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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]

This study aimed to investigate the levels of serum, gingival crevicular fluid (GCF), and salivary adipokines and their possible relationship with periodontitis and obesity. An electronic search was conducted in the following databases: PubMed/ Medline, Scopus, and EBSCOhost through February 2023. Two independent reviewers screened the titles, abstracts, and full text of all the studies. Studies comparing the levels of adipokines in GCF, serum, and/or saliva in subjects with obesity and periodontitis (group 1), subjects with normal weight and periodontitis (group 2), and subjects with obesity and gingival health (group 3) were included. Meta‐analyses and meta‐regression were performed on the data from included studies. Seventeen studies with study participants ranging from 30 to 120 were included with subjects in each group ranging from 10 to 40. There was a significant increase in levels of serum TNF‐α, leptin, IL‐6, and CRP between groups 1 and 2 (p <.05). In GCF, TNF‐α and resistin levels were significantly higher (p <.05) in Group 1 vs. 2. Serum level of leptin was higher for group 1 vs. 3 (p <.05). Meta‐regression analysis revealed that the obesity definition (body mass index (BMI) cut‐off value >25 or >30) was significant for serum resistin (p <.05) and GCF resistin (p <.05) between group 1 and 2. The current analysis indicates that both periodontitis and obesity can modulate the pro‐inflammatory cytokines at systemic and local levels. This bidirectional interaction of periodontitis and obesity via the inflammation pathway seems likely plausible. Further studies are required to elucidate this mechanism in more detail. [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]

• 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]

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

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]

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.

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]

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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: 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]

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]

Resistin is a protein involved in inflammation and angiogenesis processes and may play a role in the progression of colorectal cancer (CRC). However, it remains unclear whether resistin is associated with increased mortality after CRC diagnosis. We examined pre‐diagnostic serum resistin concentrations in relation to CRC‐specific and all‐cause mortality among 1343 incident CRC cases from the European Prospective Investigation into Cancer and Nutrition cohort. For CRC‐specific mortality as the primary outcome, hazard ratios (HRs) and 95% confidence intervals (95% CI) were estimated from competing risk analyses based on cause‐specific Cox proportional hazards models and further in sensitivity analyses using Fine–Gray proportional subdistribution hazards models. For all‐cause mortality as the secondary outcome, Cox proportional hazards models were used. Subgroup analyses were performed by sex, tumor subsite, tumor stage, body mass index and time to CRC diagnosis. Resistin was measured on a median of 4.8 years before CRC diagnosis. During a median follow‐up of 8.2 years, 474 deaths from CRC and 147 deaths from other causes were observed. Resistin concentrations were not associated with CRC‐specific mortality (HRQ4vsQ1 = 0.95, 95% CI: 0.73–1.23; Ptrend =.97; and HRper doubling of resistin concentration = 1.00; 95% CI: 0.84–1.19; P =.98) or all‐cause mortality. Results from competing risk (sensitivity) analysis were similar. No associations were found in any subgroup analyses. These findings suggest no association between pre‐diagnostic circulating resistin concentrations and CRC‐specific or all‐cause mortality among persons with CRC, and the potential insignificance of resistin in CRC progression. [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]

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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]

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.

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

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.

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.

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]

Cancer‐related fatigue is a frequent, burdensome and often insufficiently treated symptom. A more targeted treatment of fatigue is urgently needed. Therefore, we examined biomarkers and clinical factors to identify fatigue subtypes with potentially different pathophysiologies. The study population comprised disease‐free breast cancer survivors of a German population‐based case‐control study who were re‐assessed on average 6 (FU1, n = 1871) and 11 years (FU2, n = 1295) after diagnosis. At FU1 and FU2, we assessed fatigue with the 20‐item multidimensional Fatigue Assessment Questionnaire and further factors by structured telephone‐interviews. Serum samples collected at FU1 were analyzed for IL‐1ß, IL‐2, IL‐4, IL‐6, IL‐10, TNF‐a, GM‐CSF, IL‐5, VEGF‐A, SAA, CRP, VCAM‐1, ICAM‐1, leptin, adiponectin and resistin. Exploratory cluster analyses among survivors with fatigue at FU1 and no history of depression yielded three clusters (CL1, CL2 and CL3). CL1 (n = 195) on average had high levels of TNF‐α, IL1‐β, IL‐6, resistin, VEGF‐A and GM‐CSF, and showed high BMI and pain levels. Fatigue in CL1 manifested rather in physical dimensions. Contrarily, CL2 (n = 78) was characterized by high leptin level and had highest cognitive fatigue. CL3 (n = 318) did not show any prominent characteristics. Fatigued survivors with a history of depression (n = 214) had significantly higher physical, emotional and cognitive fatigue and showed significantly less amelioration of fatigue from FU1 to FU2 than survivors without depression. In conclusion, from the broad phenotype "cancer‐related fatigue" we were able to delineate subgroups characterized by biomarkers or history of depression. Future investigations may take these subtypes into account, ultimately enabling a better targeted therapy of fatigue. [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]

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]