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Approximately 50% of all global blindness is caused by cataract in adults aged ≥50 years. The mechanisms of the disease are most arguably related to a redox imbalance and inflammation; therefore, the aim of the study was to evaluate the processes associated with inflammation in cataract patients. Twenty-four patients aged 22–60 years (62.5% females) participated in the study, with 33 controls aged 28–60 years (66.7% females). Venous blood serum of the subjects was examined for alpha 1-antitrypsin, as well as selected lysosomal enzymes and adipokines. The activities of lysosomal enzymes, as well as the activity of alpha 1-antitrypsin and the concentrations of c-reactive protein and leptin, were similar in the patients versus the controls. The concentrations of interleukin 6 and resistin were lower, in turn, whereas omentin-1 and adiponectin were higher. Moreover, the study revealed the existence of many linear relationships between the parameters, including multiple linear regression, especially gender-wise. No systemic inflammation was probably noted in the cataract patients tested; nevertheless, the deregulation of adiponectin, omentin-1 and resistin secretion was observed. [ABSTRACT FROM AUTHOR]

Purpose: Obstructive sleep apnea (OSA) is characterised by increased systemic inflammation, and is often accompanied with type 2 diabetes mellitus (T2DM) and cardiovascular disease. The aim of this investigation was to evaluate gene expression of resistin, its receptor CAP1 and CD36 as the indicators of the inflammatory changes in PBMCs in relation to the severity of OSA, and the presence of type 2 diabetes mellitus (T2DM) in OSA. Methods: Severity of OSA was defined by the apnea/hypopnea index (AHI): AHI < 30: mild to moderate OSA (MM-OSA), AHI ≥ 30: severe OSA (S-OSA). Presence of T2DM was captured: OSA with T2DM (OSA + T2DM), OSA without T2DM (OSA-T2DM). PBMC resistin, CAP1, and CD36 mRNA were determined by real-time PCR. Results: Resistin mRNA was significantly upregulated in S-OSA (N = 54) compared to the MM-OSA (N = 52, P = 0.043); CAP1 and CD36 mRNA levels did not differ between the groups (P = 0.302; P = 0.166, respectively). Resistin mRNA was significantly upregulated in OSA + T2DM (N = 29) compared to the OSA-T2DM (N = 77, P = 0.029); CAP1 and CD36 mRNA levels did not differ between the groups (P = 0.662; P = 0.108, respectively). AHI and T2DM were independent predictors of resistin mRNA above the 75th percentile (OR = 3.717 [1.152–11.991]; OR = 3.261 [1.000–10.630], P = 0.042 respectively). Conclusion: Resistin gene upregulation in S-OSA indicates its possible contribution to increased inflammation in S-OSA and makes it a possible marker of the disease severity. Resistin gene upregulation in OSA + T2DM suggests that a joint effect of these two comorbidities may have a major contribution to increased inflammation and complications that arise from this state. [ABSTRACT FROM AUTHOR]

Background: Human amebiasis is caused by Entamoeba histolytica, which is found in many tropical countries. E. histolytica infections are known to have a wide range of clinical consequences. Most infections are asymptomatic; some cause diarrhea and dysentery, and only a few cause extraintestinal consequences, including liver abscess. Single nucleotide polymorphisms (SNPs) are the most prevalent kind of sequence variation in genomes and are regarded as useful genetic markers for exposing the evolutionary history and common genetic variants that explain the heritable risk for common illnesses and effected in the progression of some infections. Objective: Investigation of gene polymorphism of the parameters (interleukin 18 [IL-18], resistin) most susceptible to parasitic infection. Materials and Methods: Stool samples were collected from patients who were attending the (Kerbala Teaching Hospital for children in the holy city of Kerbala), between February 2021 and January 2022. In total, 3748 samples of feces from children between the ages of 1 and 15 years from both gender were tested using both direct smear and acid-fast stain tests in addition to rapid test techniques. Five milliliters of blood were obtained from 25 patients infected with E. histolytica, as well as 5 mL of blood from 25 healthy youngsters (sample control). Results: The result showed the distribution of genotype of IL-18 SNPs in intestinal parasites patient in contrast to the control group; there is an increase in the level of IL-18 in some SNPs, resistin concentration was statistically significantly different between resistin gene polymorphisms. Conclusion: The IL-18 and resistin polymorphism can be considered one of the genetic factors responsible for the progression of E. histolytica infection. [ABSTRACT FROM AUTHOR]

BackgroundSepsis mortality has remained unchanged for greater than a decade, and early recognition continues to be the most important factor in mortality outcome. Plasma resistin concentration is increased in sepsis, but its mechanism and clinical relevance is unclear. As one function, resistin interacts with toll-like receptor 4 in competition with lipopolysaccharide, a main component of the gram-negative bacterial cell wall. It is not known if the type of infection leading to sepsis influences resistin production. The objective of this study was to investigate whether 1) early plasma resistin concentration can predict mortality, 2) elevated plasma resistin concentration is associated with clinical disease severity scores, such as SOFA, mSOFA and APACHE II, and 3) plasma resistin concentrations differ between gram negative versus other etiologies of sepsis.MethodsThis was an exploratory study in the framework of a prospective observational design. Peripheral venous blood samples were obtained from subjects admitted to the intensive care unit at clinical recognition of sepsis (0 hour) and at 6 and 24 hours. Vasopressor utilization was not a requirement for inclusion. Plasma was analyzed for resistin concentration by ELISA. Cytokine concentrations including IL-6, IL-8, and IL-10 were determined by cytokine bead array. Cytokine data were evaluated against publicly available sepsis RNA expression datasets to compare protein versus RNA expression levels in predicting clinical disease state. Clinical data were collected from electronic health records for clinical severity index calculations and context for interpretation of resistin and cytokine concentrations. Subjects were followed up to 60 days, or until death, whichever came first. Statistical analysis was completed with R package and SPSS software.ResultsResistin levels were elevated in subjects admitted to the intensive care unit with sepsis. Four-hundred subjects were screened with 45 subjects included in the final analysis. Thirteen of 45 patients were non-survivors. Mortality within 60 days correlated with significantly higher resistin concentrations than in survivors. A resistin concentration of >126 ng/mL at clinical recognition of sepsis and >197 ng/mL within the first 24 hours were associated with mortality within 60 days with an area under the curve of 0.82 and 0.88, respectively. Most subjects with resistin concentration greater than these threshold values were deceased prior to 30 days. Resistin concentrations correlated with SOFA, mSOFA, and APACHE II scores in addition to having association with increases in inflammatory and sepsis biomarkers. These associations were validated with analysis of RNA expression datasets.ConclusionPlasma resistin concentrations of >126 ng/mL at clinical recognition of sepsis and >197 ng/mL within the first 24 hours of clinical sepsis recognition are associated with all-cause mortality. Resistin concentration within this timeframe also has comparable mortality association to well-validated clinical severity indices of SOFA, mSOFA, and APACHE II scores.

Introduction: Thyroid diseases have effects on metabolism and inflammation. Adipocytokines have autocrine, paracrine, and endocrine functions on several organs which have a central role in subclinical inflammation of adipose tissue, and obese adipose tissue secretes proinflammatory adipokines such as visfatin, and resistin. Cytokines play a role in the pathogenesis of several autoimmune thyroid diseases. Methods: All samples were conducted at Salah Aldeen General Hospital and the specific private clinic in Tikrit which started from November 2022 to February 2023, the study samples included (30) individuals with hyperthyroidism, (30) individuals with hypothyroidism, and (30) healthy individuals with age (18-76) years. Results: Adipokines (resistin and visfatin) and interleukins (IL10 and IL32) were increased in hypo and hyperthyroidism rather than control. Conclusion: The effect of inflammatory and anti-inflammatory response of some adipokines and interleukins affect the pathogenesis role in thyroid diseases.

The purpose of present study was to evaluate the effect of periodontal treatments on insulin resistance and periodontal indices in diabetic patients with chronic periodontitis based on blood glucose control in Isfahan dental faculty in years 2015-2016.Materials & Methods:This single blinded controlled clinical trial was conducted on 60 patients referred to Khoram treatment center and Isfahan dental facultyin 2015-16. Patients were divided into four groups based on blood sugar control.Before treatment, periodontal indices were measured, and insulin resistance was detected by measuring of salivary resisting. Then phase 1 of periodontal treatment was performed andfollowing three months the mentioned indices were measured again. Finally, the data was analyzed with a one-way analysis of variance test, Tukey’s Post Hoc Test and paired sample t-test. The significance level was set at α = 0.05.Results:The results showed that average of glycated hemoglobin, pocket depth, percentage of areas with bleeding and plaque index had a significant difference before and after treatment in each of the four groups p value < 0.05, although the mean changes between groups were notsignificant (45, 58, 19 & 48%).Conclusion:Non-surgical periodontal treatment improves periodontal indices and reduces glycated hemoglobin and salivary resistin, however there was no association between severity of diabetes and the mentioned indices.

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.

Resistin, an adipocyte-specific hormone involved in insulin resistance and adipocyte differentiation, was initially identified in adipose tissue and macrophages. The physiological role of this molecule in camels remains largely unexplored. This study analysed for the first time blood and tissue levels of resistin as well as expression of resistin gene by real time PCR in adipose tissue (hump, visceral & epididymal) and different muscles (gastrocnemius, heart and caecum) in dromedary camels. The re-sults revealed that resistin concentration was significantly (P

Abstract Background Asthma is a chronic inflammatory disorder of the airways with diverse overlapping pathologies and phenotypes contributing to a significant heterogeneity in clinical manifestations. Obesity may modify asthma risk, phenotype, and prognosis. A suggested mechanism linking obesity and asthma is through systemic inflammation. Adipokines secreted by adipose tissue were suggested to provide a link between obesity and asthma. Objective To have an understanding for the contribution of adiponectin, resistin and MCP-1 to development of distinct asthma phenotype in overweight/obese children through assessment of their serum level and correlation to pulmonary function tests. Subjects and methods The study included 29 normal weight asthmatics, 23 overweight/obese asthmatic children and 30 controls. All cases were subjected to detailed history taking, thorough examination and pulmonary function tests. Serum adiponectin, resistin, MCP-1 and IgE were assessed to all recruited subjects. Results Adiponectin level was significantly higher in overweight/obese asthmatics (24900 ± 1600 ng/ml) compared to normal weight asthmatics (21700 ± 1700 ng/ml) and control (23000 ± 3200 ng/ml), (p

ABSTRACT Aim/Introduction Resistin, which induces insulin resistance, is mainly expressed in monocytes/macrophages in humans. We reported previously that serum resistin was highest in the G–A haplotype defined by resistin single nucleotide polymorphisms (SNPs) at −420 (rs1862513) and − 358 (rs3219175). As sarcopenic obesity is associated with insulin resistance, we aimed to examine whether serum resistin and its haplotypes were associated with sarcopenic obesity at a latent stage. Materials and Methods We cross‐sectionally analyzed 567 community‐dwelling Japanese participants attending annual medical check‐ups in which the sarcopenic obesity index was evaluated. The age‐ and gender‐matched normal glucose tolerance subjects with G–A homozygotes and those with C–G homozygotes were examined via RNA‐sequencing and pathway analysis (each n = 3), and RT‐PCR (each n = 8). Results In multivariate logistic regression analyses, the fourth quartile (Q4) of serum resistin and G–A homozygotes were both associated with the latent sarcopenic obesity index defined by a visceral fat area of ≥ 100 cm2 and grip strength Q1 after adjustment for age and gender, with or without other confounding factors. RNA sequencing and pathway analysis showed that tumor necrosis factor (TNF) was involved in the top five pathways in the whole blood cells of G–A homozygotes compared with C–G homozygotes. RT‐PCR revealed that TNF mRNA was higher in G–A homozygotes than in C–G homozygotes. Conclusions The G–A haplotype was associated with the latent sarcopenic obesity index defined by grip strength in the Japanese cohort, could be mediated by TNF‐α.

Objective: To measure and compare the serum levels of resistin and lipid profile parameters in primigravida females with and without preeclampsia. Method: The analytical cross-sectional study was conducted at the Department of Physiology and Cell Biology, University of Health Sciences, Lahore, Pakistan, from 2018 to 2020, and comprised primigravida females having gestational age 30-36 weeks. Those with preeclampsia constituted group 1, while normotensive females constituted group 2. All the participants were subjected to detailed history and general physical examination. Serum resistin levels were measured by enzyme-linked immunosorbent assay, and lipid profile parameters were measured using the colorimetric method. Data was analysed using SPSS 20. Results: Of the 80 women, 40(50percent) were in group 1 with mean age 23.07±2.10 years and mean gestation age 33.45±2.30 weeks. There were 40(50percent) women in group 2 with mean age 23.02±2.11 years and mean gestational age 34.45±1.75 weeks. Mean serum resistin was significantly higher in group 1 compared to group 2 (p 0.02). Mean levels of lipid parameters were significantly different between the groups (p 0.05). Conclusion: Preeclampsia was found to be associated with higher levels of resistin and lipid parameters compared to normal pregnancy. Keywords: Pre-eclampsia, Resistin, Hypertension, Pregnancy outcome, Primigravida.

ABSTRACTHaemophilus parasuis (H. parasuis) causes exudative inflammation, implying endothelial dysfunction during pathogen infection. However, so far, the molecular mechanism of endothelial dysfunction caused by H. parasuis has not been clarified. By using the transwell-based cell co-culture system, we demonstrate that knocking out resistin in porcine alveolar macrophages (PAMs) dramatically attenuated endothelial monolayer damage caused by H. parasuis. The resistin secreted by PAMs inhibited the expression of the tight junction proteins claudin-5 and occludin rather than the adherens junction protein VE-cadherin in co-cultured porcine aortic endothelial cells (PAECs). Furthermore, we demonstrate that resistin regulated claudin-5 and occludin expression and monolayer PAEC permeability in an LKB1/AMPK/mTOR pathway-dependent manner. Additionally, we reveal that the outer membrane lipoprotein gene lppA in H. parasuis induced resistin expression in PAMs, as deleting lppA reduced resistin expression in H. parasuis-infected PAMs, causing a significant change in LKB1/AMPK/mTOR pathway activity in co-cultured PAECs, thereby restoring tight junction protein levels and endothelial monolayer permeability. Thus, we postulate that the H. parasuis lppA gene enhances resistin production in PAMs, disrupting tight junctions in PAECs and causing endothelial barrier dysfunction. These findings elucidate the pathogenic mechanism of exudative inflammation caused by H. parasuis for the first time and provide a more profound angle of acute exudative inflammation caused by bacteria.

The short form of the leptin receptor (LeptRa) plays a key role in the transport of leptin to the central nervous system (CNS). Here, MTS-leptin and recombinant ovine (ro) leptin-mediated expression of LeptRa and VEGFA and VEGFR2 concentration in selected hypothalamic nuclei, choroid plexus (ChP), and anterior pituitary (AP) were analyzed considering the photoperiod and acute-fasting (experiment 1), and nutritional status (experiment 2) of ewes. In experiment 1, 60 sheep were fed normally or fasted for 72 h and received one injection of saline, MTS-leptin, or roleptin 1 h prior to euthanasia. LeptRa mRNA transcript levels and VEGF system protein concentrations were detected in the ARC, ChP predominantly in the SD, and AP for the LD without detection of LeptRa in the POA and VMH/DMH. In experiment 2, an altered diet for 5 months created lean or fat sheep. Twenty sheep were divided into four groups: the lean and fat groups were given saline, while the lean-R and fat-R groups received resistin 1 h prior to euthanasia. Changes in adiposity influenced the lowering effect of resistin on the expression of LeptRa and VEGF system protein concentrations. Overall, both photoperiodic and nutritional signals influence the effects of MTS-leptin/roleptin and resistin-mediated leptin transport to the CNS via LeptRa. Resistin seems to be another adipokine involved in the adaptive/pathological phenomenon of leptin resistance in sheep.

Metabolic syndrome (MetS), a cluster of metabolic conditions that include obesity, hyperlipidemia, and insulin resistance, increases the risk of several aging-related brain diseases, including Alzheimer's disease (AD). However, the underlying mechanism explaining the link between MetS and brain function is poorly understood. Among the possible mediators are several adipose-derived secreted molecules called adipokines, including adiponectin (ApN) and resistin, which have been shown to regulate brain function by modulating several metabolic processes. To investigate the impact of adipokines on MetS, we employed a diet-induced model to induce the various complications associated with MetS. For this purpose, we administered a high-fat diet (HFD) to both WT and APP/PSN1 mice at a pre-symptomatic disease stage. Our data showed that MetS causes a fast decline in cognitive performance and stimulates Aβ42 production in the brain. Interestingly, ApN treatment restored glucose metabolism and improved cognitive functions by 50% while decreasing the Aβ42/40 ratio by approximately 65%. In contrast, resistin exacerbated Ab pathology, increased oxidative stress, and strongly reduced glucose metabolism. Together, our data demonstrate that ApN and resistin alterations could further contribute to AD pathology. [ABSTRACT FROM AUTHOR]

Adipose tissue is specialized cells that produce and release adipokines. Exercise may modulate adipokine production in adipocytes. The aim of this longitudinal study was to evaluate the acute and chronic effects of strength training (ST) on plasma levels of adiponectin, leptin, and resistin. Twelve untrained young male participants (23.42±2.67 years) were selected. The training protocol consisted of 3 exercises, with 3 sets of 65% of 1RM (one-repetition maximum) with pause of 90 s between sets with duration of 5 s/repetition (2 s conc/3 s ecc), 3 times a week for 10 weeks. Blood was collected at four time points: before and after the first ST session and before and after the last ST session. The comparisons between adipokine levels before and after the same training session showed acute changes, while the comparisons between levels before or after the first session versus before or after the last session revealed chronic alterations. ST increased adiponectin levels after the first exercise session in comparison to levels before this session [50 952 (46 568–51 894) pg/mL vs. 52 981 (49 901–54 467) pg/mL, p=0.019]. Similar differences were observed for resistin levels, which were higher after the last session compared to before [4 214.4 (±829) pg/mL vs. pre-S30 2 251.3 (±462.2) pg/mL, p=0.0008] and in the comparison between after the last and after the first ST sessions [4 214.4 (±829.0) pg/mL vs. 1 563.7 (±284.8) pg/mL, p=0.004]. Leptin levels acutely changed in the last training session. ST produced acute and chronic changes in plasma adipokines. [ABSTRACT FROM AUTHOR]

Adipokines have not been studied in acute dengue, despite their emerging role in inducing and regulating inflammation. Therefore, we sought to identify adipokine levels in patients with varying severities of acute dengue to understand their role in disease pathogenesis. We determined the levels of leptin, resistin, omentin, adiponectin, as well as IFNβ, and NS1 using quantitative ELISA in patients with dengue fever (DF = 49) and dengue haemorrhagic fever (DHF = 22) at admission (febrile phase) and at the time of discharge (recovery phase). The viral loads and serotypes of all samples were quantified using quantitative real-time RT-PCR. Resistin levels (p = 0.04) and omentin (p = 0.006) levels were significantly higher in patients who developed DHF. Omentin levels in the febrile phase also correlated with the AST (Spearman's r = 0.38, p = 0.001) and ALT levels (Spearman's r = 0.24, p = 0.04); as well as serum leptin levels with both AST (Spearman's r = 0.27, p = 0.02) and ALT (Spearman's r = 0.28, p = 0.02). Serum adiponectin levels in the febrile phase did not correlate with any of the other adipokines or with liver enzymes, but inversely correlated with CRP levels (Spearman's r = -0.31, p = 0.008). Although not significant (p = 0.14) serum IFNβ levels were lower in the febrile phase in those who progressed to develop DHF (median 0, IQR 0 to 39.4 pg/ml), compared to those who had DF (median 37.1, IQR 0 to 65.6 pg.ml). The data suggest that adipokines are likely to play a role in the pathogenesis of dengue, which should be further explored for the potential to be used as prognostic markers and as therapeutic targets. Author summary: Adipokines have not been studied in acute dengue, despite their emerging role in inducing and regulating inflammation. Therefore, we sought to identify adipokine levels in patients with varying severities of acute dengue to understand their role in disease pathogenesis. We determined the levels of leptin, resistin, omentin, adiponectin, IFNβ, and NS1 in patients with dengue fever (DF) and dengue haemorrhagic fever (DHF) at admission (febrile phase) and at the critical phase. Resistin levels and omentin levels were significantly higher in patients who developed DHF. Omentin levels in the febrile phase also correlated with the AST and ALT levels; as well as serum leptin levels with both AST and ALT. Serum adiponectin levels in the febrile phase did not correlate with any of the other adipokines or with liver enzymes, but inversely correlated with CRP levels. The data suggest that adipokines are likely to play a role in the pathogenesis of dengue, which should be further explored for the potential to be used as prognostic markers and as therapeutic targets. [ABSTRACT FROM AUTHOR]

To determine whether inhibition of kinase signaling will suppress resistin-induced liver cancer progression. Resistin is located in monocytes and macrophages of adipose tissue. This adipocytokine is an important link between obesity, inflammation, insulin resistance, and cancer risk. Pathways that resistin is known to be involved include but are not limited to mitogen-activated protein kinases (MAPKs) and extracellular signal-regulated kinases (ERK). The ERK pathway promotes cellular proliferation, migration, survival of cancer cells, and tumor progression. The Akt pathway is known to be up-regulated in many cancers including liver cancer. Using an in vitro model, HepG2 and SNU-449 liver cancer cells were exposed to resistin ± ERK, Akt, or both inhibitors. The following physiological parameters were assessed: cellular proliferation, ROS, lipogenesis, invasion, MMP, and lactate dehydrogenase activity. The inhibition of kinase signaling suppressed resistin-induced invasion and lactate dehydrogenase in both cell lines. In addition, in SNU-449 cells, resistin increased proliferation, ROS, and MMP-9 activity. Inhibition of PI3K and ERK decreased phosphorylated Akt and ERK, and pyruvate dehydrogenase. In this study, we describe the effect of Akt and ERK inhibitors to determine if inhibition suppresses resistin-induced liver cancer progression. Resistin promotes cellular proliferation, ROS, MMP, invasion and LDH activity in SNU-449 liver cancer cells which is differentially mediated by Akt and ERK signaling pathways. [ABSTRACT FROM AUTHOR]

Objective: Cinnamon is extracted from the inner bark of Cinnamomum trees. Recent studies have indicated that cinnamon is a safe and cost-effective treatment for improving body weight, lipid profiles, insulin resistance, and blood pressure. This systematic review aimed to summarize the effect of cinnamon supplementation on adipokines and appetite-regulating hormones. Materials and Methods: This comprehensive literature search was conducted using databases such as PubMed, Scopus, ISI Web of Science, and Google Scholar up to March 2022 without any limitation. The quality of eligible studies was evaluated through the Cochrane Collaboration’s tool for assessing the risk of bias. Results: This systematic review included six clinical trial studies (363 participants), among which, only one study was performed on children, and two investigations were conducted on obese participants. A decreasing effect was found in the level of leptin and visfatin after cinnamon supplementation. Two out of three studies examined adiponectin levels and revealed non-significant effects of cinnamon consumption on this parameter. Two studies evaluated ghrelin levels and found an increase after cinnamon supplementation. The result of cinnamon supplementation on other biomarkers such as glucose-dependent insulinotropic polypeptide, glucagon-like peptide 1, and resistin was inconsistent. Conclusion: The result of this systematic review indicated the increasing effect of cinnamon supplementation on ghrelin levels and decreasing effect on leptin and visfatin levels. However, more clinical data are required to clarify the beneficial effects of cinnamon on adipokines levels due to the controversial findings of the studies. [ABSTRACT FROM AUTHOR]

Background: The imbalance in pro-inflammatory and anti-inflammatory hormones secreted by the increase in fat tissue causes chronic inflammation in the fat tissue. It is thought that this chronic inflammation causes metabolic complications resulting from obesity. Kefir is a type of probiotic that has recently attracted attention in the fight against obesity. This study aimed to examine the effects of kefir consumption on lipid profile and Adiponectin, Leptin, Resistin and Irisin/FNDC5 in the high fat diet fed BALB/C mouse model. Materials and Methods: BALB/C strain male mice were divided into three groups: control group (n = 10), high fat diet (HFD) (n = 10) and HFD + Kefir (n = 10). Mice were fed specific dietary patterns for eight weeks. The control group was given standard pellet feed. The HFD group was given a high-fat diet containing 52% fat. In addition to the high-fat feed, 15 ml/kg kefir was given to the HFD+Kefir group via oral gavage. Lipid profile was measured on an autoanalyzer using commercial kits. Leptin, Adiponectin, Resistin and Irisin/FNDC5 levels were measured by enzyme-linked immunosorbent assay (ELISA) using commercially available kits. Results: As a result of the experiment, there was no difference between the live weight gains of the groups. Epididymal fat weights in the HFD and HFD+Kefir groups were found to be statistically significantly higher than the control group. There was no significant difference between the epididymal fat weights of the HFD and HFD+Kefir groups HDL Cholesterol (HDL-C), LDL Cholesterol (LDL-C) values in the HFD and HFD+Kefir groups were found to be statistically significantly higher than the control group. No statistically significant difference was detected between the HFD+Kefir group and the HFD group in terms of HDLC, LDL-C values. There was no difference between groups in triglyceride values. Adiponectin and Irisin/FNDC5 values of the HFD+Kefir group were found to be statistically significantly lower than the other groups. There was no statistically significant difference between the control group and the HFD group in terms of Adiponectin and Irisin/FNDC5 values. There was no significant difference between the groups in Leptin and Resistin values. Conclusions: It was thought that kefir may have metabolic effects through adipokines in the high-fat diet nutrition model, and it would be useful to support this with human studies. [ABSTRACT FROM AUTHOR]

Background and Objectives: In the progression and development of atherosclerosis, resistin plays a significant role. Chronic kidney disease (CKD), frequently associated with atherosclerosis, exhibits a marked increase in morbidity and mortality rates. This study set out to explore the association between aortic stiffness and serum levels of resistin in non-dialysis-dependent CKD patients ranging from stages 3 to 5. Materials and Methods: We collected fasting blood samples from 240 CKD patients across stages 3 to 5. The concentration of resistin in serum was determined using a commercially available enzyme immunoassay kit. Those patients who exhibited a carotid–femoral pulse wave velocity (cfPWV) greater than 10 m/s were identified as the aortic stiffness group. Results: Out of the 240 CKD patients, 88 (36.7%) were classified within the aortic stiffness group. This group demonstrated higher incidences of diabetes, advanced age, increased body weight, body mass index, body fat mass, systolic and diastolic blood pressure, fasting glucose, and serum resistin levels. Multivariate logistic regression analysis highlighted resistin, diabetes, and body weight as independent predictors of aortic stiffness. Additionally, body fat mass, logarithmically transformed cfPWV (log-cfPWV) values and log-triglyceride levels were independent predictors of log-resistin levels by multivariate stepwise linear regression analysis. Conclusions: In CKD patients from stages 3 to 5, a positive correlation exists between elevated serum resistin levels and cfPWV values, identifying resistin as a potential predictor of aortic stiffness. [ABSTRACT FROM AUTHOR]

Background: Adipokines are hormones secreted from adipose tissue and are associated with cardiometabolic diseases (CMD). Functional differences between adipokines (leptin, adiponectin, and resistin) are known, but inconsistently reported associations with CMD and lack of studies in Hispanic populations are research gaps. We investigated the relationship between subclinical atherosclerosis and multiple adipokine measures. Methods: Cross-sectional data from the Cameron County Hispanic Cohort (N = 624; mean age = 50; Female = 70.8%) were utilized to assess associations between adipokines [continuous measures of adiponectin, leptin, resistin, leptin-to-adiponectin ratio (LAR), and adiponectin-resistin index (ARI)] and early atherosclerosis [carotid-intima media thickness (cIMT)]. We adjusted for sex, age, body mass index (BMI), smoking status, cytokines, fasting blood glucose levels, blood pressure, lipid levels, and medication usage in the fully adjusted linear regression model. We conducted sexes-combined and sex-stratified analyses to account for sex-specificity and additionally tested whether stratification of participants by their metabolic status (metabolically elevated risk for CMD as defined by having two or more of the following conditions: hypertension, dyslipidemia, insulin resistance, and inflammation vs. not) influenced the relationship between adipokines and cIMT. Results: In the fully adjusted analyses, adiponectin, leptin, and LAR displayed significant interaction by sex (p < 0.1). Male-specific associations were between cIMT and LAR [β(SE) = 0.060 (0.016), p = 2.52 × 10–4], and female-specific associations were between cIMT and adiponectin [β(SE) = 0.010 (0.005), p = 0.043] and ARI [β(SE) = − 0.011 (0.005), p = 0.036]. When stratified by metabolic health status, the male-specific positive association between LAR and cIMT was more evident among the metabolically healthy group [β(SE) = 0.127 (0.015), p = 4.70 × 10–10] (p for interaction by metabolic health < 0.1). However, the female-specific associations between adiponectin and cIMT and ARI and cIMT were observed only among the metabolically elevated risk group [β(SE) = 0.014 (0.005), p = 0.012 for adiponectin; β(SE) = − 0.015 (0.006), p = 0.013 for ARI; p for interaction by metabolic health < 0.1]. Conclusion: Associations between adipokines and cIMT were sex-specific, and metabolic health status influenced the relationships between adipokines and cIMT. These heterogeneities by sex and metabolic health affirm the complex relationships between adipokines and atherosclerosis. [ABSTRACT FROM AUTHOR]

Introduction: This study investigated the effects of 12 weeks of high-intensity functional training (HIFT) combined with spinach-derived thylakoid supplementation on some selected Adipokines and insulin resistance in males with obesity. Method: Sixty-eight participants (mean age: 27.6 ± 8.4 yrs.; mean height: 168.4 ± 2.6 cm; mean weight: 95.7 ± 3.8 kg, mean BMI: 32.6 ± 2.6 kg/m2) were randomly divided into four groups of 17 per group: Control group (CG), Supplement group (SG), Training group (TG), and Training + supplement group (TSG). Following baseline measurements, the two training groups (TG and TSG) started the 12 weeks of exercise training program (3 sessions per week). A total of 36 sessions lasting up to 60 min were included in the HIFT program using the CrossFit program. The eligible participants received 5 g/day of thylakoid-rich spinach extract or matching placebo as 5 g/day of raw corn starch (one sachet, 30 min before lunch) for 12 weeks. Baseline assessments were obtained 48 hours before the start of the training protocols and 48 hours after the last training session in all groups. Results: There were significant interactions (p<0.001 for all) between exercise and time for adiponectin (ES:0.48), leptin (ES:0.46), resistin (ES:0.3), omentin (ES:0.65), vaspin (ES:0.46), visfatin (ES:0.62), apelin (ES:0.42), RBP4 (ES:0.63), chemrin (0.36) and semaphorin3c (ES: 0.5). Plasma levels of semaphorin3c were significantly correlated (p<0.05) with body weight (r= 0.57), BMI (r= 0.43), FFM (r= -0.612), FAT (r= 0.768), VO2peak (r=-0.53), insulin (r= 0.756), glucose (r= 0.623), and HOMA-IR (r= 0.727). There were also significant group differences in insulin (ES: 0.77), glucose (ES: 0.21), and HOM-IR (ES: 0.44) (p<0.05). Discussion: Our findings indicate that 12 weeks of HIFT supplemented with spinach-derived thylakoid reduced levels of leptin, resistin, vaspin, visfatin, apelin, RBP4, chemrin, semaphorin3c and insulin resistance while increasing adiponectin and omentin levels in men with obesity. [ABSTRACT FROM AUTHOR]

Summary: Midlife obesity and late‐life weight loss confer a greater risk for developing dementia and Alzheimer's disease (AD), but the exact mechanisms behind this phenomenon are currently unknown. The answer could lie on the involvement of gastrointestinal factors, such as adipokines (e.g., leptin, adiponectin, and resistin) and ghrelin. In this context, we conducted a pre‐registered systematic review and meta‐analysis of 42 cross‐sectional and 13 longitudinal studies targeting the associations between leptin, adiponectin, resistin, and ghrelin and the prevalence of general dementia, AD, and mild cognitive impairment (MCI). We also examined the relationship between the four gastrointestinal factors and neurocognitive outcomes and AD‐related cerebrospinal fluid biomarkers. Patients with AD had lower blood leptin and higher resistin levels than cognitively normal participants. Lower leptin and higher resistin were associated with higher degree of cognitive impairment. Additionally, lower late‐life leptin levels might be associated with higher prospective risk of dementia and AD, although more studies are needed to corroborate this. Results in ghrelin and adiponectin were not conclusive, with age, sex distribution, obesity, and severity of dementia seemingly acting as moderators across several analyses. Our work might contribute to the identification of new preclinical blood markers of MCI and AD. [ABSTRACT FROM AUTHOR]

Background: There are data supporting the idea that atherogenic dyslipidemia is a risk factor for CKD and reduced GFR. The aim was to evaluate the associations between adipocytokines and early renal dysfunction in young people with dyslipidemia. Materials and methods: A population study was conducted in IIPM—Branch of IC&G SB RAS, in 2013–2017. Furthermore, 1033 people were included in the study (469 men (45.4%) and 564 women (54.6%)). The study included blood sampling, anthropometric data, and adipokines by multiplex analysis. Results: Among people with reduced kidney function and DLP, men were 3.1 times more common than without DLP, women smoked 2 times less often, arterial hypertension was 7.8 times more common, and abdominal obesity was 2.7 times more common (and women with DLP were 3 times more likely than those without DLP). An increase in the level of resistin by 1 mcg/mL was associated with an increased chance of having renal dysfunction by 0.2%. An increase in the level of GIP was associated with an increased chance of having renal dysfunction by 1.1%. Conclusions: In young people with dyslipidemia, regardless of the presence of abdominal obesity, resistin and GIP are associated with the presence of renal dysfunction. [ABSTRACT FROM AUTHOR]

Purpose: The causal relationships between circulating adipokines and idiopathic pulmonary fibrosis (IPF) are yet to be established. We performed a two-sample Mendelian randomization (MR) study to investigate the causal roles of adipokines on IPF risk. Methods: We analyzed the summary data from genome-wide association studies (GWAS), including adiponectin, leptin, resistin and monocyte chemoattractant protein-1 (MCP-1) and IPF. The inverse-variance weighted (IVW) method was considered as the major method and the MR-Egger, weighted median, simple mode and weighted mode were utilized as complementary methods. We also performed the sensitivity analyses, including heterogeneity test, horizontal pleiotropy test and leave-one-out analysis. Results: The selected number of single nucleotide polymorphisms (SNPs) was 13 for adiponectin, 6 for leptin,12 for resistin, and 6 for MCP-1, respectively. The results showed a causal effect of the circulating adiponectin levels on the risk of IPF (OR 0.645, 95% CI 0.457–0.911, P = 0.013). However, we did not observe significant associations of genetic changes in serum leptin (OR 1.018, 95% CI 0.442–2.346, P = 0.967), resistin (OR 1.002, 95% CI 0.712–1.408, P = 0.993), and MCP-1 (OR 1.358, 95% CI 0.891–2.068, P = 0.155) with risk of developing IPF. There was no evidence of heterogeneity or horizontal pleiotropy. The sensitivity analyses confirmed that our results were stable and reliable. Conclusions: The increase in serum adiponectin was associated causally with a decreased risk of developing IPF. There is no evidence to support a causal association between leptin, resistin or MCP-1 with risk of IPF. Further studies are needed to confirm our findings. [ABSTRACT FROM AUTHOR]

Diabetes Mellitus (DM), a metabolic disease characterized by the increased blood glucose level, insulin deficiency or ineffectiveness, may cause structural and functional disorders in the brain. l -Theanine (LTN) has the relaxing, psychoactive, antidepressant, anti-inflammatory and antinecrotic properties, and regulates the functions of hippocampus (HP) in brain. In the present study, the aim was to identify the effects LTN on the levels of BDNF, insulin and adipocytokines (TNF-α, leptin, adiponectin and resistin) in both HP and serum of diabetic rats. 32 male Wistar rats were divided into four groups (n = 8/group): Control, LTN, DM and DM + LTN. Diabetes was induced by by nicotinamide/streptozotocin. 200 mg/kg/day LTN treatment was applied for 28 days. The serum and hippocampal levels of the parameters were determined by using commercial ELISA kits. Additionally, HP tissues examined histopathologically. LTN treatment significantly decreased leptin and adiponectin levels in HP tissues in diabetic rats (p < 0.05). Although it decreased the insulin level in both serum and HP, this was not statistically significant. No significant effect on other parameters was observed (p > 0.05). In histopathological analysis, although the damage was reduced by LTN in all sections of HP, this change was significant mainly in CA3 region (p < 0.05). It was concluded that LTN has the ability to reduce hippocampal degeneration and modulates adipocytokines in diabetic rats. [Display omitted] • Insulin and adipocytokines are important proteins for hippocampal functions. • l -theanine (N-Ethyl- l -glutamine), a soluble amino acid of teas (Camellia Sinensis L.), has health beneficial effects. • l -theanine affects the levels of hippocampal insulin, leptin and adiponectin. [ABSTRACT FROM AUTHOR]

Purpose: We examined the effects of aerobic exercise and detraining on adiponectin, resistin, tumor necrosis factor alpha (TNF-α), white blood cell, and pubertal signs (uterine length, ovarian volume, luteinizing hormone [LH], and follicle-stimulating hormone [FSH]) in girls with central precocious puberty (CPP). Methods: Thirty girls with CPP (7–9 yr old) were randomly divided into CPP and CPP + Exercise (EX) groups. Fifteen healthy age-matched girls without precocious puberty participated for comparison with CPP. Subjects in the CPP + EX group attended 12 wk of aerobic exercise protocol three sessions a week. In the baseline, after completing the exercise protocol and after 4 wk of detraining, all the parameters were measured. In the CPP and healthy groups, all the parameters were measured in all three stages. To measure adiponectin, resistin, and TNF-α, the ELISA method was used. LH and FSH were measured by electrochemiluminescence immunoassay. White blood cell counts were analyzed by an automated blood cell counter. Repeated-measures ANOVA was used to analyze the results. Results: CPP girls have lower adiponectin (P = 0.01) and higher TNF-α levels (P = 0.001) than healthy girls. In the CPP + EX group, after 12 wk, body weight and fat mass decreased, and adiponectin increased significantly (P = 0.02). Resistin (P = 0.02), TNF-α (P = 0.02), neutrophils (P = 0.01), and signs of puberty significantly (P < 0.05) decreased. After detraining, no significant change was observed except TNF-α, which increased significantly (P = 0.03). In the CPP group, no significant change was observed in any of the parameters; only LH (P = 0.0001) and uterine length and ovarian volume (P = 0.003, P = 0.001) decreased after 12 and 16 wk, respectively. Conclusions: Aerobic exercise can have a positive effect on the state of inflammation and pubertal signs. Positive effects remain after 4 wk of detraining. [ABSTRACT FROM AUTHOR]

Background: Obesity is a multifactorial disorder that is an important predisposing factor for a number of disorders. Genetic and epigenetic variations play important roles during the development of obesity. Method: DNA methylation is the most studied as one of the epigenetic modifications and is directly related to gene expression. Here, the methylation status of FSHR, PTH and ESRRA genes were investigated in obese patients to discover novel associations between DNA methylation and obesity phenotype. A total of 69 patients with obesity and 76 patients without obesity were enrolled in this study. DNA methylation in FSHR, PTH and ESRRA genes was analyzed. Result: There is a statistically significant association between the methylation status of ESRRA and fasting glucose (P=0.04) and BMI and methylation of the PTH gene (P=0.036) in obese subjects. In non-obese subjects, a statistically significant association was detected between adiponectin, resistin levels and FSHR methylation status. It is concluded that the methylation status of FSHR, PTH and ESRRA genes play an important role in obesity phenotype, adiponectin and resistin levels. These genes had previously been associated with obesity-related variables, but their methylation status was not highlighted. Conclusion: Our study will shed light on resolving the epigenetic contributions toward the development of obesity. Studies in the field of epigenetics will help discover predisposition markers for obesity. Based on the literature this was the first study that shows the interactions between FSHR, PTH and ESRRA methylation and obesity. [ABSTRACT FROM AUTHOR]

Background. Physical exercise exerts a positive effect on many chronic conditions, specifically lifestyle-related diseases such as overweight and obesity, type 2 diabetes mellitus (T2DM), cardiovascular conditions and osteoarthritis (OA). As a result of common risk factors, most of these patients present with multiple conditions. Exercise- and disease-related biomarkers, such as adipokines, are emerging tools in training supervision and regulation; however, their significance in subjects with multimorbidities is unknown. Subjects and Methods. To address this issue, adipokines leptin, adiponectin and resistin were assessed in a cohort of subjects with multimorbidities (n = 39) presenting with at least two of the abovementioned conditions or relevant risk factors before and after a six-month exercise and lifestyle intervention program ('MultiPill-Exercise'), and correlated with training adaptation, namely changes in relative maximum oxygen uptake ( V · O 2 max ). Results. There was a significant negative correlation between baseline leptin concentrations and training effect for relative V · O 2 max (after three months: rho = −0.54, p = 0.020 *; after six months: rho = −0.45, p = 0.013 *), with baseline leptin explaining 35% of the variance in delta relative V · O 2 max after three months and 23% after six months. Conclusions. Leptin might be a suitable surrogate biomarker in the context of exercise-based lifestyle intervention programs in subjects with multimorbidity. [ABSTRACT FROM AUTHOR]

The increase in the number of patients with obesity causes significant interest of researchers and doctors in the study and analysis of physiological and pathological processes in adipose tissue. The aim of the work is to evaluate changes in the level of hormones in adipose tissue after sleeve gastrectomy. Changes in hormone levels were studied in 3 groups of 10 animals each: a control group with a normal weight, a control group with metabolic syndrome, and the main group with metabolic syndrome, which underwent sleeve gastrectomy. Three weeks after sleeve gastrectomy, weight loss was 13.7%, and after 6 weeks - 24.8%. The level of leptin in the control group was 22.08±2.61 ng/g, in the control group with metabolic syndrome - 34.01±3.01 ng/g, and in the main group 6 weeks after surgery, it was 26.92±2, 14 ng/h. When studying the level of adiponectin in the blood of rats, we found a statistically significant difference between the level of the control group with metabolic syndrome, which was 5.16±0.75 µg/ml, and the level in the control group - 7.01±0.87 µg/ml, in the main group 6 weeks after the operation - 6.32±0.57 µg/ml. The level of resistin in the control group was 12.14±1.73 µg/l, in the second group - 17.86±1.91 µg/l, in the main group - 15.06±1.68 µg/l. Sleeve gastrectomy creates hormonal changes that have a positive effect on the main mechanism of reducing the volume of adipose tissue, leading to the normalization of adipokine levels. [ABSTRACT FROM AUTHOR]

Resistin is a small adipocyte-specific secretory hormone molecule. It has been associated with a number of cellular and metabolic processes. It has also been essentially implicated to have a vital role in the interplay between insulin resistance, obesity, and type II diabetes. Numerous clinical studies have demonstrated an association between many pathological illnesses with elevated serum resistin levels. It has also been shown to affect and modulate various molecular processes such as atherosclerosis, cancer cell metabolism, and inflammation. Periodontitis is a widespread inflammatory disease affecting human beings. Periapical periodontitis is an inflammatory disease that manifests as a sequela of untreated dental caries. Therefore, in this article, we summarize the divergent physiological roles played by resistin and its association with the mechanism of various pathologies. Moreover, current scientific studies discussing its association and role in common dental pathologies, periodontitis, and apical periodontitis are reviewed. [ABSTRACT FROM AUTHOR]

Background: A role for resistin in the pathogenesis of polycystic ovarian syndrome (PCOS) and related features were described for various ethnicities. As its expression is partly inherited, a role for RETN polymorphisms in regulating resistin levels and PCOS risk was shown, but with varied results. Aim: To investigate the association of rs34124816 (–537A>C), rs1862513 (–420C>G), rs3219175 (–358G>A), rs3745367 (+299G>A), rs3745369 (+1263G>C), and rs1423096 (+4965C>T) RETN SNPs with PCOS. Methods: Study subjects included 583 women with PCOS, and 713 eumenorrheic women serving as controls. Genotyping was done by real‐time PCR. Results: Higher minor allele frequency (MAF) of rs34124816, rs3219175, and rs3745369, and lower MAF of rs1862513 and rs1423096 were seen in PCOS cases. Reduced PCOS risk was found with rs3745367 minor‐allele homozygotes and rs1423096 minor‐allele homozygotes, while increased risk was linked with rs3745367 heterozygotes, and with rs3745369 heterozygotes and minor‐allele homozygotes. While it did not reach statistical significance, serum resistin levels were elevated in PCOS cases than in control women and major‐allele homozygotes of rs34124816 and rs1862513, and in rs1423096 minor‐allele‐containing carriers. Carriage of rs34124816 correlated positively with age and LH, whereas rs1862513 positively and rs3745367 negatively correlated with fasting glucose. Six‐locus (rs34124816‐rs1862513‐rs3219175‐rs3745367‐rs3745369‐rs1423096) haplotype analysis demonstrated a significant reduction in AGGGGG and a marked increase in AGGGCG haplotypes between cases and controls, thus assigning PCOS protective and susceptible nature to these haplotypes, respectively. Conclusions: This study is the first to document the contribution of rs34124816 and rs1423096 RETN variants to the risk of PCOS. The varied association of RETN gene variants with PCOS suggests an ethnic contribution of RETN association with PCOS. [ABSTRACT FROM AUTHOR]

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Bariatric procedures are considered to be the most effective treatment options for obesity. One of them is laparoscopic sleeve gastrectomy (LSG), which is nowadays very popular and widely used. LSG leads to weight loss and metabolic improvement and also changes adipokine levels, although it is just a restrictive operation. We describe changes in pro-inflammatory (leptin, resistin, visfatin and chemerin) and anti-inflammatory adipokines (adiponectin, omentin), with adiponectin and leptin being most studied. Their levels are markedly changed after LSG and this may partially explain the weight loss seen after LSG. Adipokines are closely connected to insulin resistance and chronic inflammation both being positively influenced after LSG. Leptin regulates amount of body fat, appetite, thermogenesis and metabolic rate and its levels are positively correlated with both weight and BMI changes after operation. Resistin influences insulin sensitivity, modulates body cholesterol trafficking and its changes after operation correlate with BMI, waist circumference, fat mass, LDL cholesterol and C-reactive protein. Chemerin, an important component of immune system, decreases after bariatric surgery and its levels correlate with BMI, triglyceride levels, and blood glucose. On the other hand, pro-inflammatory adipokine adiponectin, which influences fatty acid oxidation, browning of fat tissue and energy metabolism, is declining after LSG. This decline explains improvement of glucose status after bariatric surgery in patients with diabetes and is correlated with BMI loss, waist circumference and LDL cholesterol level. Effect of LSG goes beyond calory restriction and the changes of adipokines have a great impact on health status of the bariatric patients. [ABSTRACT FROM AUTHOR]

Cancer is a group of diseases characterized by uncontrolled cell division leading to growth of abnormal tissue, it is a common term for tumors that affect the body's organs, which are the two types of benign tumors and malignant tumors (which are known as carcinoid tumors). A distinction is made between them by examining the tissue (taking a sample). Breast cancer (BC) is formed due to a change in the functioning and growth of cells that make up breast tissue without the ability to control it, which turns them into cancer cells with the ability of these cells to spread. The aims of the study were to evaluate serum levels of resistin (RST), prolactin (PRL), aromatase (ARO), in women with breast cancer and compared with apparently healthy women (control). This study is a cross-sectional, hospital-based study, the protocol of this study was approved by the scientific committee of Tikrit University College of Medicine, and the agreement of the attendance to Kirkuk Oncology Center, Kirkuk general hospital to collect the sample from the patients was approved by the Kirkuk Health Directorate. This study was carried out at the Oncology Center in Kirkuk City-Iraq from the beginning of December 2022 to the end of May 2023. The subject enrolled in the study were divided into (44) breast cancer women and (42) apparently healthy women as control In Kirkuk city. The highest percentage of age for women with BC equal to (34.1%) in the age group (50- 59) years, with mean age, was 48.7 years and the statistical tests data obtained showed: highest significant elevation of RST, PRL, and ARO level in women with BC were 6.8±1.8 ng/ml, 58.7±8.4 ng/ml, and 1.5±0.4 pg/ml as compared to control group 4.4±0.5 ng/ml, 24.4±7.2 ng/ml, and 0.4±0.2 pg/ml respectively at (p<0.001). The present study conclude that levels of resistin, prolactin, and aromatase dismutase were significantly higher in women with breast cancer compared to the contro [ABSTRACT FROM AUTHOR]

Background: Human amebiasis is caused by Entamoeba histolytica, which is found in many tropical countries. E. histolytica infections are known to have a wide range of clinical consequences. Most infections are asymptomatic; some cause diarrhea and dysentery, and only a few cause extraintestinal consequences, including liver abscess. Single nucleotide polymorphisms (SNPs) are the most prevalent kind of sequence variation in genomes and are regarded as useful genetic markers for exposing the evolutionary history and common genetic variants that explain the heritable risk for common illnesses and effected in the progression of some infections. Objective: Investigation of gene polymorphism of the parameters (interleukin 18 [IL-18], resistin) most susceptible to parasitic infection. Materials and Methods: Stool samples were collected from patients who were attending the (Kerbala Teaching Hospital for children in the holy city of Kerbala), between February 2021 and January 2022. In total, 3748 samples of feces from children between the ages of 1 and 15 years from both gender were tested using both direct smear and acid-fast stain tests in addition to rapid test techniques. Five milliliters of blood were obtained from 25 patients infected with E. histolytica, as well as 5 mL of blood from 25 healthy youngsters (sample control). Results: The result showed the distribution of genotype of IL-18 SNPs in intestinal parasites patient in contrast to the control group; there is an increase in the level of IL-18 in some SNPs, resistin concentration was statistically significantly different between resistin gene polymorphisms. Conclusion: The IL-18 and resistin polymorphism can be considered one of the genetic factors responsible for the progression of E. histolytica infection.

Objective. Many conflicting results have been obtained in the study of leptin (LEP) and leptin receptor (LEPR) gene variants that are associated with the obesity and diabetes possibly due to differences in the study populations. The aim of this study was to evaluate changes in the metabolic hormones (leptin, ghrelin, adiponectin, resistin) levels in the blood of obese patients in relation to the GHRL (rs696217), LEP (rs7799039), LEPR (rs1137100, rs1137101, rs1805094) polymorphism in Ukrainian population.

Objective. Over the past four decades, the prevalence of obesity has tripled and limited genetic studies with specific SNPs have been conducted, but no investigations using ghrelin and obestatin prepropeptide (GHRL) gene have been reported in the Ukrainians population. The aim of this study was to evaluate changes in the level of metabolic hormones in the blood of obese patients in relation to the GHRL (rs696217) polymorphism.

Resistin is a small adipocyte-specific secretory hormone molecule. It has been associated with a number of cellular and metabolic processes. It has also been essentially implicated to have a vital role in the interplay between insulin resistance, obesity, and type II diabetes. Numerous clinical studies have demonstrated an association between many pathological illnesses with elevated serum resistin levels. It has also been shown to affect and modulate various molecular processes such as atherosclerosis, cancer cell metabolism, and inflammation. Periodontitis is a widespread inflammatory disease affecting human beings. Periapical periodontitis is an inflammatory disease that manifests as a sequela of untreated dental caries. Therefore, in this article, we summarize the divergent physiological roles played by resistin and its association with the mechanism of various pathologies. Moreover, current scientific studies discussing its association and role in common dental pathologies, periodontitis, and apical periodontitis are reviewed.

Aim: This study was performed to investigate the effect of exercise on serum resistin and leptin values in rats fed with a high-fat diet. Material and Method: 24 Wistar albino male rats were used in the study. They were randomly divided into 4 groups, with 6 rats in each group. The groups were determined as the control group (C), exercise group (E), high-fat diet (HFD) group, and high-fat diet + exercise (HFDE) Group. Results: When the findings obtained in this study were evaluated statistically, it was determined that the resistin values were similar in the C, E and HFDE groups, and higher in the HFD group compared to the other groups. It was observed that resistin value increased with high-fat diet and decreased with exercise. When evaluated in terms of leptin levels, the C and E groups showed similarity, while the HFD and HFDE groups showed similarity with each other. Although exercise decreased the leptin level, which was highly increased with a high-fat diet, it was not statistically significant. Conclusion: It has been determined that feeding with a high-fat diet causes an increase in serum resistin and leptin levels, and exercise provides a significant decrease in resistin values, but is not effective in leptin levels.

Abstract Background The development of coronary artery disease (CAD) is related to the impaired quantity and composition of inflammatory proteins found in plasma and tissue, such as interleukin 6 (IL-6), adipokines, and resistin. Therefore, the level of plasma resistin in patients with advanced CAD could be indicative of the condition of epicardial adipose tissue and thus have an impact on the frequency and severity of postoperative complications in the form of paroxysmal atrial fibrillation. Methods The study included 108 patients who qualified for elective coronary artery bypass grafting (CABG) surgery from 2017 to 2020 and were categorized into two groups. The first group consisted of patients who developed atrial fibrillation in the postoperative period – the AF group, and the second group included patients who did not have arrhythmia – the non-AF group. The analysis incorporates the history, course of treatment, anthropometric characteristics of the test subjects, biochemical laboratory tests, and echocardiography. Perivascular adipose tissue (PVAT) sections were surgically harvested from the area of the left coronary trunk. Results The resistin levels in the PVAT were significantly higher in the AF group than in the non-AF group (P = 0.000015). Similarly, plasma resistin levels increased significantly in the AF group compared to the non-AF group (P = 0.044). The values of other analyzed variables were not significantly different (analysis performed using the Mann–Whitney U test). Spearman’s rank-order correlation technique found a correlation between resistin in PVAT and plasma (r = 0.5933; P

Background and objectives: Coronary artery bypass graft (CABG) is a surgical procedure used to treat coronary heart disease. The present study aimed to investigate effects of 8 weeks of combined rehabilitation training on plasma levels of leptin, adiponectin, and resistin in middle-aged men who have undergone CABG. Methods: The present research was a quasi-experimental study with a pretest-posttest design. The statistical population included all patients who have undergone CABG in Mashhad, Iran. Overall, 26 middle-aged men who have undergone CABG were enrolled in the study. The subjects were divided into a training group (n=14) and a control group (n=12). Data were analyzed in SPSS software (version 21) using analysis of covariance and paired t-test at significance level of 0.05. Results: Plasma levels of leptin did not change significantly (p=0.709), adiponectin increased significantly (p=0.001), and resistin decreased significantly (p=0.005) after the training intervention. Conclusion: As a non-pharmacological intervention, the rehabilitation training has cardioprotective effects on patients who undergone CABG.

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.

Zhao Y, Zheng R, Ning D, Xie F. Cancer Manag Res. 2020;12:4171–4180. We, the Editors and Publisher of Cancer Management and Research, have retracted the following article. Following publication of the article, concerns were raised about the duplication of images from Figures 1 and 3 with images from other unrelated articles. Specifically, The images for Figure 1F have been duplicated with images for Figure 1C and 1D from Fang C, Jiang B, Shi X, Fan C. Hes3 Enhances the Malignant Phenotype of Lung Cancer through Upregulating Cyclin D1, Cyclin D3 and MMP7 Expression. International Journal of Medical Sciences. 2019;16(3):470-476. https://doi.org/10.7150/ijms.28139. Images for Figure 3C, A459 and 3G, H226 have been duplicated with images for Figures 2h and 2i, and 5a and 5b from Zhang X, Liu L, Deng X, et al. MicroRNA 483-3p targets Pard3 to potentiate TGF-β1-induced cell migration, invasion, and epithelial–mesenchymal transition in anaplastic thyroid cancer cells. Oncogene. 2019;38:699–715. https://doi.org/10.1038/s41388-018-0447-1. Images for Figure 3D, A549 and 3H, H226 have been duplicated with images for Figure 9A, CNE2 and 9B, 5-8F from Liang TS, Zheng YJ, Wang J, et al. RETRACTED ARTICLE: MicroRNA-506 inhibits tumor growth and metastasis in nasopharyngeal carcinoma through the inactivation of the Wnt/β-catenin signaling pathway by down-regulating LHX2. J Exp Clin Cancer Res. 2019;38:97. https://doi.org/10.1186/s13046-019-1023-4. When approached for an explanation, the authors were cooperative but were unable to provide a sufficient explanation for the image duplication or provide original data for their study. As verifying the validity of published work is core to the integrity of the scholarly record, we are therefore retracting the article and the authors have agreed with this decision. We have been informed in our decision-making by our editorial policies and COPE guidelines. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as ‘Retracted’.

Metabolic syndrome (MetS), a cluster of metabolic conditions that include obesity, hyperlipidemia, and insulin resistance, increases the risk of several aging-related brain diseases, including Alzheimer’s disease (AD). However, the underlying mechanism explaining the link between MetS and brain function is poorly understood. Among the possible mediators are several adipose-derived secreted molecules called adipokines, including adiponectin (ApN) and resistin, which have been shown to regulate brain function by modulating several metabolic processes. To investigate the impact of adipokines on MetS, we employed a diet-induced model to induce the various complications associated with MetS. For this purpose, we administered a high-fat diet (HFD) to both WT and APP/PSN1 mice at a pre-symptomatic disease stage. Our data showed that MetS causes a fast decline in cognitive performance and stimulates Aβ42 production in the brain. Interestingly, ApN treatment restored glucose metabolism and improved cognitive functions by 50% while decreasing the Aβ42/40 ratio by approximately 65%. In contrast, resistin exacerbated Aβ pathology, increased oxidative stress, and strongly reduced glucose metabolism. Together, our data demonstrate that ApN and resistin alterations could further contribute to AD pathology.

Background: High-density lipoproteins (HDLs) have antiatherogenic properties related to their chemical structure. Adipose tissue (AT) influences HDL reverse cholesterol transport and plasma HDL cholesterol levels. However, whether AT dysfunction affects HDL subpopulations and their glycation in early type 2 diabetes (T2D) is still unknown. Objective: To investigate the association of inflammation and AT dysfunction serum markers with the size and glycation of HDLs in normoglycemic, prediabetes, and T2D subjects. Methods: We assessed HDL particle size and advanced glycation end-product (AGE) content in HDLs isolated from normoglycemic (n = 17), prediabetes (n = 17), and recently T2D-diagnosed (n = 18) subjects. Insulin, adiponectin, and plasminogen activator inhibitor 1 (PAI-1) were determined using the Bio-Rad Multiplex Platform, and free fatty acids (FFAs) and high sensitivity C-reactive protein (hs-CRP) were determined by standard procedures. The AT insulin resistance (ATIR) index and ATIR/adiponectin and adiponectin/leptin ratios were calculated. Results: HDL was progressively smaller (nm) and enriched with AGE (mg-BSA-AGE/mg protein) according to the glucose categories: 8.49 and 7.5 in normoglycemic subjects, 8.44 and 12.4 in prediabetic subjects, and 8.32 and 14.3 in T2D subjects (P = 0.033 and P = 0.009 for size and AGE, respectively). In multivariable regression analysis, the ATIR/adiponectin ratio was inversely associated with HDL size (β = -0.257, P = 0.046), and the ATIR ratio was directly associated with HDL glycation (β = 0.387, P = 0.036). In contrast, adiponectin and the adiponectin/leptin ratio were not associated with alterations in HDL particles. Furthermore, HDL size was associated with resistin (β = -0.348, P = 0.007) and PAI-1 (β = -0.324, P = 0.004). HDL and AGE were related to insulin concentrations (β = 0.458, P = 0.015). Analyses were adjusted for age, sex, body mass index, triglycerides, and HDL-cholesterol. Conclusion: HDL size was significantly associated with the ATIR/adiponectin ratio and inflammation, whereas glycation was more strongly related to the ATIR index. These findings have important implications for the management and prevention of cardiovascular disease in T2D patients. [ABSTRACT FROM AUTHOR]

Adiponectin, leptin, and resistin are thought to be involved in the pathogenesis of rheumatoid arthritis (RA). However, the causal relationship between these adipokines and the risk for RA is unclear. We performed a range of two-sample Mendelian randomisation (MR) analyses to assess the causal effect of circulating adiponectin, leptin, and resistin on RA risk in European and East Asian individuals. Different sets of adiponectin-, leptin-, and resistin-related genetic variants were used as instruments for genetically determined adipokine levels. As body mass index (BMI) is a risk factor for RA and affects adipokine levels, multivariable MR was used to calculate the causal effect of each adipokine on RA risk taking BMI into account. Several MR analyses revealed no evidence of a causal relationship between circulating adiponectin, leptin, or resistin levels and RA risk in either Europeans or East Asians. Similarly, multivariable MR did not provide evidence of any causal effect of adiponectin, leptin, or resistin on RA risk when taking BMI into account. This MR study shows for the first time that genetically determined levels of adiponectin, leptin, or resistin do not have a direct causal effect on the risk of developing RA after adjustment for BMI. [ABSTRACT FROM AUTHOR]

Traditional medicines are recently being focused on to treat diabetes and its complications because of their lack of toxic and/or side effects. This report describes the effects of 7-O-galloyl-D-sedoheptulose (GS), a polyphenolic compound isolated from Corni Fructus, on type 2 diabetic db/db mice with hepatic and pancreatic damage. We examined several biochemical factors and oxidative stress- and inflammation-related markers. In the serum, levels of glucose, leptin, insulin, C-peptide, resistin, tumor necrosis factor-a, and interleukin-6 were down-regulated, while adiponectin was augmented by GS treatment. In addition, GS suppressed the reactive oxygen species and lipid peroxidation in the serum, liver, and pancreas, but increased the pancreatic insulin and pancreatic C-peptide contents. These results were derived from attenuating the expression of nicotinamide adenine dinucleotide phosphate oxidase subunit proteins, Nox-4 and p22phox. Augmented nuclear factor (NF)-E2-related factor 2 and heme oxygenase-1 were reduced with a decrease in oxidative stress during GS treatment. NF-κB-related pro-inflammatory factors were also alleviated in hepatic tissue. Moreover, GS modulated the protein expressions of pro-inflammatory NF-κB, cyclooxygenase-2, inducible nitric oxide synthase, c-Jun N-terminal kinase (JNK), phosphor-JNK, activator protein-1, transforming growth factor-ß1, and fibronectin. Based on these results, we demonstrated that the anti-diabetic action of GS may be due to its anti-oxidative stress property and anti-inflammatory action. [ABSTRACT FROM AUTHOR]