum, cardiac, and ovarian oxidative stress. Serum/ovarian adiponectin levels were lowered in LET-treated mice. In mice treated with LET, we also discovered a reduction in cardiac and serum paraoxonase 1 (PON1). Interestingly, DIC restored ovarian andcardio-metabolic abnormalities in LET-induced PCOS mice. DIC prevented the endocrine and cardio-metabolic changes brought on by letrozole-induced PCOS in mice. Conclusion: The ameliorative effects of DIC on letrozole-induced PCOS with concurrent oxidative stress, abdominal fat deposition, cardiac and ovarian substrate mishandling, glucometabolic dysfunction, and adiponectin/PON1 activation support the idea that DIC perhaps, restore compromised endocrine and cardio-metabolic regulators in PCOS. [ABSTRACT FROM AUTHOR]

Objectives Methods Results Conclusion Experimental and small human studies have indicated that high total adiponectin levels have beneficial cardiometabolic effects. In contrast, however, high total adiponectin levels are also associated with higher all‐cause and cardiovascular mortality in thoroughly adjusted epidemiological studies. To gain further insight into these seemingly contradictory results, we report results on total adiponectin from the indigenous Melanesian population of Kitava, Trobriand Islands, Papua New Guinea, where an apparent absence of cardiometabolic disease has been previously reported.Fasting levels of serum total adiponectin were measured cross‐sectionally in ≥40‐year‐old Kitavans (n = 102) and Swedish controls matched for age and sex (n = 108). Multivariable linear regression was used for the analysis of associations with total adiponectin when controlled for group, sex, smoking, hypertension and/or type 2 diabetes, age, and body mass index.Total adiponectin was lower for Kitavans compared to Swedish controls (Median [Mdn] 4.6 μg/mL, range 1.0–206 μg/mL and Mdn 9.7 μg/mL, range 3.1–104 μg/mL, respectively, r = .64, p < .001). Lower total adiponectin was associated with Kitavan group, male sex (only in Swedish controls), smoking (only in Kitavans and Swedish controls combined), younger age (not in Swedish controls), higher BMI, lower total, low‐density lipoprotein, high‐density lipoprotein (HDL) (only in Kitavans and Swedish controls combined), and non‐HDL cholesterol, and higher anti‐PC IgG (only in Kitavans and Swedish controls combined).Total adiponectin in Kitavans was significantly lower than in Swedish controls. [ABSTRACT FROM AUTHOR]

Background: The study aimed to explore the correlation between the angiotensin II (Ang II) gene and serum adiponectin expression in patients with cerebrovascular complications of H-type hypertension (HH) and its mechanism. Methods: A total of 50 cases of outpatient patients in Tianjin Fourth Central Hospital were recruited from January 2022 to June 2023 and rolled into three groups according to their blood pressure and basic information, namely the HH cerebrovascular complications group, the non-H-type hypertension (NHH) group, and the healthy control (HC) group. Peripheral blood samples were taken; one sample was utilized to test for the Ang II gene and the methylation of Ang II, and the other sample was utilized to measure serum adiponectin levels to analyze the relationship between serum adiponectin level and Ang II in patients with cerebrovascular complications of HH. Results: The ratio of male to female was 8:7 in the group of cerebrovascular complications of HH, and mean systolic blood pressure (SBP) and diastolic blood pressure (DBP) were 167.34 mm Hg and 112.56 mm Hg, respectively. In the NHH group, the mean SBP was 165.89 mm Hg, and the mean DBP was 113.47 mm Hg. The blood pressure of the HC group was in the normal range. The Ang II content was the highest in the group with cerebrovascular complications of HH, followed by the group with NHH, and the lowest in the HC group. Conclusions: Pyrosequencing chart of patients with cerebrovascular complications of HH showed that the content of deoxyphosphate ribose G was the highest, while the content of A was the highest in NHH patients. Moreover, the serum adiponectin level of patients with HH and NHH was superior to that of the HC group, and the adiponectin level between the former two groups and the HC group differed considerably. Ang II levels were high in patients with cerebrovascular complications of HH and were positively correlated with adiponectin levels. The incidence of cerebrovascular complications of HH may be related to Ang II levels in patients. [ABSTRACT FROM AUTHOR]

Polycystic ovary syndrome (PCOS) is associated with a heightened risk for various metabolic comorbidities, including glucose intolerance, type II diabetes mellitus, dyslipidaemia, metabolic syndrome, hepatic steatosis and non-alcoholic fatty liver disease (NAFLD) Objectives: the current study aims to elucidate the metabolic consequences of PCOS, with a particular focus on insulin resistance and dyslipidaemia, and their impact on hepatic function, with or without high fat diet feeding, and to investigate the potential therapeutic role of moderate-intensity exercise in mitigating these PCOS-associated metabolic and hepatic complications. For this, 55 adult female Wistar albino rats were divided into 5 equal groups: Control group, polycystic ovary syndrome group (PCO), high fat diet fed polycystic ovary syndrome group (HF-PCO), exercise-treated polycystic ovary syndrome group (PCO-EX), and high fat diet fed exercise-treated polycystic ovary syndrome group (HF-PCO-EX). At the end of the study period (8 weeks), anthropometric measures were taken. Insulin resistance, lipid profile and liver enzymes activity were also assessed and serum estradiol, testosterone, luteinizing hormone (LH), resistin and adiponectin levels were measured. Histopathological examination of ovarian and hepatic tissues was also performed. The results obtained demonstrated that glycaemic parameters significantly implied insulin resistance which was associated with a significant increase in serum triglycerides (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) and atherogenic index (AI). On the other hand, there was a significant decrease in high density lipoprotein cholesterol (HDL-C) levels in the PCO and HF-PCO compared to the control group. Also, the activity levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma glutamyl transferase (GGT) as well as serum concentration of testosterone, LH and resistin were all significantly increased while serum concentration of estradiol, adiponectin and adiponectin/resistin ratio (A/R) were significantly decreased. Swimming exercise was able to reduce serum testosterone and LH concentration levels and to elevate serum estradiol concentration and to improve all the metabolic parameters compared to their corresponding non-exercised groups through reduction of the proinflammatory cytokine resistin and elevation of adiponectin and A/R ratio. Histopathological analysis corroborated these findings revealing minimal inflammatory infiltration, apoptosis, and steatosis in the livers of exercised animals. These data allowed us to conclude that moderate intensity exercise notably improved insulin resistance and lipid metabolism, and mitigated hepatic effects through reducing the activity of liver enzymes and the levels of inflammatory cytokines, potentially preventing the development of non-alcoholic fatty liver disease (NAFLD) in PCOS rats, regardless of dietary fat content. [ABSTRACT FROM AUTHOR]

Adipocytes are key to metabolic regulation, exhibiting insulinstimulated glucose transport that is underpinned by the insulinstimulated delivery of glucose transporter type 4 (SLC2A4, also known and hereafter referred to as GLUT4)-containing vesicles to the plasmamembranewhere they dock and fuse, and increase cell surface GLUT4 levels. Adipocytokines, such as adiponectin, are secreted via a similarmechanism.We used genome editing to knock out syntaxin-4, a protein reported to mediate fusion between GLUT4-containing vesicles and the plasma membrane in 3T3-L1 adipocytes. Syntaxin-4 knockout reduced insulin-stimulated glucose transport and adiponectin secretion by ~50% and reduced GLUT4 levels. Ectopic expression of haemagglutinin (HA)-tagged GLUT4 conjugated to GFP showed that syntaxin-4-knockout cells retain significant GLUT4 translocation capacity, demonstrating that syntaxin-4 is dispensable for insulinstimulated GLUT4 translocation. Analysis of recycling kinetics revealed only a modest reduction in the exocytic rate of GLUT4 in knockout cells, and little effect on endocytosis. These analyses demonstrate that syntaxin-4 is not always rate limiting for GLUT4 delivery to the cell surface. In sum, we show that syntaxin-4 knockout results in reduced insulin-stimulated glucose transport, depletion of cellular GLUT4 levels and inhibition of adiponectin secretion but has only modest effects on the translocation capacity of the cells. [ABSTRACT FROM AUTHOR]

Background: The correlation of adiponectin and serum tumor necrosis factor alpha (TNFα) with glucometabolic parameters in diabetes mellitus (DM) needs further studies. We aimed in this study to evaluate the relationship between adiponectin and TNFα with glucometabolic parameters in patients with type 2 DM (T2DM). Methods: We conducted a cross-sectional study in the Department of Physiology, College of Medicine, King Saud University, Saudi Arabia. The sample size was 117 from the diabetes clinic of King Abdul-Aziz University hospital through the convenience sampling technique. Subjects were grouped into control (healthy) subjects (53) with no chronic diseases and the diabetic group (64) with confirmed T2DM. Socio-demographic data were collected along with the serum blood sample to analyze the variables. Results: Adiponectin was significantly high in healthy subjects compared to the diabetic group (control: 14.4 ± 4.3, T2DM: 11.0 ± 4.1, P = 0.000), while TNFα was higher in the T2DM group (7.8 ± 2.7) than in the control group (6.6 ± 2.9, P = 0.024). TNFα was negatively correlated with adiponectin in the control group (-0.279) and in diabetic subjects (-0.311) and positively correlated with HbA1c in the diabetic group (0.319) and triglycerides (0.252). Adiponectin was positively correlated with HDL in the control group (0.252) and in diabetic subjects (0.326). There was an inverse correlation between TNFα and adiponectin. Conclusion: Adiponectin is higher in healthy subjects than in diabetic patients, while TNFα is higher in diabetic patients. In addition, adiponectin is positively correlated with HDL in healthy as well as diabetic patients. TNFα is positively correlated with HbA1c and triglycerides. [ABSTRACT FROM AUTHOR]

Oral submucous fibrosis (OSF) is an oral condition characterized by chronic progression, which may lead to the development of malignancy. Currently, available treatments for OSF only provide temporary relief of symptoms, and there is a limited availability of effective interventions that can effectively cure this condition. In this study, we aimed to investigate whether adiponectin (APN) could ameliorate OSF and the mechanisms involved in it. First, human oral mucosal fibroblasts (HOMFs) were cultured, an OSF model was established using arecoline, and APN and Imiquimod treatment were administered. Then we overexpressed NLRP3 and knocked down FOXO3A. FOXO3A, fibrosis-related factors (ɑ-SMA, COL1A, CTGF), TGF-β1/Smad3 signaling-related factors (TGF-β1, p-Smad3, Smad3), NLRP3 inflammasome-related factors (NLRP3, Caspase-1, IL-1β), and ROS levels were evaluated. Finally, we explored the effect of APN on OSF in mice by in vivo experiments. We found that arecoline significantly increased ɑ-SMA, COL1A, CTGF, and TGF-β1 expressions and promoted Smad3 phosphorylation, while APN significantly inhibited the elevation of these fibrosis-related factors. ROS production was significantly elevated in HOMFs after arecoline treatment, while APN treatment inhibited ROS production. However, the addition of Imiquimod and overexpression of NLRP3 exhibited a trend of elevated ROS, resisting the inhibitory effect of APN. Furthermore, adding Imiquimod and overexpression of NLRP3 elevated ɑ-SMA, COL1A and CTGF and activated TGF-β1/Smad3 signaling pathway. Additionally, knockdown of FOXO3A enhanced APN-inhibited ɑ-SMA and COL1A. In vivo experiments further confirmed that APN ameliorated OSF in mice by inhibiting ROS/NLRP3 inflammatory pathway. In conclusion, APN ameliorated arecoline-induced OSF by promoting FOXO3A expression and downregulating the ROS/NLRP3 pathway. [ABSTRACT FROM AUTHOR]

Background & Objective: Polycystic ovary syndrome (PCOS) is a common disease in women of childbearing age. The inflammation has participated in the metabolic disorders and irregular menstruation associated with this disease. This study was carried out to correlate between the disturbance of pro-inflammatory markers resistin, adiponectin and metabolic parameters in women with PCOS. Materials & Methods: Fasting blood samples were collected from 100 PCO married infertile women (23.30±4.659 years) attending Bint AL-Hoda and Al-Shatra hospitals in Thi- Qar province - Iraq, in addition to 50 healthy age matched (23.84±4.804 years) control, through the period from June 2022 to December 2022. Results: The BMI of PCO patients (27.22±7.20) was significantly (<0.001) more that BMI of the healthy control (22.84±4.63). PCO patients showed significantly elevation of serum levels of resistin (470.00±114.00 vs 350.00±90.60 ng/l, P<0.01) and significant decline of adiponectin (5.13±1.22 vs 11.00±1.40 mg/l, P<0.001) in comparison with healthy control. PCO patients also showed significant elevation of the serum glucose (P<0.01), total cholesterol (P<0.05), triglycerides (P<0.001) and LDL (P<0.001). However, serum HDL level was insignificantly declined and VLDL was insignificantly elevated in PCO group compared with healthy control group. Conclusion: Adiponectin and resistin represented part of the pathophysiology of PCO, and may serve as beneficial indicator in the diagnosis and treatment. [ABSTRACT FROM AUTHOR]

To investigate the Levels of Nucleotide-binding, leucine-rich repeat and pyrin domain-containing protein 3 (NLRP3) and Adiponectin (APN) and their relationship with the severity of coronary artery disease in patients with Unstable Angina (UA) and Type 2 Diabetes (T2D). Methods: Two hundred and thirty-one patients with UA were diagnosed by CAG in the Department of Cardiology of the Affiliated Hospital of Xuzhou Medical University from July 2022 to May 2023 were included, and 74 healthy subjects were included as the control group. The levels of NLRP3 and APN in each group were detected by ELISA and the Gensini score in each patient according to the results of CAG. The correlations between NLRP3, APN, and Gensini score were analyzed. According to whether complicated with T2D or not, we further analyze the effect of NLRP3 and APN levels of patients with UA and T2D on the severity of coronary artery stenosis. Results: The levels of NLRP3 in UA with T2D group were the highest, followed by simple UA group, and the lowest in the control group, and the level of APN was the opposite. Spearman Correlation analysis showed that the level of NLRP3 was positively correlated with Gensini score (ρ1=0.688, P< 0.05) and the level of APN was negatively associated with Gensini score (ρ2= − 0.515, P< 0.05). There was a negative correlation between NLRP3 and the level of APN (ρ3= − 0.366, P< 0.05). High NLRP3 and low APN levels are the risk factors for atherosclerosis. Conclusion: The NLRP3 and APN were abnormally expressed in patients with UA complicated with T2D. With the aggravation of atherosclerosis, the level of NLRP3 increased and the level of APN decreased. [ABSTRACT FROM AUTHOR]