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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]

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Background/Objectives. A Mediterranean diet (MD) has been associated with neuroprotective effects. We aimed to assess the MD's association with stroke prognosis and the potential mediators involved. Methods. Seventy patients with acute anterior circulation ischemic stroke were included. Dietary patterns were evaluated using the MEDAS scale, a food-frequency questionnaire, and a 24 h recall. Circulating biomarkers including insulin resistance (HOMA index), adipokines (resistin, adiponectin, leptin), choline pathway metabolites (TMAO, betaine, choline), and endothelial progenitor cells (EPCs) were measured. Early neurological improvement (ENI) at 24 h, final infarct volume, and functional outcome at 3 months were assessed. Results. Adherence to MD and olive oil consumption were associated with a lower prevalence of diabetes and atherothrombotic stroke, and with lower levels of fasting glycemia, hemoglobinA1C, insulin resistance, and TMAO levels. Monounsaturated fatty acids and oleic acid consumption correlated with lower resistin levels, while olive oil consumption was significantly associated with EPC mobilization. Multivariate analysis showed that higher MD adherence was independently associated with ENI and good functional prognosis at 3 months. EPC mobilization, lower HOMA levels, and lower resistin levels were associated with ENI, a smaller infarct volume, and good functional outcome. Conclusions. MD was associated with better prognosis after ischemic stroke, potentially mediated by lower insulin resistance, increased EPC mobilization, and lower resistin levels, among other factors. [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]

Background and Objectives: Acute ischemic stroke (AIS) is a leading cause of death and disability with poor long-term outcomes. Creating a predictive score for long-term mortality in AIS might be important for optimizing treatment strategies. The aim of this study is to develop and validate a predictive score for three-year mortality in patients with AIS using several demographic, clinical, laboratory and imaging parameters. Materials and Methods: This study included 244 AIS patients admitted to a tertiary center and followed up for three years. The patients' data included demographics, clinical features, laboratory tests (including resistin and leptin levels) and imaging parameters. The patients were randomly divided into a predictive group (n = 164) and a validation group (n = 80). Results: Advanced age, a high NIHSS score, low levels of hemoglobin, elevated resistin levels and the presence of carotid plaques were independently associated with three-year mortality. The predictive model incorporated these variables, and it was validated in a separate cohort. Leptin levels did not significantly predict mortality. Conclusions: This study developed and validated a promising predictive score for three-year mortality in patients with AIS. Advanced age, high NIHSS scores, low hemoglobin levels, elevated resistin levels and the presence of carotid plaques were the independent predictors of long-term mortality. [ABSTRACT FROM AUTHOR]

Abstract Objectives Metabolic syndrome is a cluster of conditions that increases the risk of atherosclerotic cardiovascular diseases. The current study was a randomized, double blind, placebo-controlled study that aimed to determine the impact of green coffee (GC) in obese patients with metabolic syndrome through analysis of miRNA-155, miRNA-133a and the inflammatory biomarkers such as resistin, TNF-α, total sialic acid, homocysteine, high sensitivity C-reactive protein (hs-CRP), and the anti-inflammatory cytokine, adiponectin. Methods One hundred-sixty obese patients were randomly supplemented either with GC capsules (800 mg) or placebo daily for six months. Both groups were advised to take a balanced diet. Blood samples were collected at baseline and after six months of supplementation. Results GC supplementation for 6 months reduced BMI (p = 0.002), waist circumference (p = 0.038), blood glucose (p = 0.002), HbA1c% (p = 0.000), Insulin (p = 0.000), systolic blood pressure (p = 0.005), diastolic BP (p = 0.001) compared with placebo. GC significantly decreased total cholesterol (TC, p = 0.000), LDL-C (p = 0.001), triglycerides (TG, p = 0.002) and increased HDL-C (p = 0.008) compared with placebo group. In addition, GC significantly (p ≤ 0.005) reduced total sialic acid, homocysteine, resistin, TNF-α, hs-CRP and the oxidative stress marker malondialdehyde (MDA), but increased serum adiponectin (p = 0.000) compared to placebo group. There was a significant reduction in the gene expression of miR-133a (p = 0.000) in GC group as compared with baseline levels and with the control placebo group (p = 0.001) after 6 months. Conclusion GC administration modulated metabolic syndrome by decreasing BMI, high BP, blood glucose, dyslipidemia, miRNA-133a and inflammatory biomarkers that constitute risk factors for cardiovascular diseases. ClinicalTrials.gov registration No. is NCT05688917. Graphical Abstract

Background and objectives: Obesity is a well-known cause of cardiovascular disease and metabolic disorders. Normal-weight obesity, where the body mass index(BMI) is within the normal range but the body fat percentage is high, also adversely impacts cardiovascular and metabolic health. This study explored the effects of whole-body circuit training using a weighted vest on serum resistin, insulin resistance, and cardiovascular disease risk factors in normal-weight obese women. Methods: Thirty-six normal-weight obese women were divided into three groups: Weighted Vest Circuit Training(WVCT)(n = 12), Body Weight Circuit Training(BWCT)(n = 12), and a Control group(CON)(n = 12). Participants in the WVCT and BWCT groups engaged in whole-body circuit training three times per week for eight weeks. Serum resistin, cardiovascular disease risk factors, and insulin resistance were measured before and after the intervention. Results: The study revealed significant and impactful findings. There were substantial improvements in body composition(Skeletal Muscle Mass: +7.5 %, p = 0.042, d = 0.80), Serum Resistin(-38.2 %, p = 0.001, d = 0.85), insulin resistance(HOMA-IR: 27.1 %, p

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.

Obesity has a complex multifactorial etiology and is characterized by excessive accumulation of adipose tissue. Visceral adipose tissue has deleterious effects on health because it secretes large amounts of inflammatory cytokines. Nutritional calorie restriction associated with strength training may be useful in managing chronic systemic inflammation. This study aimed to evaluate the acute effect of a single strength-training session on plasma adipokine levels in sedentary, overweight, and obese young men. This study included twelve men (Age: [34.95 ​± ​9.77] years; Height: [174.16 ​± ​3.66] centimeter [cm]; Weight: [97.83 ​± ​12.87] kilogram (kg); body mass index [BMI]: [32.30 ​± ​4.51] kg/m2), who performed a single strength training session. The strength training protocol consisted of 4 sets of 12 repetitions in the following six exercises, 45° leg press, bench press, leg extension, machine row, leg curl, and shoulder press. Blood samples were collected before, immediately after, and 1-h subsequent after strength training. The plasma levels of resistin and leptin were measured. A significant decrease in resistin levels were found 1 ​h after the strength training session if compared to levels before the training session (pre-[before] [2 390 ​± ​1 199] picograms per milliliter [pg/mL] vs post-1 h [1-h subsequent] [1 523 ​± ​798],6 ​pg/mL, p ​= ​0.002 8). The plasma leptin levels did not differ at any time point. In conclusion, a very well controlled single session of strength training significantly decreased the plasma levels of resistin without altering the concentration of leptin in overweight and obese individuals. This effect, at least in part, supports the benefits of exercise by reducing the low grade inflammation and insulin resistance in obesity.

Obesity has a complex multifactorial etiology and is characterized by excessive accumulation of adipose tissue. Visceral adipose tissue has deleterious effects on health because it secretes large amounts of inflammatory cytokines. Nutritional calorie restriction associated with strength training may be useful in managing chronic systemic inflammation. This study aimed to evaluate the acute effect of a single strength-training session on plasma adipokine levels in sedentary, overweight, and obese young men. This study included twelve men (Age: [34.95 ± 9.77] years; Height: [174.16 ± 3.66] centimeter [cm]; Weight: [97.83 ± 12.87] kilogram (kg); body mass index [BMI]: [32.30 ± 4.51] kg/m²), who performed a single strength training session. The strength training protocol consisted of 4 sets of 12 repetitions in the following six exercises, 45° leg press, bench press, leg extension, machine row, leg curl, and shoulder press. Blood samples were collected before, immediately after, and 1-h subsequent after strength training. The plasma levels of resistin and leptin were measured. A significant decrease in resistin levels were found 1 h after the strength training session if compared to levels before the training session (pre-[before] [2 390 ± 1 199] picograms per milliliter [pg/mL] vs post-1 h [1-h subsequent] [1 523 ± 798],6 pg/mL, p = 0.002 8). The plasma leptin levels did not differ at any time point. In conclusion, a very well controlled single session of strength training significantly decreased the plasma levels of resistin without altering the concentration of leptin in overweight and obese individuals. This effect, at least in part, supports the benefits of exercise by reducing the low grade inflammation and insulin resistance in obesity. [ABSTRACT FROM AUTHOR]

Introduction: Non-alcoholic fatty liver disease (NAFLD) is a major global health problem, in which liver fat exceeds 5% of the liver weight, without secondary causes of fat accumulation or excessive alcohol consumption. Resistin plays a key role in energy homeostasis, insulin resistance, inflammation, and metabolic disorders. This study aimed to investigate the relationship between resistin (RETN) level and NAFLD. Methods: In this cross-sectional study, 80 patients with NAFLD and 80 healthy individuals as controls were evaluated. Biochemical variables, liver enzymes, insulin, and resistin were measured. Data were analyzed using SPSS version 16 software. Results: The variables of cholesterol, insulin, triglyceride, HDL, body mass index, age, and liver enzymes were significantly different between the two groups of patients with NAFLD and healthy individuals (p

Abstract Background Adipose tissue is significantly involved in inflammatory bowel disease (IBD). Vitamin D can affect both adipogenesis and inflammation. The aim of this study was to compare the production of selected adipokines, potentially involved in the pathogenesis of IBD - adiponectin, resistin, retinol binding protein 4 (RBP-4), adipocyte fatty acid binding protein and nesfatin-1 in children with IBD according to the presence of 25-hydroxyvitamin D (25(OH)D) deficiency. Methods The study was conducted as a case-control study in pediatric patients with IBD and healthy children of the same sex and age. In addition to adipokines and 25(OH)D, anthropometric parameters, markers of inflammation and disease activity were assessed in all participants. Results Children with IBD had significantly higher resistin levels regardless of 25(OH)D levels. IBD patients with 25(OH)D deficiency only had significantly lower RBP-4 compared to healthy controls and also compared to IBD patients without 25(OH)D deficiency. No other significant differences in adipokines were found in children with IBD with or without 25(OH)D deficiency. 25(OH)D levels in IBD patients corelated with RBP-4 only, and did not correlate with other adipokines. Conclusions Whether the lower RBP-4 levels in the 25(OH)D-deficient group of IBD patients directly reflect vitamin D deficiency remains uncertain. The production of other adipokines does not appear to be directly related to vitamin D deficiency.

Inflammatory bowel disease (IBD) is a clinical condition of the gastrointestinal tract that has significant incidence in childhood. Major symptoms include abdominal pain, dyspepsia, delayed gastric emptying, anorexia, diarrhea and weight loss. IBD etiopathogenesis is multifactorial, with a proven involvement of cytokines. In this regard, cytokines like resistin and adiponectin produced by adipose tissue play a crucial role in inflammation. Particularly, resistin seems related to IBD severity and is considered a promising marker of disease occurrence and progression. Unraveling its mechanism of action and downstream effectors is mandatory when designing novel therapies. This preclinical study aims to further elucidate the action of resistin in causing functional gastrointestinal alterations, comparing it with the well-defined effect of adiponectin. To this end, we carried out electrophysiological analysis on murine gastric fundus. We found that resistin, similarly to adiponectin, increases smooth muscle cell (SMC) capacitance, indicative of cell surface remodeling, which is consistent with relaxation. However, contrary to adiponectin, resistin unalters membrane potential and inward Ca2+ entry and scarcely affects outward current, suggesting its inefficacy in markedly modifying electrical phenomena on the SMC membrane. This outcome, supporting the role of resistin in gastrointestinal distention, as observed in IBD, rules out a strikingly direct effect on SMCs.

Abstract 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

Abstract 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 (

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]

Gymnema sylvestre (GS) and berberine (BBR) are natural products that have demonstrated therapeutic potential for the management of obesity and its comorbidities, as effective and safe alternatives to synthetic drugs. Although their anti-obesogenic and antidiabetic properties have been widely studied, comparative research on their impact on the gene expression of adipokines, such as resistin (Res), omentin (Ome), visfatin (Vis) and apelin (Ap), has not been reported. Methodology: We performed a comparative study in 50 adult Mexican patients with obesity treated with GS or BBR for 3 months. The baseline and final biochemical parameters, body composition, blood pressure, gene expression of Res, Ome, Vis, and Ap, and safety parameters were evaluated. Results: BBR significantly decreased (p < 0.05) body weight, blood pressure and Vis and Ap gene expression and increased Ome, while GS decreased fasting glucose and Res gene expression (p < 0.05). A comparative analysis of the final measurements revealed a lower gene expression of Ap and Vis (p < 0.05) in patients treated with BBR than in those treated with GS. The most frequent adverse effects in both groups were gastrointestinal symptoms, which attenuated during the first month of treatment. Conclusion: In patients with obesity, BBR has a better effect on body composition, blood pressure, and the gene expression of adipokines related to metabolic risk, while GS has a better effect on fasting glucose and adipokines related to insulin resistance, with minimal side effects. [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]

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]

Heart failure with preserved ejection fraction (HFpEF) is one of the major subtypes of heart failure (HF) and no effective treatments for this common disease exist to date. Cardiac fibrosis is central to the pathology of HF and a potential avenue for the treatment of HFpEF. To explore key fibrosis‐related genes and pathways in the pathophysiological process of HFpEF, a mouse model of HFpEF was constructed. The relevant gene expression profiles were downloaded from the Gene Expression Omnibus database, and single‐sample Gene Set Enrichment Analysis (ssGSEA) was performed targeting fibrosis‐related pathways to explore differentially expressed genes (DEGs) in healthy control and HFpEF heart tissues with cross‐tabulation analysis of fibrosis‐related genes. Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed on the identified fibrosis‐related genes. The two most significant DEGs were selected, and further validation was conducted in HFpEF mice. The results indicated that myocardial fibrosis was significantly upregulated in HFpEF mice compared to healthy controls, while the ssGSEA results revealed significant differences in the enrichment of nine fibrosis‐related pathways in HFpEF myocardial tissue, with 112 out of 798 DEGs being related to fibrosis. The in vivo results demonstrated that expression levels of resistin‐like molecule gamma (Relmg) and adenylate cyclase 1 (Adcy1) in the heart tissues of HFpEF mice were significantly higher and lower, respectively, compared to healthy controls. Taken together, these results suggest that Relmg and Acdy1 as well as the fibrosis process may be potential targets for HFpEF treatment. [ABSTRACT FROM AUTHOR]

Background: Adipose tissue is significantly involved in inflammatory bowel disease (IBD). Vitamin D can affect both adipogenesis and inflammation. The aim of this study was to compare the production of selected adipokines, potentially involved in the pathogenesis of IBD - adiponectin, resistin, retinol binding protein 4 (RBP-4), adipocyte fatty acid binding protein and nesfatin-1 in children with IBD according to the presence of 25-hydroxyvitamin D (25(OH)D) deficiency. Methods: The study was conducted as a case-control study in pediatric patients with IBD and healthy children of the same sex and age. In addition to adipokines and 25(OH)D, anthropometric parameters, markers of inflammation and disease activity were assessed in all participants. Results: Children with IBD had significantly higher resistin levels regardless of 25(OH)D levels. IBD patients with 25(OH)D deficiency only had significantly lower RBP-4 compared to healthy controls and also compared to IBD patients without 25(OH)D deficiency. No other significant differences in adipokines were found in children with IBD with or without 25(OH)D deficiency. 25(OH)D levels in IBD patients corelated with RBP-4 only, and did not correlate with other adipokines. Conclusions: Whether the lower RBP-4 levels in the 25(OH)D-deficient group of IBD patients directly reflect vitamin D deficiency remains uncertain. The production of other adipokines does not appear to be directly related to vitamin D deficiency. [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]

Inflammatory bowel disease (IBD) is a clinical condition of the gastrointestinal tract that has significant incidence in childhood. Major symptoms include abdominal pain, dyspepsia, delayed gastric emptying, anorexia, diarrhea and weight loss. IBD etiopathogenesis is multifactorial, with a proven involvement of cytokines. In this regard, cytokines like resistin and adiponectin produced by adipose tissue play a crucial role in inflammation. Particularly, resistin seems related to IBD severity and is considered a promising marker of disease occurrence and progression. Unraveling its mechanism of action and downstream effectors is mandatory when designing novel therapies. This preclinical study aims to further elucidate the action of resistin in causing functional gastrointestinal alterations, comparing it with the well-defined effect of adiponectin. To this end, we carried out electrophysiological analysis on murine gastric fundus. We found that resistin, similarly to adiponectin, increases smooth muscle cell (SMC) capacitance, indicative of cell surface remodeling, which is consistent with relaxation. However, contrary to adiponectin, resistin unalters membrane potential and inward Ca2+ entry and scarcely affects outward current, suggesting its inefficacy in markedly modifying electrical phenomena on the SMC membrane. This outcome, supporting the role of resistin in gastrointestinal distention, as observed in IBD, rules out a strikingly direct effect on SMCs. [ABSTRACT FROM AUTHOR]

Objective: Resistin (RETN) is an adipocyte-specific hormone that participates in metabolism and modulates cellular inflammation. Our study aimed to assess the effects of RETN treatment on autophagy and the underlying molecular and biological mechanisms in bovine alveolar macrophages (BAMs). Methods: The optimal concentration of RETN + lipopolysaccharide (LPS) on macrophages was screened and then used to co-culture with alveolar macrophages. Autophagosomes in BAMs were examined using a transmission electron microscope (TEM). Quantitative real-time PCR (qRT-PCR) was used to detect the mRNA expression of microtubule-associated protein light chain 3 (LC3) and p62. Western blot (WB) was used to detect the protein expressions of LC3 and p62. The distribution of LC3 and p62 proteins in the cells was observed by immunofluorescence (IF). The concentrations of interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) were detected using enzyme-linked immunosorbent assay (ELISA). The protein expression of adenosine-monophosphate-activated protein kinase (AMPK), p-AMPK, mammalian target of rapamycin (mTOR), and p-mTOR was detected using WB. Results: The treatment of BAMs with RETN or LPS increased the number of autophagosomes and the ratio of LC3II/LC3I and decreased the expression level of p62 protein. RETN treatment significantly triggered autophagy compared to LPS treatment. Moreover, the ratios of p-AMPK/AMPK and p-mTOR/mTOR were upregulated and downregulated, respectively, after RETN treatment, suggesting that AMPK/mTOR signaling pathway activation is required for RETN-mediated autophagy in BAMs. Additionally, the ratio of LC3-II/LC3-I was lower, and the concentrations of IL-1β, IL-6, and TNF-α significantly decreased in the LPS and RETN co-treatment groups compared to the single LPS treatment group. However, both autophagy- and LPS-induced inflammation were partially alleviated by RETN treatment. Conclusion: RETN can promote autophagy in BAMs by activating the AMPK/mTOR signaling pathway, it may help prevent LPS-induced inflammation.

Abstract 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

BackgroundObesity leads to adipocyte hypertrophy and adipokine dysregulation and is an independent risk factor for venous thromboembolism (VTE). However, the association between adipokines and VTE is not well established.ObjectivesTo examine whether adipokines are associated with increased risk of incident VTE.MethodsWe studied 1888 participants of the Multi-Ethnic Study of Atherosclerosis cohort who were initially free of VTE and had adipokine (adiponectin, leptin, and resistin) levels measured at either examination 2 or 3 (2002-2004 or 2004-2005, respectively). During follow-ups, VTE was ascertained through hospitalization records and death certificates by using ICD-9 and 10 codes. We used multivariable Cox proportional hazards regression to assess the association between 1 standard deviation (SD) log-transformed increments in adipokines and incident VTE.ResultsThe mean ± SD age was 64.7 ± 9.6 years, and 49.8% of participants were women. Medians (interquartile range) of adiponectin, leptin, and resistin were 17.3 (11.8-26.2) mcg/mL, 13.5 (5.6-28.2) ng/mL, and 15.0 (11.9-19.0) ng/mL, respectively. There were 78 incident cases of VTE after a median of 9.7 (5.0-12.4) years of follow-up. After adjusting for sociodemographics, smoking, and physical activity, the hazard ratios (95% CIs) per 1 SD increment of adiponectin, leptin, and resistin were 1.14 (0.90-1.44), 1.29 (1.00-1.66), and 1.38 (1.09-1.74), respectively. The association for resistin persisted after further adjustments for body mass index and computed tomography-derived total visceral adipose tissue area.ConclusionHigher resistin levels were independently associated with greater risk of incident VTE. Larger prospective cohort studies are warranted to confirm this association.

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]

The aim of the study was to assess the impact of two lengths of Nordic walking (NW) training interventions combined with time-restricted eating (TRE) on improving body-composition parameters, lipid profiles, and levels of selected adipokines in women with elevated body mass. Overweight and obese women (n = 55, age: 21–85) were recruited. Four groups were selected: 6 weeks (SG6, n = 13) and 12 weeks intervention (SG12, n = 13); and two control groups: CON6 (n = 13) and CON12 (n = 13). The training sessions took place three times a week (60 min each) and were conducted outdoors under the supervision of a professional coach. The training intensity was determined individually. The extended NW program combined with TRE induced a significant weight reduction in SG12 by 1.96 kg (p = 0.010) and fat tissue by 1.64 kg (p = 0.05). The proposed interventions did not affect LBM, TBW [kg], VFA, and lipid profile. The LDL/HDL ratio changed with a small size effect. The leptin concentration differed between groups (p = 0.006), but not over time. For resistin, the differentiating factor was time (p = 0.019), with lower results observed after the intervention. The change in leptin concentration was negatively correlated with its baseline concentration (p = 0.025). Extended to 12 weeks, this intervention allows for an improvement in body composition. Neither 6 nor 12 weeks of training and fasting affected the lipoprotein profile. It is, therefore, indicated to recommend prolonged training protocols and to inform patients that beneficial effects will be seen only after prolonged use of training and time-restricted eating. [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]

Whole blood models are rapid and versatile for determining immune responses to inflammatory and infectious stimuli, but they have not been used for bacterial discrimination. Staphylococcus aureus, S. epidermidis and Escherichia coli are the most common causes of invasive disease, and rapid testing strategies utilising host responses remain elusive. Currently, immune responses can only discriminate between bacterial 'domains' (fungi, bacteria and viruses), and very few studies can use immune responses to discriminate bacteria at the species and strain level. Here, whole blood was used to investigate the relationship between host responses and bacterial strains. Results confirmed unique temporal profiles for the 10 parameters studied: IL-6, MIP-1α, MIP-3α, IL-10, resistin, phagocytosis, S100A8, S100A8/A9, C5a and TF3. Pairwise analysis confirmed that IL-6, resistin, phagocytosis, C5a and S100A8/A9 could be used in a discrimination scheme to identify to the strain level. Linear discriminant analysis (LDA) confirmed that (i) IL-6, MIP-3α and TF3 could predict genera with 95% accuracy; (ii) IL-6, phagocytosis, resistin and TF3 could predict species at 90% accuracy and (iii) phagocytosis, S100A8 and IL-10 predicted strain at 40% accuracy. These data are important because they confirm the proof of concept that host biomarker panels could be used to identify bacterial pathogens. [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]

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]

Aim. To evaluate the associations of abdominal obesity (AO), adipokines and premature coronary artery disease (CAD) in young people for a deeper understanding of the pathogenesis of atherosclerotic diseases.Material and methods. A total of 1457 people were examined, including 653 (44,8%) men. Mean age was 36,7±6,0 years. Premature CAD was detected in 46 people, while 4 following subgroups were formed (138 people in total): with CAD and AO; with CAD, without AO; control groups by age and sex: without CAD, with AO; without CAD, without AO.Results. Premature CAD in young people is associated with an increase in non-high-density lipoprotein cholesterol (non-HDL-C). Univariate analysis found that the probability of CAD increased by 1% with an increase in adiponectin level, and by 0,2% with an increase of 1 ng/ml in resistin level. Multivariate regression analysis, including sex, age, waist circumference, non-HD-C, adiponectin, and resistin, significant associations were obtained for non-HDL-C and adiponectin. With AO, the CAD probability increased by 0,6% with an increase in plasminogen activator inhibitor-1 level (PAI-1). However, when non-HDL-C was included in the model, significance for this biomarker was not achieved.Conclusion. In young people, CAD is associated with increased levels of non-HDL cholesterol, adiponectin, resistin and PAI-1. Independent associations with premature CAD were obtained only for adiponectin, which makes this marker promising for study in young people.

AimsResistin is a circulating inflammatory biomarker that is associated with cardiovascular disease. We investigated the associations of resistin and incident heart failure (HF) and its subtypes, as well as specific measures of subclinical HF (myocardial fibrosis and relevant biomarkers).MethodsWe analysed data from 1968 participants in the Multi-Ethnic Study of Atherosclerosis with measurements of plasma resistin levels at clinic visits from 2002 to 2005. Participants were subsequently followed for a median of 10.5 years for HF events. The associations between resistin levels and incident HF, HF with reduced ejection fraction (HFrEF), and HF with preserved ejection fraction (HFpEF) were examined using multivariable Cox proportional hazards models. Linear regression models assessed the associations between resistin levels and myocardial fibrosis from cardiac magnetic resonance imaging, as well as hs-cTnT and NT-proBNP.ResultsThe mean age of the cohort was 64.7 years, and 50.0% were female. Seventy-four participants (4%) developed incident HF during follow-up. In a Cox proportional hazards model adjusted for age, gender, education level, race/ethnicity, and traditional risk factors, higher resistin levels were significantly associated with incident HF (HR 1.44, CI 1.18-1.75, P = 0.001) and HFrEF (HR 1.47, CI 1.07-2.02, P = 0.016), but not with HFpEF (HR 1.25, CI 0.89-1.75, P = 0.195). Resistin levels showed no significant associations with myocardial fibrosis, NT-proBNP, or hs-cTnT levels.ConclusionsIn a multi-ethnic cohort free of cardiovascular disease at baseline, elevated resistin levels were associated with incident HF, more prominently with incident HFrEF than HFpEF, but not with subclinical myocardial fibrosis or biomarkers of HF.

Interleukin (IL) 6 is one of the key cytokines whose role in the inflammation development in rheumatoid arthritis (RA), is well proven. The pleiotropic effects of the cytokine and biologic agents that inhibit its action have been studied much worse. The review provides information on the effects of IL-6 and blocking its signaling pathway on adipose tissue, glucose metabolism and adipocytokine levels in RA. It has been shown that prolonged blockade of IL-6 receptors does not lead to the adipose tissue accumulation and improves glycemic control, although it is not clear whether such effect is associated only with the anti-inflammatory properties of tocilizumab and sarilumab. Moreover, the mechanism of this beneficial effect is not fully understood, since the data on increased sensitivity of peripheral tissues to insulin during tocilizumab treatment are ambiguous. Perhaps changes in the relationship of adipocytokines or hormones play a certain role.

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 urethane-anesthetized 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 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.

Background/Objectives. A Mediterranean diet (MD) has been associated with neuroprotective effects. We aimed to assess the MD’s association with stroke prognosis and the potential mediators involved. Methods. Seventy patients with acute anterior circulation ischemic stroke were included. Dietary patterns were evaluated using the MEDAS scale, a food-frequency questionnaire, and a 24 h recall. Circulating biomarkers including insulin resistance (HOMA index), adipokines (resistin, adiponectin, leptin), choline pathway metabolites (TMAO, betaine, choline), and endothelial progenitor cells (EPCs) were measured. Early neurological improvement (ENI) at 24 h, final infarct volume, and functional outcome at 3 months were assessed. Results. Adherence to MD and olive oil consumption were associated with a lower prevalence of diabetes and atherothrombotic stroke, and with lower levels of fasting glycemia, hemoglobinA1C, insulin resistance, and TMAO levels. Monounsaturated fatty acids and oleic acid consumption correlated with lower resistin levels, while olive oil consumption was significantly associated with EPC mobilization. Multivariate analysis showed that higher MD adherence was independently associated with ENI and good functional prognosis at 3 months. EPC mobilization, lower HOMA levels, and lower resistin levels were associated with ENI, a smaller infarct volume, and good functional outcome. Conclusions. MD was associated with better prognosis after ischemic stroke, potentially mediated by lower insulin resistance, increased EPC mobilization, and lower resistin levels, among other factors.