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• In patients with kidney failure undergoing dialysis, neutrophils are dysfunctionally activated. • Plasma levels of MPO and resistin correlate with overall and cardiovascular mortality risk in kidney failure patients undergoing dialysis. • Inflammatory markers can mediate the high risk of death and CV events and can prove useful tools in risk stratification of patients undergoing dialysis. In patients with kidney failure (KF) undergoing dialysis, neutrophils are dysfunctionally activated. Such chronic activation does not correspond to increased protection against infections and is thought to cause direct vascular damage accounting for the higher incidence of cardiovascular (CV) events. We hypothesized that circulating levels of neutrophil degranulation products (i.e. myeloperoxidase (MPO) and resistin) can predict overall and CV-specific mortality in dialysis patients. MPO and resistin levels were assessed in plasma samples from n = 1182 dialysis patients who were followed-up for median 2.9 years (IQR: 1.7–4.2). Patients were 65 ± 14 (SD) years old and 36 % women. Median value of MPO and resistin were 78 ng/mL (IQR: 54 - 123) and 72 ng/mL (IQR: 46 - 110), respectively. MPO and resistin levels correlated with biomarkers of organ damage, nutritional status and inflammation. Both MPO and resistin levels predicted all-cause mortality even after adjustment for traditional risk factors and inflammation, nutritional and KF-related indexes (MPO, HR for 1 ln unit increase : 1.26, 95 %CI 1.11 – 1.42, P < 0.001; Resistin, HR for 1 ln unit increase : 1.25, 95 %CI 1.09 – 1.44, P = 0.001). Similarly, their predictive ability held true also for CV death (MPO, HR for 1 ln unit increase : 1.19, 95 %CI 1.01 – 1.41, P = 0.04; Resistin, HR for 1 ln unit increase : 1.29, 95 %CI 1.07 – 1.56, P = 0.007). Plasma levels of MPO and resistin correlate with prospective overall and CV-specific mortality risk in KF patients undergoing dialysis and might be useful prognostic tools. Mediators of inflammation may be potential target to improve survival of those patients. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA) is a chronic, progressive, degenerative joint disease characterized by joint pain, stiffness, and limited movement. It presents significant intra- and inter-individual variability—in particular, between genders. Recent research has increasingly focused on the role of adipokines—especially leptin, adiponectin, and resistin—in the development of OA. Adipokines, peptide hormones primarily secreted by adipose tissue, are involved in crucial physiological processes related to metabolism and immunity. They can also impact bone and cartilage turnover by interacting with joint cells such as osteoblasts, osteoclasts, chondrocytes, and mesenchymal stem cells, thereby linking inflammation with bone cartilage homeostasis. This review aims to elucidate the structure and functions of various adipokines, their serum and synovial levels, and their association with clinical presentation and radiographic progression in OA patients, with a focus on differences between sexes. A narrative literature review was conducted using three databases specifically analyzing sex differences. OA patients generally show elevated serum and synovial levels of leptin, chemerin, and visfatin, as well as high plasma levels of resistin and visfatin. In contrast, synovial levels of adiponectin and omentin are reduced in OA patients compared to healthy individuals, with an inverse relationship to disease severity, suggesting a potential protective role. Resistin and leptin were positively correlated with pain severity and radiographic progression, while adiponectin's role in OA remains controversial. Regarding sex differences, male OA patients exhibited higher serum levels of leptin, chemerin, and omentin compared to healthy controls, with a positive correlation to the BMI and estrogen levels, potentially explaining the sexual dimorphism observed in this condition. Studies on visfatin and lipocalin did not reveal significant differences in synovial or serum levels between the sexes. The role of resistin remains controversial. Adipokines influence the joint microenvironment and contribute to the progression of osteoarthritis (OA). However, the precise biological mechanisms are not yet fully understood due to the complex interactions between the metabolic, mechanical, and immune systems. Further research is needed to clarify their roles in OA and to identify targeted therapies for managing this degenerative disease. [ABSTRACT FROM AUTHOR]

Chemerin and resistin are adipokines studied as potential markers for early diagnosis and disease severity in patients with knee osteoarthritis (KOA) Therefore, we aimed to investigate the associations serum and synovial levels of chemerin and resistin with inflammatory parameters and ultrasonographic scores (US) in KOA individuals. Serum was collected from 28 patients with KOA and synovial fluid was obtained from 16 of them. Another 31 age and sex matched cases with no joint disease were included as healthy controls. Concentrations of chemerin, resistin, interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) were determined with ELISA. Erythrocyte sedimentation rate (ESR), C-reactive protein, serum uric acid (UA) were measured in the patients group. Participants with KOA underwent US assessment using the Outcome Measures in Rheumatology (OMERACT) scores. Patients with KOA had statistically significant higher level of serum resistin than healthy controls [11.05 (3.78–24.13) ng/mL and 7.23 (3.83–12.19) respectively, p < 0.001]. A strong correlation was found between serum chemerin and ESR (r = 0.434, p = 0.021), uric acid (r = 0.573, p = 0.001) as well as the US (r=-0.872, p < 0.001). Serum resistin demonstrated significant association with TNF-alpha (r = 0.398, p = 0.044). In conclusion, both chemerin and resistin might contribute to inflammatory changes associated with KOA. Further studies are needed to elucidate their potential role in the pathogenesis of the disease. [ABSTRACT FROM AUTHOR]

Indroduction: Cryptoglandular perianal fistula represents a prevalent benign anorectal condition, primarily addressed through surgical interventions, occasionally posing considerable therapeutic challenges. The associated decline in patient quality of life underscores the significance of effective management. However, the lack of a fully understood pathogenesis complicates the treatment approach. Recent research has proposed the involvement of adipose fat tissue in the inflammatory response and pathogenesis of cryptoglandular anal fistula. Aim: The study aims to characterize the role of adipose fat tissue in the pathogenesis of cryptoglandular anal fistula, with a specific focus on understanding the potential involvement of proinflammatory cytokines in the development of chronic inflammation. Materials and methods: This study involved the characterization of serum levels of inflammatory cytokines and adipose tissue hormones. A total of 35 samples from both simple and complex cryptoglandular perianal fistula cases were collected during surgical procedures. Results: Serum levels of leptin, resistin, IL-1β, and IL-8 were significantly elevated in patients operated on due to complex cryptoglandular perianal fistula when compared to patients with simple fistula. Adiponectin was significantly lowered in samples from complex perianal fistula in comparison to simple fistula. Conclusions: Complex perianal cryptoglandular fistula has a reduced level of anti-inflammatory adipokines i.e. adiponectin, and an increased level of proinflammatory resistin, leptin, IL-1β, and IL-8. [ABSTRACT FROM AUTHOR]

Background & Aims: Adipokines are among the biomarkers that have been studied in chronic pancreatitis (CP), as well as in pancreatic cancer (PC). So far, the existing findings are contradictory and inconclusive. Therefore, we assessed the levels of three major adipokines in CP in comparison to controls and PC, adiponectin, leptin, and resistin. Methods: A systematic electronic search was carried out in November 2022 using PubMed, Embase, and Scopus, reviewing observational studies. By using the Newcastle-Ottawa Scale, the included studies' quality was evaluated (NOS). In the examination of the estimated overall effect size, we employed the random-effects model in conjunction with the mean difference (MD) analysis. The MD with 95% confidence interval (CI) served as the primary summary outcome. Results: Our systematic review included a total of 14 studies, out of which nine were considered in our metaanalysis. A significant MD related to leptin levels in CP patients vs. controls (-1.299, 95%CI: -2.493 - -0.105), resistin levels in CP patients vs. controls (8.356, 95%CI: 3.700-13.012), and adiponectin levels in PC patients vs. controls (11.240, 95%CI: 5.872-16.60) was reported. However, no significant MD was reported in leptin levels between CP vs. PC patients (-0.936, 95%CI: -3.325-1.454), as well as adiponectin levels in CP patients vs. controls (0.422. 95%CI -5.651-6.535]) and in CP vs. PC patients (-6.252, 95%CI -13.269-0.766). Conclusions: CP was significantly associated with decreased leptin levels and increased resistin levels. Furthermore, increased levels of adiponectin are associated with PC. Yet, no significant MD was seen for leptin and adiponectin levels between CP and PC patients, and likewise for adiponectin levels between CP patients and controls. Results should be interpreted with caution due to the high heterogeneity among the included studies. [ABSTRACT FROM AUTHOR]

Introduction: Obesity is a prevalent co-morbidity in Polycystic Ovarian Syndrome (PCOS), causing metabolic disturbances that lead to changes in endocrinological homeostasis. Adipokines are proinflammatory molecules secreted by adipose tissues that affect metabolic and endocrinological mechanisms. Excess androgen secretion alters fat distribution and deposition, leading to increased visceral obesity in PCOS, which is a major concern for the development of cardiometabolic events. Aim: To assess the Visceral Adiposity Index (VAI) and levels of different adipokines in non obese and obese PCOS patients, and to establish the relationship between VAI and circulating adipokines in both non obese and obese phenotypes of PCOS patients. Materials and Methods: This cross-sectional study was conducted at the Mayo Institute of Medical Sciences, Barabanki, Uttar Pradesh, India from November 2019 to August 2021. A total of 144 patients diagnosed with PCOS according to the Rotterdam criteria were divided into non obese and obese categories based on Body Mass Index (BMI). VAI was calculated using a sex-specific formula, and serum levels of adiponectin, resistin, and leptin were measured by Enzyme Linked Immuno Sorbent Assay (ELISA). Fasting glucose, insulin, and serum lipid profiles were evaluated. Data were statistically analysed using Student's t-tests and Pearson's correlation coefficient. Weighted linear regression was used to detect any relationships between adipokines, obesity indicators, and VAI. Results: A total of 144 female patients with a mean age of 27.47±0.33 years suffering from PCOS were included in this study. VAI was significantly higher (p-value=0.034) in non obese patients than in obese patients. There was a significant correlation between VAI and resistin (r-value=0.302, p-value=0.011) and leptin (r-value=0.308, p-value=0.009) in the non obese PCOS group. Additionally, there was a significant association between obesity indicators {BMI, Body Fat Percentage (BFP), Waist Circumference (WC), and Hip Circumference (HC)} and VAI; this association was absent in the obese subgroup. According to the regression model, leptin was the only statistically relevant predictor for VAI among the studied PCOS patients (t-value=2.278, p-value=0.024). Conclusion: VAI was higher in non obese PCOS patients. An imbalance in adipokines (leptin and resistin) may lead to the accumulation of visceral fat without significantly affecting BMI. [ABSTRACT FROM AUTHOR]

Obesity, which leads to metabolic dysregulation and body function impairment, emerges as one of the pressing health challenges worldwide. Excessive body fat deposits comprise a dynamic and biologically active organ possessing its own endocrine function. One of the mechanisms underlying the pathophysiology of obesity is low-grade systemic inflammation mediated by pro-inflammatory factors such as free fatty acids, lipopolysaccharides, adipokines (including leptin, resistin and visfatin) and cytokines (TNF-α, IL-1β, Il-6), which are secreted by adipose tissue. Together with obesity-induced insulin resistance and hyperandrogenism, the exacerbated immune response has a negative impact on the hypothalamic–pituitary–gonadal axis at all levels and directly affects reproduction. In women, it results in disrupted ovarian function, irregular menstrual cycles and anovulation, contributing to infertility. This review focuses on the abnormal intracellular communication, altered gene expression and signaling pathways activated in obesity, underscoring its multifactorial character and consequences at a molecular level. Extensive presentation of the complex interplay between adipokines, cytokines, immune cells and neurons may serve as a foundation for future studies in search of potential sites for more targeted treatment of reproductive disorders related to obesity. [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]

Background: In a great many of observational studies, whether there is a relevance of resistin levels on bone mineral density (BMD) and fracture occurrence has been inconsistently reported, and the causality is unclear. Methods: We aim to assess the resistin levels on BMD and fracture occurrence within a Mendelian randomization (MR) analysis. Exposure and outcome data were derived from the Integrative Epidemiology Unit (IEU) Open genome wide association studies (GWAS) database. Screening of instrumental variables (IVs) was performed subject to conditions of relevance, exclusivity, and independence. Inverse variance weighting (IVW) was our primary method for MR analysis based on harmonized data. Weighted median and MR-Egger were chosen to evaluate the robustness of the results of IVW. Simultaneously, heterogeneity and horizontal pleiotropy were also assessed and the direction of potential causality was detected by MR Steiger. Multivariable MR (MVMR) analysis was used to identify whether confounding factors affected the reliability of the results. Results: After Bonferroni correction, the results showed a suggestively positive causality between resistin levels and total body BMD (TB-BMD) in European populations over the age of 60 [β(95%CI): 0.093(0.021, 0.165), P = 0.011]. The weighted median [β(95%CI): 0.111(0.067, 0.213), P = 0.035] and MR-Egger [β(95%CI): 0.162(0.025, 0.2983), P = 0.040] results demonstrate the robustness of the IVW results. No presence of pleiotropy or heterogeneity was detected between them. MR Steiger supports the causal inference result and MVMR suggests its direct effect. Conclusions: In European population older than 60 years, genetically predicted higher levels of resistin were associated with higher TB-BMD. A significant causality between resistin levels on BMD at different sites, fracture in certain parts of the body, and BMD in four different age groups between 0–60 years of age was not found in our study. [ABSTRACT FROM AUTHOR]

Background/Objectives: Understanding the prognostic factors of acute ischemic stroke (AIS) is essential for improving patient outcomes. The aim of this study was to establish the predictive role of plasmatic resistin and leptin on short-term mortality in adult patients with a first episode of AIS. Methods: This study enrolled 277 patients who were consecutively hospitalized for AIS. Demographic data, cardiovascular risk, comorbidities, and laboratory tests were collected. Death was noted if it occurred during hospitalization. Results: Death was recorded in 33 (11.9%) patients. Conducting multivariate analysis, the following variables were independent variables associated with in-hospital mortality: a resistin value of >11 ng/mL (OR 10.81 (95%CI 2.31;50.57), p = 0.002), a lesion volume of >18.8 mL (OR 4.87 (95%CI 1.87;12.67), p = 0.001), a NIHSS score of >7 (OR 5.88 (95%CI 2.01;17.16), p = 0.001), and the presence of IHD (OR 4.33 (95%CI 1.66;11.27), p = 0.003). This study has some limitations: single-center design (which may affect the generalizability of the results) and the potential impact of the COVID-19 pandemic on patient outcomes. Conclusions: This study demonstrated that resistin is a significant predictor of in-hospital mortality in AIS patients. Other established factors, such as a high NIHSS score, large lesion volume, and the presence of IHD, were reaffirmed as important predictors. [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 Psoriasis is a chronic inflammatory skin disorder characterized by an increase in epidermal turnover and inflammation of the dermis. Resistin is one of the adipokines that promotes the production of proinflammatory mediators involved in the pathogenesis of psoriasis. This study aimed to assess the correlation between serum resistin levels with the severity of psoriasis vulgaris. Methods The disease severity was recorded based on Psoriasis Area and Severity Index (PASI) score, and serum resistin levels were obtained for each subject. The independent t test and One-Way ANOVA were applied for comparative analysis and the Pearson test was used to measure correlation analysis. Results Serum resistin levels didn't differ significantly between men and women (p=0.998) or also between the normal, overweight and obese subjects (p=0.624). Serum resistin levels were significantly higher in subjects with psoriasis vulgaris compared with controls (p<0.001). High serum resistin levels were markedly correlated (r=0.848; p<0.001) with the increased severity of psoriasis vulgaris based on the Psoriasis Area Severity Index (PASI) scores. Conclusion Serum resistin levels mediates the degree of inflammation of psoriasis and correlates with the severity of psoriasis vulgaris. [ABSTRACT FROM AUTHOR]

• Wheat germ improved markers of glucose homeostasis in overweight adults. • Wheat germ reduced the pro-inflammatory adipokine, resistin. • Gut microbiota and gut integrity markers were unaffected by wheat germ. Wheat germ (WG), a by-product of flour milling, is rich in bioactive substances that may help improve health complications associated with increased adiposity. This study investigated the effects of WG on gut health, metabolic, and inflammatory markers in adults classified as overweight. We hypothesized that WG, because of its many bioactive components, would improve gut health and metabolic, and inflammatory markers in overweight adults. Forty adults (18–45 years old) and with a body mass index between 25 and 30 kg/m2 participated in this single-blinded randomized controlled pilot study. Participants consumed the study supplements containing 30 g of either cornmeal (control, CL) or WG daily for 4 weeks. Primary outcome variables were gut health markers including gut microbiota, gut integrity markers, and fecal short-chain fatty acids, whereas secondary outcome variables included metabolic and inflammatory parameters assessed at baseline and at the end of supplementation. Thirty-nine participants (n = 19 and 20 for CL and WG group, respectively) completed the study. The genus Faecalibacterium was significantly higher in the WG group compared to CL post-supplementation but no significant changes in other gut health markers, short-chain fatty acids, inflammatory markers, and lipid profiles were observed. Compared with baseline, WG improved markers of glucose homeostasis including insulin (P =.02), homeostatic model assessment of insulin resistance (P =.03), glycated hemoglobin (P =.07), and the pro-inflammatory adipokine, resistin (P =.04). However, these parameters after intervention were not different with control. Our findings suggest that WG supplementation have modest effects on gut health but may provide an economical option for individuals to improve glycemic control. Daily consumption of 30 g of wheat germ supplement for 4 weeks by adults classified as overweight maintained the bacterial genus Faecalibacterium and improved several markers of glucose homeostasis including insulin, HOMA-IR, and HbA1c, and reduced the pro-inflammatory adipokine, resistin. Abbreviations: HbA1c, glycated hemoglobin; HOMA-IR, homeostatic model assessment of insulin resistance. [Display omitted] [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]

Purpose: The primary objective of this investigation is to systematically screen and identify differentially expressed proteins (DEPs) within the plasma of individuals afflicted with sepsis. This endeavor employs both Data-Independent Acquisition (DIA) and enzyme-linked immunosorbent assay (ELISA) methodologies. The overarching goal is to furnish accessible and precise serum biomarkers conducive to the diagnostic discernment of sepsis. Method: The study encompasses 53 sepsis patients admitted to the Affiliated Hospital of Southwest Medical University between January 2019 and December 2020, alongside a control cohort consisting of 16 individuals devoid of sepsis pathology. Subsequently, a subset comprising 10 randomly selected subjects from the control group and 22 from the sepsis group undergoes quantitative proteomic analysis via DIA. The acquired data undergoes Gene Ontology (GO) and Kyoto Encyclopedia of Genes (KEGG) analyses, facilitating the construction of a Protein-Protein Interaction (PPI) network to discern potential markers. Validation of core proteins is then accomplished through ELISA. Comparative analysis between the normal and sepsis groups ensues, characterized by Receiver Operating Characteristic (ROC) curve construction to evaluate diagnostic efficacy. Result: A total of 187 DEPs were identified through bioinformatic methodologies. Examination reveals their predominant involvement in biological processes such as wound healing, coagulation, and blood coagulation. Functional pathway analysis further elucidates their engagement in the complement pathway and malaria. Resistin emerges as a candidate plasma biomarker, subsequently validated through ELISA. Notably, the protein exhibits significantly elevated levels in the serum of sepsis patients compared to the normal control group. ROC curve analysis underscores the robust diagnostic capacity of these biomarkers for sepsis. Conclusion: Data-Independent Acquisition (DIA) and Enzyme-Linked Immunosorbent Assay (ELISA) show increased Resistin levels in sepsis patients, suggesting diagnostic potential, warranting further research. [ABSTRACT FROM AUTHOR]

Background: Abnormal remodeling of distal pulmonary arteries in patients with pulmonary arterial hypertension (PAH) leads to progressively increased pulmonary vascular resistance, followed by right ventricular hypertrophy and failure. Despite considerable advancements in PAH treatment prognosis remains poor. We aim to evaluate the potential for using the cytokine resistin as a genetic and biological marker for disease severity and survival in a large cohort of patients with PAH. Methods: Biospecimens, clinical, and genetic data for 1121 adults with PAH, including 808 with idiopathic PAH (IPAH) and 313 with scleroderma-associated PAH (SSc-PAH), were obtained from a national repository. Serum resistin levels were measured by ELISA, and associations between resistin levels, clinical variables, and single nucleotide polymorphism genotypes were examined with multivariable regression models. Machine-learning (ML) algorithms were applied to develop and compare risk models for mortality prediction. Results: Resistin levels were significantly higher in all PAH samples and PAH subtype (IPAH and SSc-PAH) samples than in controls (P <.0001) and had significant discriminative abilities (AUCs of 0.84, 0.82, and 0.91, respectively; P <.001). High resistin levels (above 4.54 ng/mL) in PAH patients were associated with older age (P =.001), shorter 6-min walk distance (P =.001), and reduced cardiac performance (cardiac index, P =.016). Interestingly, mutant carriers of either rs3219175 or rs3745367 had higher resistin levels (adjusted P =.0001). High resistin levels in PAH patients were also associated with increased risk of death (hazard ratio: 2.6; 95% CI: 1.27–5.33; P <.0087). Comparisons of ML–derived survival models confirmed satisfactory prognostic value of the random forest model (AUC = 0.70, 95% CI: 0.62–0.79) for PAH. Conclusions: This work establishes the importance of resistin in the pathobiology of human PAH. In line with its function in rodent models, serum resistin represents a novel biomarker for PAH prognostication and may indicate a new therapeutic avenue. ML-derived survival models highlighted the importance of including resistin levels to improve performance. Future studies are needed to develop multi-marker assays that improve noninvasive risk stratification. [ABSTRACT FROM AUTHOR]

Aims/Introduction: Gene–environment interactions are considered to critically influence type 2 diabetes mellitus development; however, the underlying mechanisms and specific interactions remain unclear. Given the increasing prevalence of low birthweight (LBW) influenced by the intrauterine environment, we sought to investigate genetic factors related to type 2 diabetes development in individuals with LBW. Materials and Methods: The interaction between 20 reported type 2 diabetes susceptibility genes and the development of type 2 diabetes in LBW (<2,500 g) individuals in a population‐based Japanese cohort (n = 1,021) was examined by logistic regression and stratified analyses. Results: Logistic regression analyses showed that only the G/G genotype at the rs1862513 locus of the resistin gene (RETN), an established initiator of insulin resistance, was closely related to the prevalence of type 2 diabetes in individuals with LBW. Age, sex and current body mass index‐adjusted stratified analyses showed a significant interaction effect of LBW and the RETN G/G genotype on fasting insulin, homeostatic model assessment 2‐insulin resistance, Matsuda index and the prevalence of type 2 diabetes (all P‐values for interaction <0.05). The adjusted odds ratio for type 2 diabetes in the LBW + G/G genotype group was 7.33 (95% confidence interval 2.43–22.11; P = 0.002) compared with the non‐LBW + non‐G/G genotype group. Similar results were obtained after excluding the influence of malnutrition due to World War II. Conclusions: Simultaneous assessment of LBW and the RETN G/G genotype can more accurately predict the risk of future type 2 diabetes than assessing each of these factors alone, and provide management strategies, including early lifestyle intervention in LBW population. [ABSTRACT FROM AUTHOR]

Objective: Increasing evidence revealed the role of adipokines in carbohydrates and fat metabolism. The present study was designed to evaluate the adiponectin, leptin, and resistin levels in prediabetes subjects and evaluate the relationship between these adipokines and insulin resistance. Methods: A hospital-based descriptive study was conducted for one year. 200 individuals who met the inclusion criteria were enrolled in the study. Based on the oral glucose tolerance test, the study subjects were grouped into healthy controls (n = 100), prediabetic non-obese (n = 61), and prediabetic obese (n = 39). Blood glucose estimation was done by the glucose oxidase peroxidase method. Chemiluminescent immunoassay was used for the measurement of insulin level and homeostasis model assessment-estimated insulin resistance was used for the assessment of insulin resistance. Serum adipokines levels were determined by ELISA. Statistical analysis was performed by using SPSS Software. Results: Serum adiponectin levels decreased significantly in obese prediabetes (7.21 ± 2.15 µg/ml) when compared to non-obese prediabetes (7.28 ± 2.41 µg/ml) and healthy control subjects (13.64 ± 2.88 µg/ml, p < 0.001). Serum leptin levels increased significantly in obese prediabetes (13.59 ± 2.59 ng/ml) when compared to non-obese prediabetes (9.84 ± 2.66 ng/ml) and healthy control subjects (12.28 ± 2.65 ng/ml, p < 0.001). Serum resistin levels increased significantly in obese prediabetes (17.67 ± 3.60 ng/ml) when compared to non-obese prediabetes (17.2 ± 3.93 ng/ml) and healthy control subjects (14.46 ± 4.16 ng/ml, p < 0.001). Adiponectin-leptin ratio decreased significantly in obese prediabetes (0.56 ± 0.22) when compared to non-obese prediabetes (0.79 ± 0.4) and healthy control subjects (1.15 ± 0.37; p < 0.001). Fasting insulin resistance was statistically significant (p < 0.001) in all groups. Conclusion: The present study strongly suggests that the adipokine profile is an ideal diagnostic tool to predict prediabetes and metabolic syndrome, especially among those with insulin resistance. [ABSTRACT FROM AUTHOR]

Epidemiological studies have shown that the levels of serum adipokine such as leptin and resistin are associated with the risk of developing systemic lupus erythematosus (SLE). Nevertheless, whether either leptin or resistin has causal impacts on the risk of SLE is still unknown. In this study, two-sample univariable MR analyses and multivariable MR analysis were performed to explore the causal relationships between adipokines and SLE. Additionally, the potential causal effects of SLE on major adipokines were evaluated using reverse MR analyses. The results of inverse-variance weighted (IVW), weighted median, weighted mode and MR‒Egger methods concordantly supported that major adipokines have no causal effects on the risk of SLE. In the multivariable MR IVW analysis with leptin and resistin as covariates, neither leptin (odds ratio (OR) = 3.093, P = 0.067) nor resistin (OR = 0.477, P = 0.311) was identified as an independent risk factor for SLE, which is in line with the univariable MR results. In conclusion, our analyses revealed no evidence to support that these three major adipokines are risk factors for SLE. [ABSTRACT FROM AUTHOR]

Few studies have reported the cardiovascular health effects of different high-intensity interval training (HIIT) protocols among sedentary young women. We investigated the impact of a traditional HIIT programme and a high-intensity circuit training (HICT) programme on lipid profiles and inflammatory cytokine levels in sedentary young women. Forty-two women were randomly assigned to HICT (body weight-based training), HIIT (cycling-based training), or control groups (n = 14 each). HICT and HIIT participants completed an 8-week training programme of three sessions per week. Total cholesterol (TC), triglyceride, high- and low-density lipoprotein, leptin, resistin, tumour necrosis factor-alpha (TNF-α), interleukin-8, and interferon-gamma levels were measured before and after the intervention. Post-intervention, TC and leptin were decreased in the HICT group. The HICT group also demonstrated increased lean mass, upper and lower limb strength, and balance, while the HIIT group displayed improved lower limb strength. Additionally, the control group showed significant increases in triglyceride levels, weight, body mass index, and fat mass. In conclusion, although both HICT and HIIT interventions showed improvements in cardiovascular health and physical fitness, participants in the HICT group experienced more health benefits. [ABSTRACT FROM AUTHOR]

Summary: Obesity is reported to increase stroke risk, with adipocyte‐derived cytokines or adipokines implicated as mediators. However, the relationship between adipokines and stroke is not well clarified. Thus, we aimed to evaluate the association of adipokines with stroke using fully adjusted risk estimates that incorporated body mass index in a meta‐analysis. Data from 52 studies (62,428 patients) were pooled in a random‐effects meta‐analysis. Adiponectin was independently associated with a lower risk of pre‐existing stroke (adjusted odds ratio: 0.64 [95% confidence interval: 0.46–0.88], p < 0.01), whereas leptin (1.08 [1.00–1.17], p = 0.04), resistin (1.06 [1.04–1.08], p < 0.01) and visfatin (1.04 [1.01–1.07], p = 0.01) are associated with a higher risk of stroke, but none with incident stroke. Adipokines independently associated with an ischaemic stroke subtype were adiponectin (0.48 [0.30–0.77], p < 0.01), leptin (1.10 [1.01–1.20], p = 0.04), and resistin (1.06 [1.04–1.08], p < 0.01). Fatty acid‐binding protein‐4 (FABP‐4) independently predicted 6‐month poor functional outcomes in stroke patients (adjusted hazard ratio: 1.09 [1.06–1.12], p < 0.01); whereas both FABP‐4 (1.17 [1.03–1.34], p = 0.01) and visfatin (1.24 [1.00–1.55], p = 0.05) were predictive of 6‐month mortality. Adipokines are associated with a greater risk of pre‐existing stroke, but not with the relationship with incident stroke. Adipokines, such as FABP‐4 and visfatin, may serve as biomarkers of stroke severity and worsening of stroke outcomes. [ABSTRACT FROM AUTHOR]

Gestational diabetes mellitus (GDM) is a complex metabolic disorder that has short- and long-term effects on maternal and offspring health. This study aimed to assess the impact of maternal hyperglycemia severity, classified as GDM-G1 (diet treatment) and GDM-G2 (insulin treatment) on colostral appetite-regulating molecules. Colostrum samples were collected from hyperglycemic (N = 30) and normoglycemic (N = 21) mothers, and the concentrations of milk hormones were determined by immunoenzymatic assay. A difference was found for milk ghrelin, but not for molecules such as adiponectin, leptin, resistin, or IGF-I levels, in relation to maternal hyperglycemia. The colostral ghrelin in the GDM-G1 cohort (0.21 ng/mL) was significantly lower than for GDM-G2 (0.38 ng/mL) and non-GDM groups (0.36 ng/mL). However, colostral resistin was higher, but not significantly, for GDM-G1 (13.33 ng/mL) and GDM-G2 (12.81 ng/mL) cohorts than for normoglycemic mothers (7.89 ng/mL). The lack of difference in relation to hyperglycemia for milk leptin, adiponectin, leptin–adiponectin ratio, resistin, and IGF-I levels might be the outcome of effective treatment of GDM during pregnancy. The shift between ghrelin and other appetite-regulating hormones might translate into altered ability to regulate energy balance, affecting offspring's metabolic homeostasis. [ABSTRACT FROM AUTHOR]

Purpose: This systematic review aims to gain the studies regarding the effect of Nigella Sativa (N. sativa) on adipokines including leptin, adiponectin and resistin. Design/methodology/approach: Search was carried out using databases Scopus, Web of Science, PubMed and Google Scholar with no restriction on language or date until February 2023 and alert services were applied to identify any paper after the primary search. Findings: Eighteen animal and human studies were eligible for the current systematic review. Leptin and resistin levels showed a downward tendency after consuming N. sativa and its ingredients [e.g. oil, thymoquinone (TQ) and thymol] as well as its extracts (e.g. water extract). Furthermore, considering 4 of 8 animal research studies and 2 of 5 human studies that evaluated adiponectin levels, a significant increase was observed after using N. sativa and its ingredients (e.g. oil, TQ and thymol). Originality/value: The present paper collates evidence from animal and human studies regarding the effect of N. sativa on adipokines including leptin, adiponectin and resistin. [ABSTRACT FROM AUTHOR]

Background: Assessing fetal growth constitutes a fundamental aim within the realm of prenatal care. Impaired prenatal growth increases the risk of perinatal mortality, morbidity, and poor newborn outcomes. Growth restriction increases the risk of premature birth problems, as well as the risk of poor neurodevelopmental outcomes and future non-communicable disorders such as hypertension and metabolic syndrome as adults. The objective of this systematic review is to accumulate current literature evidence to assess the patterns of serum adipokine levels among women with growth-restricted fetuses and assess their potential alterations in those high-risk pregnancies. Methods: Medline, Scopus, CENTRAL, Clinicaltrials.gov, and Google Scholar databases were systematically searched from inception until 31 March 2023. All observational studies reporting serum adipokine values among women with appropriately grown and growth-restricted fetuses were held eligible. Results: The current systematic review encompassed a total of 20 studies, incorporating a patient population of 1850 individuals. Maternal blood leptin emerged as the adipokine most investigated, as evidenced by 13 studies encompassing a collective sample size of 1081 patients, all of which explored its potential correlation with intrauterine growth restriction. Elevated levels of leptin were detected in fetuses with intrauterine growth restriction, although the observed difference did not reach statistical significance. Furthermore, regarding adiponectin, the meta-analysis conducted indicated that there were not any statistically significant differences observed in the mean values of adiponectin. The available data on the remaining three adipokines were extremely limited, making it difficult for any solid conclusions to be extracted. Conclusions: Though limited and inconsistent, the existing data suggest that fetal growth restriction is not linked to leptin, adiponectin, visfatin, resistin, or RBP4. More substantial prospective studies are needed to comprehend the importance of established and novel adipokines. [ABSTRACT FROM AUTHOR]

Background: Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is a chronic relapsing-remitting systemic disease of the gastrointestinal tract with rising incidence. Studies have shown that adipocytes play a crucial role in patients with IBD by actively participating in systemic immune responses. The present study was designed to investigate the correlation between the circulatory levels of resistin, as an adipokine, and active and remission phases of IBD in comparison with healthy controls. Methods: Relevant articles were retrieved from PubMed, Embase, the Web of Science, and Scopus from inception until June 2023. Estimation of the standardized mean difference (SMD) and 95% confidence interval (CI) for comparison of plasma/serum resistin levels between IBD patients, patients in remission, and healthy controls were conducted through random-effect meta-analysis. Results: A total of 19 studies were included, assessing 1836 cases. Meta-analysis indicated that generally, serum/plasma resistin levels were higher in IBD patients in comparison with healthy controls (SMD 1.33, 95% CI 0.58 to 2.08, p-value < 0.01). This was true for each of the UC and CD separate analyses, as well. Moreover, it was shown that higher serum/plasma resistin levels were detected in the active phase of IBD than in the remission phase (SMD 1.04, 95% CI 0.65 to 1.42, p-value = 0.01). Finally, higher serum/plasma resistin levels were found in the remission phase compared to healthy controls (SMD 0.60, 95% CI 0.15 to 1.06, p-value < 0.01). Conclusion: The results of this systematic review and meta-analysis support the conclusion that circulating resistin levels are increased in IBD (both UC and CD). Also, higher resistin levels were recorded in the remission phase of IBD in comparison with healthy controls. This indicates that further studies may provide valuable insights into the role of resistin in the pathogenesis of IBD. [ABSTRACT FROM AUTHOR]

Introduction: Nitric oxide (NO) and resistin play significant roles in the inflammatory processes and pathogenesis of psoriasis, and are associated with comorbidities often seen in psoriasis patients. Objective: We evaluated the correlation between the level of resistin gene expression in peripheral blood mononuclear cells (PBMCs) and the serum NO levels in patients with psoriasis. Material and methods: We studied 60 cases with psoriasis and 40 healthy controls. The serum level of NO in the blood of the study groups, psoriasis and healthy control respectively, was determined using the Griess technique and the Kiazist kit (Kiazist, Iran). In addition, we performed real-time PCR to assay resistin gene expression in PBMCs from both groups. Results: The serum NO levels in patients with psoriasis were significantly higher than in healthy controls (p = 0.001). The resistin gene expression in PBMCs was significantly elevated in psoriatic patients group (p = 0.001). Conclusions: The findings revealed that, in addition to having higher levels of platelets and WBC in their serum, patients with psoriasis, have higher levels of NO and upregulated resistin gene expression, which is likely due to the pathological role of these factors in the occurrence or maintenance of psoriasis. The rise in NO levels and resistin gene expression suggests they may play a role in the pathology of psoriasis. [ABSTRACT FROM AUTHOR]

Objectives: Matrix metalloproteinases (MMPs) are calcium-dependent zinc-containing endo-peptidases engaged in many biological processes including adipogenesis, angiogenesis, and tissue remodeling. Fat tissue infiltration by peripheral leukocytes plays an important role in transition of fat tissue residual, non-inflammatory status into the pro-inflammatory one, resulting in fat tissue inflammation and expansion as well as production of many mediators like adipokines and cytokines. The aim of this study was to investigate the expression of MMPs, their endogenous tissue inhibitors (TIMPs), and selected inflammatory mediators in leukocytes and plasma of children with simple obesity to find their associations with obesity-related phenotypes. Material and methods: Twenty-six overweight/obese children and twenty-three healthy volunteers participated in the study. The leukocyte mRNA expression levels of MMP-2, -9, -12 -14, TIMP-1, -2, and IL-6 were analyzed by the real time quantitative PCR. Plasma MMP-9/TIMP-1 and MMP-2/TIMP-2 ratios as well as the concentrations of MMP-9, TIMP-1, IL-1 beta, IL-6, TNF- alpha, leptin and resistin were tested by ELISA assays. Gelatin zymography was used to assess the activity of the leukocyte MMPs proteins. Results: The obese children showed the following: a) increased expression of leukocyte TIMP-1 and slight elevation (close to statistical significance) of leukocyte MMP-9 (p = 0.054), the decline in MMP-2, b) elevation of plasma MMP-9, leptin, and MMP9/TIMP1 ratio, c) reduced expression of plasma TNF-alpha and MMP-2/TIMP-2 ratio. Several negative correlations were found: TIMP2 vs. ALT (r = −0.536), AST (r = −0.645) and TTG (r = −0.438), IL-6 vs. GGTP (r = −0.815), and MMP12 vs. TTG (r = −0.488), leptin vs. ALT (r = −0.569), MMP-9 vs. total cholesterol (r = −0.556). The only positive correlation was that of plasma leptin level vs. GGTP (r = 0.964). Conclusions: At the beginning of obesity development (children), possibly compensatory reactions prevail, reflected here by an increase in the expression of leukocyte MMPs inhibitor TIMP-1, decrease in the level of leukocyte MMP-2 and plasma MMP-2, MMP2/TIMP-2 ratio, low plasma TNF-alpha and negative correlations between the expression of TIMP-2 and liver (AST, ALT) or fat (TTG) inflammatory markers. [ABSTRACT FROM AUTHOR]

Depressive disorder is a complex mental health condition in which the etiopathogenesis involves several factors. Suitable biomarkers for the development of depression have not yet been established. Alterations in cytokines are assumed to be involved in the pathophysiology of depressive disorder. Adipokines (also known as adipocytokines) are important factors that not only regulate the energy balance but also regulate the inflammatory and immune responses. This study investigated the serum levels of adiponectin, leptin, resistin, chemerin, and fetuin A and the possible role of these adipokines in depressive disorder. We recruited a total of 73 patients diagnosed with recurrent depressive disorder (rDD) and 54 age- and sex-matched healthy controls (HCs). Serum adipocytokines were determined using ELISA kits (R&D, USA). The serum levels of the investigated molecules between depressive patients and HCs were compared, and diagnostic values were evaluated using the receiver operating characteristic (ROC) curve method for discriminating depressive patients from HCs. Correlations between the molecules and clinical variables were also evaluated. Patients with rDD had lower levels of serum adiponectin and chemerin and higher levels of serum leptin, resistin and fetuin A (p < 0.05) vs. controls. Moreover, ROC curve analysis showed that the area under the curve (AUC) values of above set of adipocytkines were >0.7, with a sensitivity and specificity over 80% in discriminating patients with rDD from HCs. Conclusions: These results suggest that circulating adipocytokies may hold promise as biomarkers for the diagnosis of rDD. [ABSTRACT FROM AUTHOR]

Background: the single nucleotide polymorphism (SNP) (rs3138167) is a polymorphism that has been associated with metabolic disorder in obese subjects and its effect on the metabolic response after a dietary intervention has not been evaluated. Objective: our aim was to analyze the effects of the rs3138167 on metabolic changes secondary to weight loss with a hypocaloric diet with a Mediterranean pattern. Method: one thousand and eight Caucasian obese patients were evaluated. Before and after 12 weeks on a hypocaloric diet with Mediterranean pattern, an anthropometric evaluation and a biochemical analysis were performed. The statistical analysis was performed as a dominant model (CC vs. CT + TT). Results: the values of insulin, HOMA-IR and resistin were higher in T allele carriers than non-T allele carriers in pre- and post-intervention time. In non-T allele carriers, resistin, insulin, HOMA-IR, triglycerides and C-reactive protein levels decreased. The improvement was statistically superior in non-T allele carriers; resistin (-1.2 ± 0.2 ng/dl; p = 0.02), triglycerides (-18.3 ± 4.3 mg/dl; p = 0.02), C-reactive protein (-2.6 ± 0.3 mg/dl; p = 0.02), insulin -4.4 ± 1.9 mUI/l; p = 0.02) and HOMA-IR (-2.1 ± 0.7; p = 0.03). Conclusion: we report an association of rs3138167 with a worse metabolic response (insulin, HOMA-IR, triglyceride and C-reactive protein) in T allele carriers after weight loss with a hypocaloric diet with Mediterranean pattern. [ABSTRACT FROM AUTHOR]

Childhood obesity has been related to metabolic syndrome and low-grade chronic inflammation. This study aimed to evaluate the impact of physical activity intensities and practice on inflammation, endothelial damage, and cardiometabolic risk factors in children. There were 513 participants, aged 6–14 years, recruited for the study. Physical activity was measured by accelerometry, and the children were classified into four groups according to quartiles of moderate to vigorous physical activity (MVPA) practice as very low active, low active, moderate active, and high active. Anthropometric measures, blood pressure, and plasma metabolic and proinflammatory parameters were analyzed. Very low active group presented a worse lipid profile and higher insulin, leptin, adiponectin, resistin, matrix metallopeptidase-9, and tissue plasminogen activator inhibitor-1, while lower levels of tumor necrosis factor-alpha, Type 1 macrophages, and interleukin 8 than high-active children. Regression analyses showed that a higher MVPA practice was associated with lower levels of triacylglycerols (β: −0.118; p =.008), resistin (β: −0.151; p =.005), tPAI (β: −0.105; p =.046), and P-selectin (β: −0.160; p =.006), independently of sex, age, and body mass index (BMI). In contrast, a higher BMI was associated with higher levels of insulin (β: 0.370; p <.001), Homeostasis Model Assessment (β: 0.352; p <.001), triacylglycerols (β: 0.209; p <.001), leptin (β: 0.654; p <.001), tumor necrosis factor-alpha (β: 0.182; p <.001), Type 1macrophages (β: 0.181; p <.001), and tissue plasminogen activator inhibitor (β: 0.240; p <.001), independently of sex, age, and MVPA. A better anthropometric, metabolic, and inflammatory profile was detected in the most active children; however, these differences were partly due to BMI. These results suggest that a higher MVPA practice and a lower BMI in children may lead to a better cardiometabolic status. [ABSTRACT FROM AUTHOR]

Resistin, a cytokine hormone predominantly secreted by adipose tissue, is elevated in various metabolic disorders such as obesity, type 2 diabetes, and cardiovascular disease. In addition to its involvement in metabolic regulation, resistin has been implicated in the pathogenesis of psoriasis, a chronic inflammatory skin disorder. Numerous studies have reported increased resistin levels in psoriatic skin lesions, suggesting a possible association between resistin and psoriasis. Recent studies have suggested the potential involvement of resistin in the development and progression of certain cancers. Resistin is overexpressed in breast, colorectal, and gastric cancers. This suggests that it may play a role in the development of these cancers, possibly by inducing inflammation and cell growth. The link between resistin and cancer raises the possibility of shared underlying mechanisms driving the pathogenesis of psoriasis. Chronic inflammation, one such mechanism, is a hallmark of psoriasis and cancer. Further research is needed to fully understand the relationship between resistin and psoriasis. Identifying potential therapeutic targets is crucial for effective management of psoriasis. By doing so, we may be able to develop more effective treatment options for individuals living with psoriasis and ultimately improve their quality of life. Ultimately, a more comprehensive understanding of the mechanisms underlying the impact of resistin on psoriasis is essential for advancing our knowledge and finding new ways to treat and manage this challenging condition. [ABSTRACT FROM AUTHOR]

The remission of obesity-related diseases following bariatric surgery appears to result from the reorganization of metabolic and hormonal pathways involving adipokines. This study aimed to investigate the relationship between changes in body adiposity and serum adipokine levels, as well as the association between variations in adiponectin or resistin levels and cardiometabolic risk blood biomarkers before and after Roux-en-Y gastric bypass. A longitudinal and prospective study was conducted with bariatric surgery patients. Anthropometric, body composition and blood biochemical parameters were measured before and at 2 and 6 months post-surgery. The data were analyzed using ANOVA, Pearson or Spearman correlation, and simple linear regression with a significance level of p < 0.05. Among 36 mostly female patients aged 30 to 39 years, significant reductions in body weight (−26.8%), fat mass (−50%), waist circumference (−18%) and waist-to-height ratio (−22%) were observed post-surgery. Serum adiponectin levels increased (+107%), while resistin (−12.2%), TNF-α (−35%), and PAI-1 (−11.1%) decreased. Glucose, insulin, CRP, cholesterol, LDL-c, triglycerides, and vitamin D also decreased. Waist circumference variation showed a positive correlation with PAI-1 and TNF-α and a negative correlation with adiponectin. The total fat mass showed a positive correlation with PAI-1. Adiponectin variation correlated negatively with glucose, resistin, and CRP but positively with HDL-c. Resistin showed a positive correlation with insulin and CRP. In conclusion, 6 months post-bariatric surgery, reducing abdominal adiposity had a more significant impact on serum adipokine levels than total fat mass. Adiponectin increase and resistin decrease acted as endocrine mediators driving the remission of cardiometabolic risk biomarkers in individuals with obesity following Roux-en-Y gastric bypass. [ABSTRACT FROM AUTHOR]

The cryptoglandular perianal fistula is a common benign anorectal disorder that is managed mainly with surgery and in some cases may be an extremely challenging condition. Perianal fistulas are often characterized by significantly decreased patient quality of life. Lack of fully recognized pathogenesis of this disease makes it difficult to treat it properly. Recently, adipose tissue hormones have been proposed to play a role in the genesis of cryptoglandular anal fistulas. The expression of adipose tissue hormones and epithelial-to-mesenchymal transition (EMT) factors were characterized based on 30 samples from simple fistulas and 30 samples from complex cryptoglandular perianal fistulas harvested during surgery. Tissue levels of leptin, resistin, MMP2, and MMP9 were significantly elevated in patients who underwent operations due to complex cryptoglandular perianal fistulas compared to patients with simple fistulas. Adiponectin and E-cadherin were significantly lowered in samples from complex perianal fistulas in comparison to simple fistulas. A negative correlation between leptin and E-cadherin levels was observed. Resistin and MMP2 levels, as well as adiponectin and E-cadherin levels, were positively correlated. Complex perianal cryptoglandular fistulas have a reduced level of the anti-inflammatory adipokine adiponectin and have an increase in the levels of proinflammatory resistin and leptin. Abnormal secretion of these adipokines may affect the integrity of the EMT in the fistula tract. E-cadherin, MMP2, and MMP9 expression levels were shifted in patients with more advanced and complex perianal fistulas. Our results supporting the idea of using mesenchymal stem cells in the treatment of cryptoglandular perianal fistulas seem reasonable, but further studies are warranted. [ABSTRACT FROM AUTHOR]

Background: Severe acute pancreatitis (SAP) is a dangerous condition with a high mortality rate. Many studies have found an association between adipokines and the development of SAP, but the results are controversial. Therefore, we performed a meta-analysis of the association of inflammatory adipokines with SAP. Methods: We screened PubMed, EMBASE, Web of Science and Cochrane Library for articles on adipokines and SAP published before July 20, 2023. The quality of the literature was assessed using QUADAS criteria. Standardized mean differences (SMD) with 95% confidence intervals (CI) were calculated to assess the combined effect. Subgroup analysis, sensitivity analysis and publication bias tests were also performed on the information obtained. Result: Fifteen eligible studies included 1332 patients with acute pancreatitis (AP). Pooled analysis showed that patients with SAP had significantly higher serum levels of resistin (SMD = 0.78, 95% CI:0.37 to 1.19, z = 3.75, P = 0.000). The difference in leptin and adiponectin levels between SAP and mild acute pancreatitis (MAP) patients were not significant (SMD = 0.30, 95% CI: -0.08 to 0.68, z = 1.53, P = 0.127 and SMD = 0.11, 95% CI: -0.17 to 0.40, z = 0.80, P = 0.425, respectively). In patients with SAP, visfatin levels were not significantly different from that in patients with MAP (SMD = 1.20, 95% CI: -0.48 to 2.88, z = 1.40, P = 0.162). Conclusion: Elevated levels of resistin are associated with the development of SAP. Resistin may serve as biomarker for SAP and has promise as therapeutic target. [ABSTRACT FROM AUTHOR]

Objective: Regular physical activity (PA) regulates important interactive pathways linking energy balance, neuroendocrine function, and hypothalamic pituitary ovarian axis. Consistent physical activities are known to improve insulin sensitivity which exerts its effects via adipokines. The purpose of the study is to determine insulin resistant (IR) status and the effect of brisk walking on the levels of adipocytokines in women with polycystic ovarian syndrome (PCOS). Design: It is a prospective study. Materials and methods: The study included 143 married women with PCOS (as per Rotterdam's criteria) and 110 married women as controls with at least one child through natural conception. Anthropometric measurements were documented. Adiponectin and resistin were analyzed. Homeostatic Model Assessment of IR (HOMA-IR) and HOMA-adiponectin were calculated to assess IR. A follow-up task of 150 minutes/week of PA of brisk walking of moderate intensity was advised for 12 weeks and the status was reassessed. Results: Infertile women with PCOS, hypoadiponectinemia, and hyperesistinemia with elevated markers of IR (HOMA-IR and HOMA-adiponectin) were observed. The baseline data were compared with estimates after 12 weeks, it was found that adiponectin levels were increased with 4.75% weight loss, and decreased levels of resistin, HOMA-IR, and HOMA-adiponectin were observed. Participants who met 150 minutes/week of brisk walking revealed an increase in adiponectin levels and a strong positive correlation (r = 0.76) was observed with regression analysis of metabolic equivalents of tasks (METs) PA with adiponectin levels. Diagnostic sensitivity and specificity of adiponectin at a cutoff value of 7.3 µg/mL with 150 minutes/week of PA were found to be 93.8 and 82.1%, respectively. It was observed a 16.6% reduction of HOMA-IR and 29% of HOMA-adiponectin in the women who completed 12 weeks of PA had statistically significant p-values. An ovarian follicular study revealed positive ovulation in 80% of the participants with >150 minutes/week of brisk walking. Conclusion: Brisk walking of 150 minutes/week resulted in increased adiponectin levels. Beneficial adiponectin facilitates the ovulatory menstrual cycle and thereby the chance of ovulation is increased in PCOS women. [ABSTRACT FROM AUTHOR]

The coexistence of stunting and excess weight in the same individual is defined as a double burden of malnutrition (DBM) and is associated with noncommunicable diseases. In this study, we evaluated the impact of DBM on adipokine concentrations and metabolic profiles in children compared with weight excess alone. Children were allocated to the weight excess group (n = 23) (height-for-age (HAZ) > 0.0 and < 2.0 Z-score and body mass index-for-age (BMI/A) > 1.0 Z-score) or DBM (n = 22) group (HAZ < −1.0 Z-score (including mild stunting) and BMI/A > 1.0 Z-score). Lipid, glycemic profile, resistin, plasminogen activator inhibitor-1, leptin, and adiponectin concentrations were analyzed. Glycemia was significantly higher in the DBM group compared to the weight excess group (5.05 (4.76–5.31) mmol/L vs. 4.57 (4.35–4.81) mmol/L), although no differences were found in insulin and homeostasis model assessment of insulin resistance (HOMA-IR). Adipokine concentrations did not differ between the groups. However, the DBM group showed higher resistin concentrations normalized by body fat mass than those of the weight excess group (1.44 (0.98–1.93) ng/mL vs. 0.76 (0.55–1.45) ng/mL). Insulin and HOMA-IR showed a negative correlation with adiponectin (r = −0.590 and −0.624, respectively, both p < 0.01). DBM was associated with increased glucose and resistin concentrations adjusted by fat mass compared to that associated with excess weight alone. Therefore, this association between mild stunting and weight excess has deleterious potential for long-term metabolic function, highlighting an additional precaution against weight gain in children, especially in those with stunting. [ABSTRACT FROM AUTHOR]

Objective(s): High levels of resistin are associated with metabolic diseases and their complications, including hypertension. The paraventricular nucleus (PVN) is also involved in metabolic disorders and cardiovascular diseases, such as hypertension. Therefore, this study aimed to study cardiovascular (CV) responses evoked by the injection of resistin into the lateral ventricle (LV) and PVN and determine the mechanism of these responses in the rostral ventrolateral medulla (RVLM). Materials and Methods: Arterial pressure (AP) and heart rate (HR) were evaluated in urethaneanesthetized male rats (1.4 g/kg intraperitoneally) before and after all injections. This study was carried out in two stages. Resistin was injected into LV at the first stage, and AP and HR were evaluated. After that, the paraventricular, supraoptic, and dorsomedial nuclei of the hypothalamus were chosen to evaluate the gene expression of c-Fos. Afterward, resistin was injected into PVN, and cardiovascular responses were monitored. Then to detect possible neural mechanisms of resistin action, agonists or antagonists of glutamatergic, GABAergic, cholinergic, and aminergic transmissions were injected into RVLM. Results: Resistin injection into LV or PVN could increase AP and HR compared to the control group and before injection. Resistin injection into LV also increases the activity of RVLM, paraventricular, supraoptic, and dorsomedial areas. Moreover, the CV reflex created by the administration of resistin in PVN is probably mediated by glutamatergic transmission within RVLM. Conclusion: It can be concluded that hypothalamic nuclei, including paraventricular, are important central areas for resistin actions, and glutamatergic transmission in RVLM may be one of the therapeutic targets for high AP in obese people or with metabolic syndrome. [ABSTRACT FROM AUTHOR]

The rising incidence of obesity has coincided with rising levels of poor reproductive outcomes. The molecular basis for the association of infertility in obese males is now being explained through various mechanisms. Insulin resistance, hyperglycemia, and changes in serum and gonadal concentrations of adipokines, like leptin, adiponectin, resistin, and ghrelin have been implicated as causes of male infertility in obese males. The effects of obesity and hypogonadism form a vicious cycle whereby dysregulation of the hypothalamic–pituitary–testicular axis—due to the effect of the release of multiple mediators, thus decreasing GnRH release from the hypothalamus—causes decreases in LH and FSH levels. This leads to lower levels of testosterone, which further increases adiposity because of increased lipogenesis. Cytokines such as TNF-α and interleukins, sirtuins, and other inflammatory mediators like reactive oxygen species are known to affect fertility in obese male adults. There is evidence that parental obesity can be transferred through subsequent generations to offspring through epigenetic marks. Thus, negative expressions like obesity and infertility have been linked to epigenetic marks being altered in previous generations. The interesting aspect is that these epigenetic expressions can be reverted by removing the triggering factors. These positive modifications are also transmitted to subsequent generations. [ABSTRACT FROM AUTHOR]

The design of a novel electrochemical impedimetric biosensor for label-free analysis of resistin, a biomarker for obesity, is reported. For the fabrication of the immunosensor, a novel approach composed of electrochemical copolymerization of double epoxy groups-substituted thiophene (ThidEp) and 3,4-Ethylenedioxythiophene (EDOT) monomers was utilized. Anti-resistin antibodies were covalently attached to the copolymer-coated electrode. The capture of resistin antigens by anti-resistin antibodies caused significant variations in charge transfer resistance (Rct) because of the immunoreactions between these proteins. Under optimum experimental variables, the changes in impedance signals were employed for the determination of resistin antigen concentration, and the prepared immunosensor based on conjugated copolymer illustrated a wide linear range between 0.0125 and 22.5 pg/mL, a low detection limit (LOD) of 3.71 fg/mL, and a good sensitivity of 1.22 kΩ pg−1mL cm2. The excellent analytical performance of the resistin immunosensor in terms of selectivity, sensitivity, repeatability, reproducibility, storage stability, and low detection limit might be attributed to the conductive copolymer film layer generation on the disposable indium tin oxide (ITO) platform. The capability of this system for the determination of resistin in human serum and saliva samples was also tested. The immunosensor results were in accordance with the enzyme-linked immunosorbent assay (ELISA) results. The matrix effects of human serum and saliva were also investigated, and the proposed immunosensor displayed good recovery ranging from 95.91 to 106.25%. The engineered immunosensor could open new avenues for obesity monitoring. [ABSTRACT FROM AUTHOR]

Purpose: Resistin is an inflammatory cytokine secreted mostly by adipocytes and immune cells that plays a role in the development of insulin resistance, diabetes, and cancer. We hypothesized that resistin’s inflammatory activity influences the free radical and oxidative stress pathways. Methods: We used human breast carcinogenic (MCF-7 and MDA-MB-231) and non-carcinogenic (MCF-10A) cells in this investigation and correlated the absorbed resistin concentration with the change in oxidative stress (TBARS, carbonated proteins) and antioxidant activity (Antioxidant Capacity, SuperOxideDismutase, CATalase, Glutathione Peroxidase). Results: Resistin was substantially more effective as a prooxidant at lower (12.5 ng/ml) concentrations, than at higher concentrations (25.0 ng/ml). Vitamin C did not appear to be an effective oxidative stress protector at antioxidant concentrations of 5.10–4 M. Leptin, at 100 ng/ml, did not result in conclusive oxidative stress or antioxidant defence stimulation, as expected. Conclusion: Taken together, the findings support resistin’s role as a non-oxidative stress marker and a metabolic signaling molecule. [ABSTRACT FROM AUTHOR]

Background: PCOS, considered to be a common endocrinological disorder of females of reproductive age is often associated with obesity, dyslipidemia, hyperandrogenism, metabolic syndrome and infertility. Adipokines levels in PCOS is also reported to be altered may play a key role in obesity and dyslipidemia and insulin resistance. This study explored the relation among Adiponectin to Resistin Ratio, Tryglyceride to HDL cholesterol, HOMA IR and BMI. Materials & Methods: In this cross sectional comparative study 144 PCOS patients were included. Anthropometric and Biochemical parameters were evaluated. Patient population was categorized into Obese and No-obese groups depending on BMI and all the parameters were compared. Correlation among Adiponectin to Resistin Ratio, Triglyceride to HDL cholesterol, HoMA IR and BMI was assessed. Result: Significant difference was observed between lipid profile of Obese and Non-Obese groups. TG: HDL Ratio also had strong association (r = 0.79) with BMI. A:R Ratio and TG: HDL Ratio correlated significantly (r= - 0.78). HOMA IR had moderate correlation with BMI (p = 0.54), A:R Ratio (r = -0.41) and TG: HDL Ratio (r = 0.59). Conclusion: In Obese PCOS patients Adiponectin and Resistin decrease significantly and A:R Ratio decrease significantly exposing the subjects to the more cardio-metabolic risk. TG:HDL Ratio can predict A:R Ratio, independent of HOMA IR. [ABSTRACT FROM AUTHOR]

Adipokines are substances secreted by adipose tissue that are receiving increasing attention. The approach to adipose tissue has changed in recent years, and it is no longer looked at as just a storage organ but its secretion and how it influences systems in the human body are also looked at. The role of adipokine seems crucial in developing future therapies for pathologies of selected systems. In this study, we look at selected adipokines, leptin, adiponectin, chemerin, resistin, omentin-1, nesfatin, irisin-1, visfatin, apelin, vaspin, heparin-binding EGF-like growth factor (HB-EGF), and TGF-β2, and how they affect systems in the human body related to physical activity such as the musculoskeletal and cardiovascular systems. [ABSTRACT FROM AUTHOR]

Resistin is an adipokine with metabolic and inflammatory functions. Epidemiological and translational studies report that an increase in plasma levels and tissue expression of resistin increases the aggressiveness of prostate tumor cells. Extracellular vesicles (EVs) are secreted constitutively and induced by cytokines, growth factors, and calcium and are found in multiple biological fluids such as saliva, serum, semen, and urine. In particular, EVs have been shown to promote tumor progression through the induction of proliferation, growth, angiogenesis, resistance to chemotherapy, and metastasis. However, the role of resistin in the migration, invasion, and secretion of EVs in invasive prostate tumor cells remains to be studied. In the present study, we demonstrate that resistin induces increased migration and invasion in PC3 cells. In addition, these phenomena are accompanied by increased p-FAK levels and increased secretion of MMP-2 and MMP-9 in resistin-treated PC3 cells. Interestingly, EVs isolated from supernatants of PC3 cells treated with resistin induce an increase in migration and invasion accompanied by high MMP-2 and MMP-9 secretion in an autocrine stimulation model. In summary, our data for the first time demonstrate that resistin induces migration and invasion, partly through the secretion of EVs with pro-invasive characteristics in PC3 cells. [ABSTRACT FROM AUTHOR]

Resistin, a diminutive secretory adipokine, has been linked to obesity and its related ailments. A growing body of evidence suggests that resistin may also be related to the pathogenesis preeclampsia. However, results of previous studies were not consistent. We performed a systematic review and meta-analysis to evaluate the level of circulating resistin in women with PE. A systematic search of Medline, Web of Science, and Embase databases from inception to April 28, 2023, was conducted to identify studies that compared blood resistin levels in pregnant women with and without PE. A random-effects model was utilized to pool the results, accounting for heterogeneity. The present study analyzed eighteen datasets from sixteen observational studies. The results of the meta-analysis demonstrated a statistically significant increase in blood resistin levels among women with PE compared to the control group. (standardized mean difference=0.35, 95% confidence interval: 0.16 to 0.54, p<0.001; I2=74%). The findings of the subgroup analysis indicate that various study characteristics, including study design, timing, and methods for measuring resistin, matching of body mass index between cases and controls, and study quality scores did not exert a significant impact on the outcomes. Nonetheless, it is noteworthy that the diagnostic criteria for PE employed in the studies included in the analysis may have influenced the results (p for subgroup difference=0.001). Women with preeclampsia exhibit a greater concentration of resistin in circulation when compared to healthy pregnant controls. [ABSTRACT FROM AUTHOR]

Numerous chronic conditions including obesity exhibit autophagic dysfunction. Association of immune cell autophagic marker regulation by body fat percentage (%BF) is unknown. Investigate autophagy activity in peripheral blood mononuclear cells (PBMCs) of adults with distinct %BFs and obesity-related circulating inflammatory markers. Sixteen individuals (eight males) with %BF above (n = 8, 36.9 ± 3.6 years, 27.1 ± 8.1%BF) and below (n = 8, 37.1 ± 3.7 years, 13.3 ± 3.7%BF) their age- and sex-specific 50th percentile value based on the American College Sports Medicine guidelines participated. Body fat percentage was calculated from hydrostatic weighing. PBMCs were isolated from venous blood, and PBMC autophagic flux markers (LC3-I, LC3-II, and p62) were measured via Western blot. CRP, resistin, leptin, and adiponectin were measured via ELISA. LC3-II/LC3-I ratio correlated with %BF (r=–0.56, p=.023). Insulin (p=.05) and CRP (p=.018) were higher in high %BF participants. Autophagic activity markers in PBMCs correlate with %BF, but are not different between %BF groups. [ABSTRACT FROM AUTHOR]

The aim of the study was to systematically explore the relationships between various adipokines and risks of endometrial atypical hyperplasia (EAH), type I endometrial cancer (EC), and type II EC. We enrolled 219 patients in this study, including 39 EAH, 87 type I EC, 38 type II EC and 55 control individuals. We subsequently explored the association of adipokine levels and the leptin-to-adiponectin (L/A) ratio with EAH, type I EC, and type II EC. The plasma leptin level and L/A ratio were significantly higher in the EAH group than in the control group (p = 0.012). Leptin, resistin, vaspin, and visfatin levels were significantly higher in the type I EC group; however, the adiponectin level was lower in the type I EC, which resulted in a higher L/A ratio. Notably, the L/A ratio and visfatin level in the type II EC group were significantly higher. Multiple logistic regression analysis revealed that a higher leptin level was significantly associated with a higher EAH risk (p = 0.012). Higher leptin level (p = 0.042) and L/A ratio (p = 0.027) were significantly associated with an increased type I EC risk. By contrast, higher leptin (p = 0.059) and visfatin (p = 0.003) levels, higher L/A ratio (p = 0.033), and lower adiponectin level (p = 0.042) were associated with an increased type II EC risk. We suggested that adipokines are potentially correlated with EAH and EC risks. What is already known on this subject? EAH and EC are considered significantly correlated with obesity and the related insulin resistance. Studies reported that some of the adipokines mediate obesity-related EC risk. What do the results of this study add? We systematically explored whether the adipokines produced from adipose tissue, including leptin, adiponectin, resistin, vaspin, and visfatin as well as the L/A ratio were associated with increased EAH, type I EC, and type II EC risks; whether they are independent risk factors for EAH and EC. Moreover, we analysed the underlying roles of these adipokines in EC tumorigenesis and development. What are the implications of these findings for clinical practice and/or further research? This study aimed to systematically explore the relationships between various adipokines and risks of EAH, type I EC, and type II EC, to suggest that adipokine levels correlated with EAH and EC risks, and to analyse the underlying molecular mechanisms linking adipokines with endometrial carcinogenesis. It is helpful to improve our understanding of EC tumorigenesis and development. [ABSTRACT FROM AUTHOR]

Purpose: Resistin, a novel pro-inflammatory protein implicated in inflammatory processes, has been suggested to play a role in colorectal development. However, evidence from observational studies has been inconsistent. Mendelian randomization may be a complementary method to examine this association. Methods: We conducted a two-sample Mendelian randomization to estimate the association between genetically determined circulating resistin concentrations and risk of colorectal cancer (CRC). Protein quantitative trait loci (pQTLs) from the SCALLOP consortium were used as instrumental variables (IVs) for resistin. CRC genetic summary data was obtained from GECCO/CORECT/CCFR (the Genetics and Epidemiology of Colorectal Cancer Consortium, Colorectal Cancer Transdisciplinary Study, and Colon Cancer Family Registry), and FinnGen (Finland Biobank). The inverse variance weighted method (IVW) was applied in the main analysis, and other robust methods were used as sensitivity analyses. Estimates for the association from the two data sources were then pooled using a meta-analysis approach. Results: Thirteen pQTLs were identified as IVs explaining together 7.80% of interindividual variation in circulating resistin concentrations. Based on MR analyses, genetically determined circulating resistin concentrations were not associated with incident CRC (pooled-IVW-OR per standard deviation of resistin, 1.01; 95% CI 0.96, 1.06; p = 0.67. Restricting the analyses to using IVs within or proximal to the resistin-encoding gene (cis-IVs), or to IVs located elsewhere in the genome (trans-IVs) provided similar results. The association was not altered when stratified by sex or CRC subsites. Conclusions: We found no evidence of a relationship between genetically determined circulating resistin concentrations and risk of CRC. [ABSTRACT FROM AUTHOR]

Diabetes is a metabolic disease with multifactorial causes. There are two types of diabetes in humans: type-1 diabetes, which occurs when the immune system attacks and eliminates insulin secreting cells, and type-2 diabetes, which can be triggered by a variety of factors, the most important being lifestyle, but can also be caused by various genotypes. Date palm sugar (DPS) is nutritive with good potential in treating diabetes due to the presence of polyphenols that have strong antioxidant properties. We assess various parameters in normal rats, sugar-treated rats and diabetes-induced rats, including body weight, food intake, water intake, blood glucose level, insulin level, insulin resistance, lipid profile, atherogenic index, adiponectin, resistin and TNF-α. The study results reveal that DPS contributes to significant improvement in diabetic rats. Thus, DPS is a beneficial substitute compared to other sugars in treating diabetes. [ABSTRACT FROM AUTHOR]

Obesity is a complicated disease characterized by abundant fat accumulation. It is associated with cardiovascular disease. The current study aimed to appreciate the role of synthesized zinc oxide nanoparticles (ZnONPs) (18.72 nm in size) in curbing cardiovascular disease in an obesity model of a high fat/sucrose diet in male rats. For 16 weeks, 24 rats were fed a high-fat diet and a 25% sucrose solution to develop obesity, and after that, the rats were randomly allocated into four groups of rats. Group 1 served as the control group and consisted of normal, non-obese rats. Group 2 comprised obese rats that were injected with an equivalent volume of a neutral substance, serving as vehicle control. In Group 3 or 4, obese rats were treated with an intraperitoneal injection of 5 or 10mg/kg of zinc oxide nanoparticles (ZnONPs) for eight weeks. The treatment of obese rats with ZnONPs decreased plasma levels of monocyte chemoattractant Protein-1 (MCP-1), resistin, ENA78, tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL6), and C reactive protein (CRP). Also, the remediation of obese rats with ZnONPs led to a significant decrease in body mass index (BMI), body weight gain, leptin, cholesterol, triglycerides, LDL (Low-density lipoprotein), glucose, and insulin resistance index (HOMA-IR). Moreover, ZnONPs treatment lowered troponin, creatine phosphokinase-MB (CK-MB), lactate dehydrogenase (LDH), cardiac or adipose tissue iron content, and malondialdehyde (MDA) either in blood or heart tissue. Otherwise, treating obese rats with ZnONPs enhanced plasma adiponectin levels, cardiac-reduced glutathione (GSH), and superoxide dismutase (SOD). In addition, ZnONPs displayed a significant influence on the cardiovascular system since they combat the rise in blood pressure and the pathological changes of the heart and aorta besides maintaining plasma nitric oxide levels. The results showed a positive correlation between BMI and MDA, MPC-1, CK-MB, and LDH. ZnONPs are convenient in treating cardiovascular disease in obese rats via reduced blood pressure, oxidative stress, cardiac iron accumulation, insulin resistance, and inflammatory markers. [ABSTRACT FROM AUTHOR]

Background: The correlation between plasma adipose factor levels and Alzheimer's patients is not entirely clear. Objective: We aimed to investigate associations between AD and plasma levels of three adipokines including plasma adiponectin, leptin, and resistin. Methods: A single-center, cross-sectional study recruited AD patients (n = 148) and cognitively normal (CN) controls (n = 110). The multivariate logistic regression analysis was applied to determine associations of adiponectin, leptin, and resistin with the presence of AD. The receiver operating characteristic (ROC) analysis was employed to determine the diagnostic power of adiponectin, leptin and resistin for AD. Results: After adjusted for the conventional risk factors, plasma levels of leptin (OR = 0.417, 95% CI: 0.272-0.638, p < 0.0001) and adiponectin (OR = 1.249, 95% CI: 1.151-1.354, p < 0.0001) were associated with the presence of AD. In total participants, the plasma adiponectin level was negatively correlated with MMSE scores (p < 0.0001) and was positively with CDR scores (p < 0.0001) and age (p < 0.0001). The plasma level of leptin was negatively correlated with CDR scores (p < 0.0001) and positively correlated with MMSE scores (p < 0.0001). Both adiponectin (p < 0. 0001) and leptin (p < 0. 0001) featured higher AUC than the random chance. Conclusions: Plasma adiponectin and leptin were associated with the presence, symptomatic severity, and diagnostic power of AD, suggesting a potential role of adipokines in the pathogenesis of AD. [ABSTRACT FROM AUTHOR]