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Background In current intensive care treatment, there are patients with severe burns who cannot be saved due to progressive organ failure. Further investigation of the pathogenesis of severe burns is needed to improve the mortality rate. In burns, inflammatory cytokines form a network that leads to an inflammatory response. Adipocytes secrete physiologically active substances (adipokines). The roles of adipokines have not been completely clarified in burn patients. This study aimed to determine the relation between serial changes of adipokines and clinical course in severely burned patients. Methods This was a single-center, retrospective, observational study. Patients’ blood samples were collected on the day of injury and around 1 week later. Adipokines (adiponectin, angiotensinogen, chemerin, CXCL-12/SDF-1, leptin, resistin, vaspin, visfatin), various inflammatory cytokines, syndecan-1 and C1 esterase inhibitor were measured. Results Thirty-eight patients were included. Resistin levels were significantly higher in the non-survivors versus survivors on Day 1 after burn injury. Hierarchical clustering analysis showed common clusters on Day 1 and at 1 Week after burn injury (resistin, IL-6, IL-8, IL10 and MCP-1). The correlation coefficient of resistin to SOFA score at 1 Week was significant. Logistic regression analysis showed a significant relation of resistin levels on Day 1 with prognosis; the area under the ROC curve for resistin was 0.801. Conclusions In the acute phase of burns, resistin was associated with other pro-inflammatory cytokines and was related to the severity and prognosis of major burns.

The adipose tissue secretes adipokines and influences the release of inflammatory mediators contributing to a state of low-grade systemic inflammation that may change lung function.To correlate levels of adipokines and inflammatory mediators with lung function in individuals with obesity and bronchial asthma symptoms.A cross-sectional study, including women with obesity (grade II and III) with symptoms and clinical diagnosis of asthma. Anthropometric measurements (weight, height, BMI), pulmonary function test (spirometry), asthma control test questionnaire, collection of systemic inflammatory markers (blood collection) and pulmonary markers (sputum collection) were collected and were analyzed: IL-6, IL-8, TNF-α, adiponectin, resistin, leptin and C-reactive protein (CRP). The patients were stratified into two groups according to asthma control.80 women were analyzed and 40% had an ACT score greater than or equal to 18 and were classified as "controlled asthma". More than half of the patients of ACT18 score obtaining measures of FEV1, PEF and FEF25-75% below and 80% of predicted. There was a significant and negative correlation between IL-6 in the sputum with FVC and FEF25-75% in the group ACT18 and with FVC and FEV1 in the group ACT≥18.Therefore, we concluded that the increase of interleukin-6 in the sputum is related to worse pulmonary function even in patients with controlled asthma, especially in the translate airway permeability measures.

The objective of the study — to assess the correlation between resistin and indexes of the functional state of the liver in patients with non-alcoholic fatty liver disease (NAFLD), type 2 diabetes mellitus (DM) and with their combination. Materials and methods. 110 patients were examined, among them 20 patients with NAFLD, 20 patients with DM type 2 and 70 patients with comorbidity (NAFLD + DM type 2), they were divided into 2 subgroups — 20 patients with normal body weight and 50 obese patients. The control group consisted of 20 apparently healthy individuals. Comprehensive clinical, laboratory (with determination of indicators of protein, pigment, enzyme and carbohydrate metabolism, resistin level), instrumental (ultrasound of the liver and liver biopsy (8 patients)) examinations were carried out. Results. Significant increase in plasma resistin levels in patients with comorbidity was revealed. Significant correlations between resistin levels and indicators of the functional state of the liver in these patients were established. Conclusion. In patients with NAFLD, DM type 2 and their combination, especially with concomitant obesity, there is an imbalance of fatty tissue products, a sign of which is the increase of resistin level. The relationship between resistin and indicators of the functional state of the liver mainly in the subgroup with comorbid disorders and obesity give reason to believe that hormone and metabolic disorders that affect liver function activate and worsen in obesity.

The differential diagnosis of psoriatic arthritis (PsA) and rheumatoid arthritis (RA) is difficult because of the lack of diagnostic clinical signs and reliable biomarkers. This study investigated microRNAs (miRNA) and adipokines as potential additional markers to discriminate PsA from RA. The expression profile of miRNA (miR-21, miR-140, miR-146a, miR-155, miR-181b, miR-223, miR-let-7e) and inflammatory cytokines (IL-1β, IL-6, IL-17a, IL-23a, TNF-α) from peripheral blood mononuclear cells of PsA and RA patients compared to healthy controls (HC) were evaluated by real-time PCR, and serum adipokines (adiponectin, chemerin, leptin, resistin, visfatin) and cytokines by ELISA assay. Univariable binary logistic regression was used to find the association between PsA and potential predictors. The gene expression of miRNA and cytokines and the serum levels of adipokines were found significantly different in PsA and RA patients compared to HC, as well as in PsA versus RA. MiR-140 gene expression resulted up-regulated in PsA patients and reduced in RA in comparison to HC, and, for the first time, significantly higher in PsA compared with RA. Serum levels of IL-23a and leptin were significantly increased in PsA and RA populations than in HC, as well as in PsA versus RA. Furthermore, circulating TNF-α was up-regulated in PsA and RA in comparison to controls, while resulted higher in RA than in PsA. Univariable binary logistic regression analysis found the above-mentioned markers associated to PsA versus RA. Our results first demonstrated an increased expression of circulating miR-140 and serum leptin in PsA patients compared to RA, which were identified as potential additional biomarkers to discriminate PsA from RA. Since the differential diagnosis of PsA and RA poses challenges in clinical practice, our data may help to enhance the diagnostic performance of PsA in daily practice.

Recent research has closely linked adipocytokines to liver inflammation and fibrosis progression in patients with non-alcoholic liver disease. This study aimed to determine the relationship of serum adiponectin and resistin levels with the severity of liver fibrosis in patients with chronic hepatitis B (CHB), depending on the duration of antiviral therapy.The cross-sectional study included 75 patients with CHB divided into two groups: the T1 group (undergoing antiviral therapy for up to 2 years) and the T2 group (undergoing antiviral therapy over 2 years). The control group consisted of 40 healthy people. Serum concentrations of adiponectin and resistin were estimated with the ELISA method, while the degree of liver fibrosis was determined using FIB-4 and APRI score.There were no statistically significant differences in the mean serum adiponectin levels in relation to the duration of antiviral therapy. Higher values of serum resistin concentration were confirmed in patients of the T1 group compared to healthy controls (p=0.001) and to the T2 group (p=0.031). The mean level of serum resistin concentration was significantly higher in the group of patients with a higher FIB-4 score (9.12±3.39 vs 5.58±3.36 ng/mL, p=0.001) and higher APRI score (17.45±3.96 ng/mL vs 4.82±1.11 ng/mL, p=0.001). A positive correlation was found between serum resistin levels and the degree of liver fibrosis (p0.001). There was no significant difference between mean serum adiponectin levels according to the values of FIB-4 and APRI scores.Progression of liver fibrosis estimated by FIB4 and APRI scores as well as the length of antiviral treatment had a significant effect on serum resistin values in CHB patients on antiviral therapy.Novija istraživanja su usko povezala adipocitokine sa progresijom upale i fibroze jetre kod bolesnika koji imaju bolesti jetre koje nisu povezane sa konzumiranjem alkohola. Cilj ovog istraživanja bio je da se utvrdi odnos serumskog nivoa adiponektina i rezistina sa težinom fibroze jetre kod pacijenata sa hroničnim hepatitisom B (CHB), u zavisnosti od trajanja antivirusne terapije.Studija preseka je obuhvatila 75 pacijenata sa HHB koji su bili podeljeni u dve grupe: T1 grupa (na antivirusnoj terapiji do 2 godine) i T2 grupa (na antivirusnoj terapiji preko 2 godine). Kontrolnu grupu je činilo 40 zdravih osoba. Serumske koncentracije adiponektina i rezistina su procenjene uz pomoć ELISA metode, dok je stepen fibroze jetre određen pomoću FIB-4 i APRI skora.Nije bilo statistički značajnih razlika u srednjim nivoima adiponektina u serumu u odnosu na trajanje antivirusne terapije. Veće vrednosti koncentracije rezistina u serumu su potvrđene kod pacijenata iz T1 grupe u poređenju sa zdravim pacijentima iz kontrolne grupe (p = 0,001) i pacijentima iz grupe T2 (p=0,031). Prosečan nivo koncentracije rezistina u serumu bio je značajno veći u grupi pacijenata sa većim skorom FIB-4 (9,12 ± 3,39 naspram 5,58 ± 3,36 ng/mL, p = 0,001) i većim skorom APRI (17,45 ± 3,96 ng/mL naspram 4,82 ± 1,11 ng/mL, p=0,001). Utvrđena je pozitivna korelacija između serumskog nivoa rezistina i stepena fibroze jetre (p0,001). Nije bilo značajne razlike između srednjih nivoa adiponektina u serumu prema vrednostima FIB-4 i APRI skoru.Napredovanje fibroze jetre procenjeno rezultatima FIB-4 i APRI, kao i du'ina antivirusnog lečenja su imali značajan uticaj na vrednosti rezistina u serumu kod pacijenata sa hroničnim hepatitisom B na antivirusnoj terapiji.

Background: Epicardial adipose tissue (EAT) surrounds the epicardium and can mediate harmful effects related to coronary artery disease (CAD). Objective: We explored the regional differences between adipose stores surrounding diseased and non-diseased segments of coronary arteries in patients with advanced CAD. Methods: We enrolled 32 patients with known CAD who underwent coronary artery bypass graft (CABG) surgery. Inflammatory mediators were measured in EAT biopsies collected from a region of the left anterior descending artery (LAD) with severe stenosis (diseased segment) and without stenosis (non-diseased segment). Results : Mean age was 64.3±11.1 years, and mean EAT thickness was 7.4±1.9 mm. Dyslipidemia was the most prevalent comorbidity (81% of the patients). Out of a total of 11 cytokines, resistin (p=0.039), matrix metallopeptidase 9 (MMP-9) (p=0.020), C-C motif chemokine ligand 5 (CCL-5) (p=0.021), and follistatin (p=0.038) were significantly increased in the diseased compared with the non-diseased EAT segments. Indexed tumor necrosis factor-alpha (TNF-α), defined as the diseased to non-diseased cytokine levels ratio, was significantly correlated with increased EAT thickness both in the whole cohort (p=0.043) and in a subpopulation of patients with dyslipidemia (p=0.009). Treatment with lipid-lowering agents significantly decreased indexed TNF-α levels (p=0.015). No significant alterations were observed in the circulating levels of these cytokines with respect to CAD-associated comorbidities. Conclusion: Perivascular EAT is a source of cytokine secretion in distinct areas surrounding the coronary arteries in patients with advanced CAD. Adipocyte-derived TNF-α is a prominent mediator of local inflammation.

Метою дослідження було вивчення впливу препарату метформін на рівень деяких гормонів жирової тканини та медіаторів генералізованого неспецифічного запалення при цукровому діабеті 2-го типу. Обстежено 38 пацієнтів з уперше виявленим цукровим діабетом 2-го типу перед початком і після 12 місяців цукрознижувальної монотерапії Глюкофажем. Отримані результати свідчать, що нормалізація показників вуглеводного обміну, зниження маси тіла пацієнтів на тлі проведеного лікування спричинено не лише прямим впливом метформіну на поліпшення поглинання глюкози периферичними тканинами, а і його здатністю модулювати секрецію адипоцитокінів.

Background and aims Extra-coronary calcification (ECC) is a marker of atherosclerosis and independently associated with cardiovascular disease (CVD). Adipokines may mediate the effect of obesity on atherosclerosis. However, the relationship of adipokines with ECC is not well-established. We examined the associations of leptin, resistin and adiponectin with ECC in a diverse community-based cohort. Methods We performed a cross-sectional analysis of 1897 adults without clinical CVD in the MESA cohort. Serum adipokine levels and non-contrast cardiac CT scans were obtained at Exam 2 or 3 (randomly assigned). ECC was quantified by Agatston score and included calcification of the mitral annulus (MAC), aortic valve (AVC), ascending thoracic aorta (ATAC) and descending thoracic aorta (DTAC). We used multivariable regression to evaluate the associations between leptin, resistin and adiponectin [per 1 SD ln(adipokine] with ECC prevalence (score >0) and extent [ln(score+1)]. Results The mean age of participants was 65 ± 10 years; 49% women. After adjusting for demographic factors, adiponectin was inversely associated with AVC prevalence and extent; leptin positively associated with MAC prevalence and extent; and resistin positively associated with ATAC prevalence and extent and DTAC extent. After adjustment for BMI and other CVD risk factors, adiponectin remained inversely associated with AVC prevalence, and resistin remained associated with greater ATAC prevalence and extent. Leptin was not associated with measures of ECC after full adjustment. No adipokine was associated with MAC after full adjustment. Conclusions We identified significant associations between select adipokines and specific markers of ECC. Adipokines may play a role in the development of systemic atherosclerosis.

Vertebral osteomyelitis (VO) is an infection of the spine mainly caused by bacterial pathogens. The pathogenesis leading to destruction of intervertebral discs (IVDs) and adjacent vertebral bodies (VBs) is poorly described. The present study aimed at investigating the connection between infection and bone/disc metabolism in VO patients. 14 patients with VO (infection group) and 14 patients with burst fractures of the spine (fracture group; control) were included prospectively. Tissue biopsies from affected IVDs and adjacent VBs were analysed by RT-qPCR for mRNA-expression levels of 18 target genes including chemokines, adipokines and genes involved in bone metabolism. Most importantly, the receptor activator of NF-κB/osteoprotegerin (RANK/OPG) expression ratio was drastically elevated in both VBs and IVDs of the infection group. In parallel, expression of genes of the prostaglandin-E2-dependent prostanoid system was induced. Such genes regulate tissue degradation processes via the triad OPG/RANK/RANKL as well as via the chemokines IL-8 and CCL-20, whose expression was also found to be increased upon infection. The gene expression of the adipokine leptin, which promotes inflammatory tissue degradation, was higher in IVD tissue of the infection group, whereas the transcription of omentin and resistin genes, whose functions are largely unknown in the context of infectious diseases, was lower in infected VBs. In summary, similar expression patterns of pro-inflammatory cytokines and pro-osteoclastogenic factors were identified in VBs and IVDs of patients suffering from VO. This suggests that common immuno-metabolic pathways are involved in the mechanisms leading to tissue degradation in VBs and IVDs during VO.

Background The prevalence of precocious puberty is increasing. Obesity has been demonstrated to be associated with changes in the adipokine profile and incidence of early puberty in girls. This study assessed the pubertal signs, the levels of adiponectin, resistin, and tumor necrosis factor-alpha (TNF-α) after 12 weeks of combined exercise and 4 weeks of detraining in overweight and obese girls with precocious puberty. Methods Thirty overweight and obese girls (aged 7–9) with precocious puberty, who had received Triptorelin, were randomly divided into two groups (15 exercise and 15 control). Initially, serum levels of adiponectin, resistin, TNF-α, luteinising hormone (LH), and follicle-stimulating hormone (FSH) and the signs of puberty progression (bone age, uterine length, and ovarian volume) were measured. The exercise group performed 60 min of combined (aerobic and resistance) exercise three times/week for 12 weeks. The control group did not receive any exercise. 48 h after the last training session and after 4 weeks of detraining, all research variables were measured (also in the control group). The statistical method used for data analysis was repeated measures ANOVA. Results In the exercise group, adiponectin significantly increased and resistin significantly decreased after 12 weeks. After 4 weeks of detraining, adiponectin significantly decreased, but resistin significantly increased. TNF-α levels did not change significantly during the study. There was no significant difference in all of the factors in the control group. Throughout the 16-week study period, the rate of puberty and LH significantly decreased in both exercise and control groups, but FSH, LH/FSH and ovarian volume significantly decreased in the exercise group alone (P Conclusions Combined exercise increased adiponectin and decreased resistin and the rate of puberty. However, after 4 weeks of detraining, these effects diminished but did not disappear. Trial registration IRCT, IRCT56471. Registered 25 may 2021 - Retrospectively registered, https://fa.irct.ir/user/profile

Purpose The role of adipokines in causing inflammation and insulin resistance in normal weight and obese patients is generally well studied. However, there are often conflicting results regarding their levels in type 1 diabetes mellitus (T1DM) patients and their relationship to micro- and macrovascular disease. We therefore investigated which serum adipokine levels are independently associated with markers of early atherosclerosis and microvascular complications in patients with T1DM. Methods A cross-sectional study was performed in the Diabetes Outpatient Clinic of Hippokrateion General Hospital, Thessaloniki, Greece. Sixty T1DM patients (30 females, mean age 38.8 ± 10.6 years, mean diabetes duration 17.4 ± 9.9 years) were included. Plasma adiponectin, leptin, and resistin, carotid artery intima media thickness (cIMT), and arterial stiffness (pulse wave velocity, PWV/SpygmoCor CP System and Mobil-O-Graph 24 h PWA) were assessed. Results Leptin and resistin levels were significantly higher in overweight and obese patients (p = 0.002 and p = 0.039, respectively). Adiponectin was the only adipokine negatively correlated with BMI (rs = - 0.41, p = 0.001). We report a bivariate association between serum adiponectin levels and retinopathy (p = 0.007). Resistin was the only adipokine that showed significant correlation with systolic (rs = 0.42, p = 0.001) and diastolic (rs = 0.29, p = 0.024) hypertension and PWV (p = 0.035). Conclusions Serum adipokine levels demonstrate similar bivariate associations with anthropometric variables in patients with T1DM to those in normal weight subjects. Although microvascular complications are associated with serum adipokine levels by bivariate analysis, only resistin, an inflammatory marker, is independently associated with arterial stiffness in patients with T1DM.

Resistin is associated with atherosclerosis progression by affecting inflammation and insulin resistance. There are controversial data regarding the prognostic value of resistin in stable coronary artery disease (CAD) patients. We prospectively investigated the long-term prognostic value of resistin in patients with stable CAD. A total 741 consecutive patients with stable CAD were followed for a median of 5.5 years. Serum resistin, lipids, high-sensitivity C-reactive protein (hsCRP) and interleukin-6 (IL-6) levels were measured at baseline. Primary endpoints were cardiac death and secondary hospitalizations for acute coronary syndrome, arrhythmic event or ischemic stroke. Follow-up data were obtained from 703 patients of whom 79 had a cardiac death (11.2%) and 205 (29.2%) met the secondary endpoints. Resistin was positively correlated with hsCRP (r = 0.159, p

To explore the role of adiponectin-resistin (AR) index as a better indicator of obesity-related hypertension.This study continued a case control study that had finished recruiting 153 subjects divided as four characteristic groups. Fasting serum resistin levels (FSR) and Fasting serum adiponectin levels (FSA) were tested by ELISA. And, other related anthropometric clinical and metabolic data were collected. Analyzation on correlations between research index and differences between groups were done by SPSS. AR index's performance was also validated by the receiver operating characteristic (ROC) curves, the net reclassification improvement (NRI), and the integrated discrimination improvement (IDI).The AR index was defined as 1+ logThe AR index was more strongly associated with increased risk of obesity-related hypertension than the solely index of FSR or FSA and was useful for early diagnosis of obesity-related hypertension.

Research question Can the adipocytokine milieu of the follicular niche improve the ability to predict treatment outcomes in infertile patients? Design Follicular fluid samples from overweight patients were analysed and compared with samples from matched normal-weight patients. Concentrations of adiponectin, chemerin, C-reactive protein, interleukin-6 (IL-6), IL-10, IL-18, insulin, leptin, prolactin, resistin, tumour necrosis factor alpha (TNF-α) and bone morphogenetic protein-15 (BMP-15) were assessed by multiple magnetic bead immunoassay (MMBI) and enzyme-linked immunosorbent assay and correlated with fertility treatment outcomes. Results Analysis of samples from 22 overweight and 22 normal-weight patients demonstrated that TNF-α can predict oocyte maturation rate. When stratified by body mass index (BMI), IL-10 emerges as a better predictor of oocyte maturation in normal-weight patients. Prolactin was a negative predictor for fertilization rate in the full cohort, and this prediction power was lost upon stratification. No adipocytokines were predictive of blastulation rate, and only age remained predictive. BMP-15 was a strong predictor of high-quality blastulation in the full cohort, more so in the normal-weight population. Conclusions The adipocytokine milieu of the follicular fluid provides a snapshot of the growing oocyte's environment and can help predict fertility treatment outcomes, fine-tuning understanding of the dysregulation caused by increasing BMI. Inflammatory cytokines can predict oocyte maturation; prolactin, oocyte competence; and BMP-15, high-quality blastulation. Further analysis of these findings with a larger sample size and assessing individual oocytes will help shed more light on the clinical significance of these findings.

Aim of the work: To evaluate resistin level in systemic lupus erythematosus (SLE) patients and to assess the relationship with insulin resistance, disease characteristics, inflammatory markers and carotid intima-media thickness (CIMT) as a marker of subclinical atherosclerosis. Patients and methods: Thirty adult SLE patients and twenty age and sex-matched control were enrolled. All patients were subjected to history taking, clinical examination and assessment of anthropometric measurements. Laboratory investigations included serum resistin, measures of insulin resistance, highly sensitive C-reactive protein (hs-CRP), erythrocyte sedimentation rate (ESR) and lipid profile. Carotid duplex was performed for measurement of CIMT. SLE disease activity index (SLEDAI-2k) and damage index were evaluated. Results: The 30 patients were 23 (76.7%) females and 7 (23.3%) males (F:M 3.3:1) with a mean age of 30.9 ± 7.9 years. The disease duration was 4.8 ± 1.8 years. The mean serum resistin in patients was 7.7 ± 2.9 ng/dl and in control was 8.5 ± 5.1 ng/dl (p = 0.8). The ESR and hs-CRP were significantly increased (p

Introduction/Purpose Obesity increases significantly every year worldwide. Since 1980, the prevalence of individuals with obesity has practically doubled. Obesity plays an important role in the pathophysiology of diseases that arise from a complex interaction of nutritional, genetic, and metabolic factors, characterizing a chronic inflammatory state. This study aimed to verify the systemic inflammatory response through the analysis of IGF-1, IL-23, and resistin levels and the lipid profile in severely obese women undergoing surgery for obesity and weight-related diseases. Materials and Methods This randomized controlled clinical trial includes female patients clinically diagnosed with severe obesity with an indication for bariatric surgery. Results In the initial evaluation, no significant difference was observed between the control (CG) and bariatric surgery (BSG) groups. The weight, BMI, systolic and diastolic blood pressures, total cholesterol, LDL, HDL, total non-HDL cholesterol, and glucose in BSG patients showed a significant change after surgery. Pre- and post-surgery levels of resistin, IGF-1, and IL-23 showed a significant difference in the BSG group, but only IL-23 was changed after 6 months in the CG. Conclusion The results of this study confirmed that weight loss induced by surgery for obesity and weight-related diseases improved the lipid profile and reduced the chronic inflammatory status in women with severe obesity.

Obesity is a globally common metabolic condition that causes or exacerbates many diseases. High-intensity interval training (HIIT) and orlistat may affect cytokines and adipokines related to obesity. The purpose of this study was to investigate the independent and combined effects of 8 weeks of HIIT and orlistat on body weight, body mass index (BMI), neck circumference, aerobic power, interleukin‑6 (IL-6), tumor necrosis factor α (TNF-α), resistin, and adiponectin in young, obese women. 48 obese individuals were randomly divided into 4 groups: control-placebo (n = 12), HIIT-placebo (n = 12), control-orlistat (n = 12), and HIIT-orlistat (n = 12), and received group-specific interventions. Participant blood samples were taken 48 h before the intervention and 48 h after the last training session. Two-way multivariate analysis of covariance (MANCOVA) was used to investigate the effects of interventions, with significance set at P ≤ 0.05. The results showed that HIIT decreased body weight, BMI, neck circumference, TNF‑α, and resistin concentration, while increasing aerobic power, IL‑6, and adiponectin concentration. Orlistat decreased body weight, BMI, neck circumference, and resistin, and increased plasma IL‑6 levels. In conclusion, although the combined effects of HIIT and orlistat were significant in many factors, no synergistic effect was observed, and there appears to be a limit for changes in each factor that can be reached by either HIIT or medication interventions.

Background Adipokines are hormones secreted by adipose tissue with roles in energy homeostasis and regulation of metabolism. Their dysregulation is suggested to contribute to the increased risk of dementia seen with midlife obesity, but longitudinal studies investigating this are scarce. We determined the association between plasma levels of adiponectin, leptin, and resistin with the risk of dementia. Methods We performed a case–cohort study embedded in the prospective, population-based Rotterdam Study. Plasma levels of the adiponectin, leptin, and resistin were measured at baseline (1997–1999) in a random subcohort of 945 participants without dementia, and additionally in 177 participants, who were diagnosed with dementia during follow-up (until January 1, 2018). Results Higher levels of leptin and resistin were associated with a decreased risk of dementia (adjusted hazard ratio [95% confidence interval] per SD increase of log-transformed values: 0.85 [0.72–1.00] for leptin; 0.82 [0.71–0.95] for resistin). The association of leptin with dementia was further modified by body mass index and by APOE ε4 carrier status. Adiponectin levels were not associated with the risk of dementia. Conclusions These findings support the hypothesis that adipokines have a role in the pathophysiology of dementia. Future studies are warranted to confirm the findings and to explore the underlying mechanisms.

The escalating global burden of type 2 diabetes mellitus necessitates the implementation of strategies that are both more reliable and faster in order to improve the early identification of insulin resistance (IR) in high-risk groups, including overweight and obese individuals. The use of salivary biomarkers offers a promising alternative to serum collection because it is safer, more comfortable, and less painful to obtain saliva samples. As obesity is the foremost contributory factor in IR development, the adipocytokines such as leptin, adiponectin, resistin, and visfatin secreted from the adipose tissue have been studied as potential reliable biomarkers for IR. Measurement of salivary adipokines as predictors for IR has attracted widespread attention because of the strong correlation between their blood and salivary concentrations. One of the adipokines that is closely related to IR is resistin. However, there are conflicting findings on resistin's potential role as an etiological link between obesity and IR and the reliability of measuring salivary resistin as a biomarker for IR. Hence this study reviewed the available evidence on the potential use of salivary resistin as a biomarker for IR in order to attempt to gain a better understanding of the role of resistin in the development of IR in obese individuals.

Background Increasing protein intake (above the Recommended Dietary Amount) alone or with resistance‐based exercise is suggested to improve cardiometabolic health; however, randomized controlled trials (RCTs) are needed to confirm this. Methods The Liverpool Hope University‐Sarcopenia Aging Trial (LHU‐SAT) was a 16 week RCT (ClinicalTrials.gov Identifier: NCT02912130) of 100 community‐dwelling older adults [mean age: 68.73 ± 5.80 years, body mass index: 27.06 ± 5.18 kg/m2 (52% women)] who were randomized to four independent groups [Control (C), Exercise (E), Exercise + Protein (EP), Protein (P)]. E and EP completed supervised and progressive resistance‐based exercise (resistance exercise: two times per week, functional circuit exercise: once per week), while EP and P were supplemented with a leucine‐enriched whey protein drink (three times per day) based on individual body weight (0.50 g/kg/meal, 1.50 g/kg/day). Outcome measures including arterial stiffness (pulse wave velocity), fasting plasma/serum biomarkers [glucose/glycated haemoglobin, total cholesterol, low‐density lipoprotein (LDL), high‐density lipoprotein, insulin, resistin, leptin, adiponectin, C‐reactive protein, tumour necrosis factor‐alpha, interleukin‐6, cystatin‐C, & ferritin], insulin resistance (HOMA‐IR), and kidney function (eGFR) were measured before and after intervention. Results Total protein intake (habitual diet plus supplementation) increased to 1.55 ± 0.69 g/kg/day in EP and to 1.93 ± 0.72 g/kg/day in P, and remained significantly lower (P 0.05), and kidney function (eGFR) remained unaltered. Conclusions Sixteen weeks of leucine‐enriched whey protein supplementation alone and combined with resistance‐based exercise improved cardiometabolic health markers in older adults.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) comorbidity with adipose tissue dysfunction is not new and studies have focused on how adipose tissue influences NAFLD pathophysiology. OBJECTIVE: Quantification of nature and magnitude of the association between serum resistin and also insulin resistance, by calculating pooled Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) score, with NAFLD pathophysiology was the objective of the current study. METHODS: Using systematic review and meta-analysis and standardized mean difference (SMD) as the effect size, the levels of resistin and HOMA-IR scores have been investigated in NAFLD subjects in comparison with controls in the case-control studies using random-effects models. RESULTS: This meta-analysis retrieved a total number of 665 and 522 cases and 671 and 555 control subjects until May 2020 for serum levels of resistin and HOMA-IR score until May 2020. The final analyses demonstrated that pooled SMD of resistin and HOMA-IR score was 0.687 (95% confidence interval, 0.070–1.304) and 1.368 (95% confidence interval, 1.080–1.655); respectively. Moreover, the p-value for the test of significance for each pooled SMD was examined by the z-test and calculated as 0.029 and 0.000 for resistin and HOMA-IR score (clearly considered as statistically significant). CONCLUSION: Based on the findings, the HOMA-IR score and the serum levels of resistin in NAFLD subjects are associated with disease pathogenesis.

A body of studies has examined the circulating concentration of adipokines including apelin, vapin, resistin, and chemerin in polycystic ovary syndrome (PCOS) patients. However, their findings have been inconclusive. Therefore, we systematically reviewed available studies to illuminate the overall circulating concentration of adipokines in PCOS subjects. Cochrane’s Library, PubMed, Scopus, and ISI Web of Science databases were searched from the earliest available date up to April 2021 for relevant articles. The quality of each study was assessed by the Newcastle–Ottawa Quality Assessment Scale. The pooled effect size was estimated based on the random effects model, and the standard mean differences (SMD) with a 95% confidence interval (CI) were reported. A total of 88 studies met the inclusion criteria and were included in the current systematic review and meta-analysis. The results of the analysis showed that serum levels of vaspin (SMD 0.69; 95% CI, 0.22 to 1.17; P = 0.004; I2 = 90.6%), chemerin (SMD 1.87; 95% CI, 1.35 to 2.40; P

Chronic kidney disease (CKD) is the leading cause of death from non-communicable diseases, and its prevalence in 2017 ranged from 8.5 to 9.8%. Depending on the stage of CKD, stage 1 was diagnosed in 3.5%, stage 2 in 3.2% and stage 3 in 7.6%, while stages 4 and 5 took place in 0.4 and 0.1% of the world’s population respectively. Obesity also contributes to the increase in the prevalence and severity of CKD, and their combination occurs in 3.1% of patients. Kidney damage and their structural and functional changes in patients with obesity are associated with high metabolic activity of adipose tissue, due to the synthesis of adipocytokines, including resistin. The purpose of the work: to study changes of resistin level in the blood in patients with early stages of chronic kidney disease, its relation to the level of endothelin, markers of lipid metabolism and inflammation. Materials and methods: 70 patients with stage 1 and 88 patients with stage 2 of CKD with different stages of obesity were examined. Glomerular filtration rate (GFR) was calculated by the formula CKD-EPI based on creatinine, cystatin C and their combination (CKD-EPIcysC / cr). The levels of cystatin C, resistin, tumor necrosis factor-alpha (TNF-α) and endothelin-1 were determined by enzyme-linked immunosorbent assay. Determination of total cholesterol and low-density lipoprotein cholesterol levels in the blood serum was performed by colorimetric method. Statistical analysis of the results was performed with the help of Statistica 6.0 statistical software package using Student’s t-test and Spearman’s rank correlation coefficient. Results: an increase of the resistin level in the blood by 1.3 times in the patients with stage 1 CKD and by 1.6 times in the patients with stage 2 CKD and obesity was determined (p1.2 < 0.05), and there was a weak correlation between its concentration in the blood and body mass index. A significant average negative correlation between resistin and GFR was detected. Increased serum resistin level correlates with increased TNF-α. In patients of both groups, the level of resistin and LDL increases simultaneously, and the correlation between them increases as CKD progresses. Similar changes are observed with respect to increasing concentrations of resistin and endothelin-1. Thus, an increase of resistin level in the blood in patients with the early stages of CKD initiates a number of pathological changes, such as systemic inflammation, hyperlipidemia and endothelial dysfunction.

Obesity is associated with the development of liver disease and its progression to hepatocellular carcinoma. This link may be attributed to adipocytokines such as visfatin and resistin which have been shown to promote liver cancer incidence and progression. Studies have yet to determine the role of visfatin and resistin in liver cancer, specifically in the context of obesity. The objective of this study was to investigate the effect of neutralizing visfatin and resistin in obese (OB) or normal weight (NW) sera to determine the contribution of these proteins in obesity-induced invasive liver cancer. Sera from OB or NW males was used to determine the efficacy of neutralizing visfatin and resistin to reduce the obesity-induced liver cancer phenotype. HepG2 and SNU-449 cells were exposed to OB and NW sera ± antibodies for visfatin or resistin. The neutralizing antibodies differentially suppressed invasion, reactive oxygen species production, and matrix metalloproteinase-9 secretion. These changes corresponded with a decrease in phosphorylated extracellular signal-regulated kinases and protein kinase B in HepG2 cells, but differences were not observed in CAP1 or β-catenin. In conclusion, visfatin and resistin have differential roles in obesity-associated liver cancer and may be potential targets to reverse the impact of obesity on liver cancer progression.

Higher serum resistin levels were reported to be associated with increased mortality risk. We aimed to assess the predictive value of resistin levels in perivascular adipose tissue (PVAT) around the left main coronary artery (LMCA) for mid-term survival of patients with advanced coronary artery disease (CAD). This was a prospective study including patients referred for elective coronary artery grafting in 2016 and 2017, performed using a standard approach. A sample of PVAT was harvested and resistin levels were measured using an enzyme-linked immunosorbent assay. Patients were followed from the day of the procedure until March 2021. In each patient, the SYNTAX score and EuroSCORE II were calculated. The study included 108 patients aged 68.1 ±7.9 years, including 83 men (76.9 %). The duration of follow-up was 731 (range, 275-1020) for nonsurvivors and 1418 median (range, 1174-1559) for survivors (p

Systemic sclerosis (SSc) is autoimmune disease characterized by endothelial dysfunction and microvascular damage. Resistin has been implied in microvascular dysfunction. Objective of this study is to evaluate the association between baseline resistin and development of new digital ulcers (DUs) in SSc patients. At baseline, serum resistin has been assessed in 70 female SSc patients and 26 healthy controls (HC). In SSc patients, clinical assessment was performed at baseline and after a 52-weeks follow-up. Serum resistin level was increased in SSc patients compared to HC [5.89 ng/ml (2.5 ng/ml–8.1 ng/ml) vs 2.3 ng/ml (0.4 ng/ml–2.4 ng/ml), p = 0.0004)]. Resistin was lower (p = 0.005) in SSc patients with early capillaroscopic pattern than patients with active or late capillaroscopic pattern [2.49 ng/ml (0.89 ng/ml–5.81 ng/ml) vs 7.11 ng/ml (3.48 ng/ml–11.35 ng/ml) and 6.49 ng/ml (3.35 ng/ml–8.87 ng/ml), respectively]. After a 52-weeks follow-up, 34 (48.6%) patients developed new DUs. Median serum resistin was significantly higher in patients with new DUs than in patients without new DUs [6.54 ng/ml (3.35 ng/ml–11.02 ng/ml) vs 4.78 ng/ml (1.06 ng/ml–7.6 ng/ml), p = 0.019]. Kaplan–Meier curves show a significantly reduced free survival from DUs in patients with increased resistin (p = 0.002). In multivariate analysis, resistin is associated with the development of new DUs. Increased serum resistin level is a predictive marker of new DUs in SSc.

Body fat has regulatory functions through producing cytokines and adipokines whose role in the pathogenesis of systemic sclerosis (SSc) is currently emerging. Changes in body mass, either over‐ or underweight, entail a dysregulation of the cytokine/adipokine network that may impact upon SSc disease activity. We evaluated serum levels of adipokines and cytokines in SSc patients and correlated them to clinical features and body mass index (BMI) categories. The study included 89 SSc patients and 26 healthy donors (HD). Serum levels of adiponectin, leptin, resistin, visfatin, tumor necrosis factor (TNF)‐α, interferon (IFN)‐γ, interleukin (IL)‐2, IL‐10 and IL‐17A were measured by multiplex immunoassay and correlated to BMI and disease‐specific features. Student’s t‐test or analysis of variance (ANOVA) were used for comparisons between groups. Spearman’s or Pearson’s tests were used for correlation analysis. Serum levels of TNF‐α, IL‐2, leptin and resistin were significantly higher in SSc than in HD. Leptin levels were significantly higher in interstitial lung disease (ILD)‐ and pulmonary arterial hypertension (PAH)‐SSc subgroups. The highest levels of IL‐17A, IL‐2, IL‐10, leptin and visfatin were detected in SSc patients with obesity (p, Adpokines and cytokines are regulated in Systemic Sclerosis across BMI categories. Leptin levels raise with BMI increase, but did not seem to be correlated with disease activity. Interestingly, TNFα levels were lowest in underweight patients suggesting its possible role in SSc associated sarcopenia.

Background Chronic hepatitis C (CHC) virus is associated with insulin resistance and diabetes which have been linked to progressive liver fibrosis and sustained virologic response (SVR) to antiviral treatment. Resistin is a polypeptide hormone belonging to adipokines that may contribute to the development of obesity, insulin resistance, and metabolic syndrome. Also, the link between resistin and insulin resistance in patients with chronic hepatitis C and the effect of new direct acting antivirals on them seems unclear at present. The aim of this study is to evaluate the role of Resistin in detecting Insulin Resistance and their impact on response to direct acting antiviral in chronic hepatitis C patients. Results The Study was prospective Cohort clinical study, in Hepatology outpatient clinic at Ain Shams University Hospitals .This study was performed on 40 Egyptian patients who have Chronic viral hepatitis C, divided into 3 groups: GROUP I includes: 20 patients with Chronic viral hepatitis C on Sofosbovir- Daclatasvir before start of treatment and Sustained viral response after 12 weeks [SVR 12]. GROUP II includes: 20 patients with Chronic viral hepatitis C and non-responders before start of 2nd line of treatment and SVR 12. GROUP III includes: 10 subjects not infected with HCV as control group. The following investigations were done: body mass index calculation, Laboratory investigations including CBC, complete hepatic function tests, FIB-4 calculation, fasting serum insulin, HOMA-IR and serum Resistin level at baseline and re-assessed 12 weeks post end of treatment. Fasting serum Insulin, HOMA-IR and Resistin level were statistically significant higher in both naïve & relapser chronic HCV infected patients than in control group (p value p value 0,001, p value 0,002). Serum Resistin at a cut off value >1800 ng/ml had 38.89 % sensitivity, 86.36 % specificity, 70 % PPV, 63.3 % NPV (with an overall accuracy of 57.1 %) in predicting absence of liver cirrhosis based on FIB-4. And at a cutoff value ≥2400 ng/ml had 93.55% sensitivity, 33.3% specificity, 82.9% positive predictive value, and 60% negative predictive value with an overall accuracy of 62.4% in prediction of significant insulin resistance among chronic HCV patients. Conclusion Serum Resistin level was significantly up regulated in patients with chronic HCV, with significant reduction in its level after achievement of SVR. Resistin has the potential to be a biomarker for screening of insulin resistance among chronic HCV patients.

Fresh camel milk was widely accepted to help to prevent and control of diabetes, especially in Africa, Middle East, and cooler dry areas of Asia. In this study, type 2 diabetic patients were enrolled to supplement with 10 g of camel milk powder twice a day for 4 weeks (n = 14), cow milk powder served as the placebo (n = 13). It was found that camel milk supplement decreased fasting blood glucose, 2‐hr postprandial blood glucose, serum content of total cholesterol, resistin, and lipocalin‐2. There was also a significant increase in serum content of osteocrin, amylin, and GLP‐1in camel milk group, indicating an improvement on adipose tissue and skeletal muscle. Camel milk powder supplement significantly enriched the relative abundance of Clostridium_sensu_stricto_1 and [Eubacterium]_eligens_group compared with cow milk after the 4‐week intervention. This study suggested that camel milk powder can be used as a functional food help to treat type 2 diabetes., It was found that camel milk supplement decreased fasting blood glucose, 2‐hr postprandial blood glucose, serum content of total cholesterol, resistin, and lipocalin‐2. There was also a significant increase in serum content of osteocrin, amylin, and GLP‐1in camel milk group, indicating an improvement on adipose tissue and skeletal muscle. Camel milk powder supplement significantly enriched the relative abundance of Clostridium_sensu_stricto_1 and [Eubacterium]_eligens_group compared with cow milk after the 4‐week intervention.

Objective: This study aimed to investigate the serum levels of inflammatory markers in adolescents with major depressive disorder (MDD) using selective serotonin reuptake inhibitors. Methods: This was an 8-month observational study, involving 30 adolescents with and 38 without (control) MDD diagnosis. Demographic (age and gender) and anthropometric data (weight, height, and calculated body mass index [BMI] z score) were collected. Body composition was assessed with whole-body DXA scan. Depressive and anxiety symptoms were assessed using the Beck Depression and Anxiety Inventories (BDI-II and BAI), respectively. Serum levels of interleukin (IL)-6, IL-8, IL-1β, tumor necrosis factor, monocyte chemoattractant protein-1 (MCP-1), leptin, resistin, and adiponectin were measured using Bio-Plex Multiplex Immunoassays at baseline and after 8 months. Results: At baseline, patients with MDD and controls did not differ in age, gender, BMI z score, and fat mass index (FMI) z score. At follow-up, 58.3% (21/36) of patients with MDD were in full remission. Patients with MDD had higher levels of resistin at baseline (26274.16 pg/mL [16162.68–54252.72]) than controls (21678.53 pg/mL [11221.17–37343.27]; p

Background and Purpose: Unstable carotid plaques are a common cause of ischemic strokes. Identifying markers that reflect/contribute to plaque instability has become a prominent focus in cardiovascular research. The adipokines, resistin and chemerin, and ChemR23 (chemerin receptor), may play a role in carotid atherosclerosis, making them potential candidates to assess plaque instability. However, the expression and interrelationship of resistin and chemerin (and ChemR23) protein and mRNA within the carotid atherosclerotic plaque remains elusive. Thus, we investigated herein, the association between plaque mRNA and protein expression of resistin and chemerin (and ChemR23) and carotid plaque instability in humans, and whether sex differences exist in the relationship between these adipokines and plaque instability. Methods: Human carotid plaques were processed for immunohistochemical/mRNA analysis of resistin, chemerin, and ChemR23. Plaque instability was assessed by gold-standard histological classifications. A semi-quantitative scoring system was used to determine the intensity of adipokine expression on macrophages/foam cells, as well as the percentage of inflammatory cells stained positive. Plaque adipokine protein expression was also digitally quantified and mRNA expression was assessed by qRT-PCR. Results: Resistin and chemerin mRNA expression was 80% and 32% lower, respectively, in unstable versus stable plaques ( P P P Conclusions: This study examined the relationship between resistin, chemerin, and ChemR23, and carotid plaque instability, with a specific analysis at the plaque level. We reported a positive association between plaque instability and protein levels of resistin, chemerin, and ChemR23 but a negative association with resistin and chemerin mRNA expression. This suggests these adipokines exert proinflammatory roles in the process of carotid atherosclerosis and may be regulated via a negative feedback regulatory mechanism.

OBJECTIVE To explore the effect of electro-acupuncture (EA) on glucose and lipid metabolism in unmarried patients with polycystic ovary syndrome (PCOS). METHODS Fifty-four PCOS patients were equally randomized into true acupuncture group and sham acupuncture group (control) for totally 16 weeks of treatment by random method with a computerized randomization program. Patients in true acupuncture group accepted traditional acupuncture methods with EA and two sets of acupoint groups were used alternatively. The first set consisted of Zhongji (CV 3), Qihai (CV 6), Guilai (ST 29), Sanyinjiao (SP 6), Yinlingquan (SP 9), Hegu (LI4) and Baihui (GV 20), and the second set consisted of Tianshu (ST 25), ST 29, CV 3, CV 6, SP 6, Taichong (LR 3), Neiguan (PC) 6 and GV 20. Patients in the sham acupuncture group accepted shallow acupuncture methods through EA without electricity at 4 non-meridian points in each shoulder and upper arm. Outcome measures included body mass index (BMI), waist-hip-ratio (WHR), oral glucose tolerance test (OGTT), insulin release test, glucose and lipid metabolism indicators such as total cholesterol (TC), triglycerides, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol, adiponectin, leptin, visfatin, resistin, and interleukin (IL-6). RESULTS Twenty-six subjects in the true acupuncture group and 20 subjects in the sham group completed the clinical trial. After 16 weeks of treatment, no significant difference in the outcome measures were observed between the two groups (P>0.05). However, as compared with baseline data, a reduction in weight, BMI, hipline, WHR, fasting glucose, homeostatic model assessment of insulin sensitivity, visfatin and HDL-C, and an increase in resistin and IL-6 were observed in the true acupuncture group (P

Background: NAFLD is a metabolic syndrome that manifests in the liver and is associated with type 2 diabetes mellitus (type 2 DM), insulin resistance, obesity and hyperlipidemia. The number of sufferers continues to increase worldwide in line with the increasing prevalence of obesity and diabetes. Resistin is a potential marker for NAFLD, which also have an important relationship with obesity and insulin resistance. Purpose: to analyze the relationship between resistin level and the degree of NAFLD. Methods: This cross sectional study was conducted at the Gastroentero-hepatology Department of Haji Adam Malik General Hospital, Medan, from January to March 2020. Patients with NAFLD diagnosed with abdominal ultrasound underwent measurement of body mass index (BMI), examination of resistin levels, fasting blood glucose, platelet count, albumin, AST and ALT, and the degree of NAFLD Fibrosis Score (NFS) was determined. Results: From 67 samples, based on abdominal ultrasound, the largest proportion was grade I NAFLD (40.4%). There was a statistically significant relationship between resistin levels and the degree of NAFLD (p value

Diabetic nephropathy causes chronic kidney disease and renal failure globally. We investigated the mRNA expression of resistin, TNF-α, and microRNA 124-3p (miR-124-3p) in peripheral blood mononuclear cells (PBMCs) of diabetic patients with and without nephropathy. The mRNA expression of target genes in isolated PBMCs from whole blood was determined using real-time quantitative reverse transcription (RT) polymerase chain reaction (qRT-PCR). Demographic and clinical characteristics of study patients were also measured by standard methods. Relative expression of resistin and TNF-α was significantly increased (approximately 10-fold, and 1.5-fold respectively) in patients with nephropathy compared to that in patients without nephropathy (p

Cardiovascular diseases (CVDs) are associated with socioeconomic and, most importantly, with clinical problems. Accordingly, the identification of early and specific biomarkers indicating metabolic changes that underlie disease development and/or progression is important and may improve preventive and treatment strategies. A recently discovered protein - resistin (ADSF, FIZZ3) - whose expression is increased in carbohydrate metabolism and adipose tissue disorders, seems to be worth of interest in this context. The current publication was based on a detailed review of available literature, including Medline, EBSCO, Scopus, and Cochrane Library databases. The search period was between January 1, 2001 and December 20, 2020. The following keywords were used: "resistin", "resistin AND cardiology" and "resistin AND cardiosurgery". Our review covered a total of 4476 records, 594 of which were review publications. The presented article summarizes the current knowledge on the role of resistin in prevention and treatment of CVDs. Available literature shows that resistin may be a predictor for various pathological states; however, data from some studies on the pathophysiological mechanisms of action are contradictory. There is a need for further investigations to explore the exact role of resistin in CVDs.

Metabolic syndrome is a symptom complex that is based on visceral obesity and insulin resistance. Its prevalence is quite high, which is a big problem, since this condition increases the risk of developing cardiovascular diseases and mortality from them. Metabolic syndrome includes, in addition to abdominal obesity, arterial hypertension, disorders of carbohydrate, lipid and purine metabolism. Visceral adipose tissue plays a key role in the formation of insulin resistance and other components of the metabolic syndrome. This is due to the fact that abdominal fat, in contrast to subcutaneous fat, synthesizes pro-inflammatory cytokines, as well as adipokines — adipose tissue hormones that are involved in the formation of insulin resistance, affect carbohydrate and fat metabolism and the cardiovascular system. These include leptin, adiponectin, resistin, apelin and others. Some adipokines have an adverse effect on metabolism and increase cardiovascular risks, while others, on the contrary, have a positive effect. Taking into account their role in the development of the components of the metabolic syndrome, the possibilities of a therapeutic effect on the hormones of adipose tissue to improve metabolic processes and prevent complications associated with it are discussed.

Objective Previous studies have reported a link between metabolic parameters and disease activity in rheumatoid arthritis (RA), although the evidence is limited in early RA. We aimed to investigate the relationship between disease activity and adipocytokine levels in subjects with early RA. Methods Forty-seven patients with early RA (symptom duration ≤12 months) were enrolled. Disease activity was determined by DAS28-CRP. Patients were treated with DMARDs according to the EULAR recommendations. Subjects were tested before and five months after treatment. Results Early RA patients with high disease activity (DAS28-CRP > 4.9) had greater BMI (31.2 ± 6.8 kg/m2 vs. 26.7 ± 4.1 kg/m2; p = 0.006) and higher leptin levels (14.62 ± 15.60 ng/mL vs. 7.82 ± 8.00 ng/mL; p = 0.048). Levels of other adipocytokines were not significantly different. Leptin levels were similar in subjects with mild/moderate disease activity and controls. DAS28-CRP was correlated with leptin (r = 0.303, p = 0.039). Leptin levels decreased significantly after treatment (from 10.86 ± 12.34 ng/mL to 9.22 ± 9.29 ng/mL; p = 0.047) along with insulin levels (from 13.68 ± 21.90 mU/L to 7.09 ± 4.72 mU/L; p = 0.010) and HOMA-IR (from 4.39 ± 9.53 to 1.70 ± 1.38; p = 0.012). HDL cholesterol levels increased (from 41 ± 10 mg/dL48 ± 10 mg/dL; p Conclusion Leptin levels were associated with disease activity in patients with early RA and these levels decreased after treatment with DMARDs. Further research is needed to elicit leptin's role to regulate disease activity in early RA.

The frequent coexistence of obesity and metabolic syndrome in patients with alopecia areata may indicate the common pathogenetic pathway in these conditions with an important role of adipokines. The aim of the study was to evaluate the serum level of adiponectin, resistin and leptin in patients with alopecia areata in comparison to healthy controls. The study included 65 patients with alopecia areata and 71 healthy controls. The concentration of adipokines was determined with the enzyme-linked immunosorbent assay. The mean concentrations of adiponectin and resistin were significantly lower in the sera of patients with alopecia areata when compared to healthy controls (7966 $$\pm$$ ± 4087 vs 9947 $$\pm$$ ± 5692 ng/ml; p = 0.0312 and 11.04 $$\pm$$ ± 3.88 vs 14.11 $$\pm$$ ± 8.69 ng/ml; p = 0.0176, respectively). A negative correlation between the serum level of adiponectin and severity of alopecia tool (SALT) score was observed (r = − 0.26; p $$\pm$$ ± 2499 vs 8525 $$\pm$$ ± 4085 ng/ml; p = 0.0135). No significant difference in the serum concentration of leptin was observed between patients with alopecia areata and healthy controls. The negative correlation between the serum level of adiponectin and hair loss severity indicates that adiponectin may be considered a marker of hair loss severity in alopecia areata. Further studies are needed to evaluate the role of resistin in patients with alopecia areata and its decreased level irregardless of severity or activity of the disease.

Intravenous lipid emulsions in parenteral nutrition may cause different metabolic responses and immune effects in critically ill patients with sepsis. The aim of this study is to investigate the effects of different lipid emulsions on changes in concentrations of adipokine and cytokine and their relationship with mortality in patients.Patients enrolled in this prospective, single-center, observational cohort study, were estimated to require more than ten days of parenteral nutrition. They were treated with soybean oil-based or olive oil-based parenteral lipid emulsions. Adipokine and cytokine concentrations of septic patients were determined at enrollment and ten days after, in accordance with the diagnostic criteria of SEPSIS-3. The concentrations levels were measured in an enzyme-linked immunosorbent assay. Mortality was analyzed using the Kaplan-Meier method and Cox regressions.Over a 25-month period, 145 patients were assessed for eligibility and consequently, 40 patients were analyzed. On admission, both groups had comparable physiological scores, comorbidities, malnutrition risk, anthropometric measurements, metabolic/hematologic biomarkers and concentrations of adipokines and cytokines (p .05). Serum leptin, resistin, and cytokines (IL-6, IL-10, IL-1β and TNF-α) decreased significantly in the entire cohort over ten days following sepsis (p .05). Serum resistin decreased in both olive oil-based and soybean oil-based lipid emulsions groups. Serum adiponectin only decreased in soybean oil-based lipid emulsions group (p .05). There was association between survival and percentage changes in adiponectin, resistin and visfatin concentrations (log rank test: p .05).Adipokine and cytokine responses are affected by medical nutritional therapy in the sepsis process and adipokines may represent functional prognostic biomarkers in critically ill patients with sepsis.

This study was undertaken to elucidate the effect of omega-3 and omega-6 supplementation on the levels of different adipokines and cytokines, as well as the antioxidant system, in relation to male reproductive hormones and testicular functions. Adult male Sprague-Dawley rats were daily gavaged with either physiological saline (control group), sunflower oil (omega 6 group; 1 mL/kg body weight), or fish oil (omega-3 group; 1000 mg/kg body weight) for 12 weeks. The administration of omega-3 or omega-6 resulted in decreased serum concentrations of kisspeptin 1, gonadotropin-releasing hormone, luteinizing hormone, follicle-stimulating hormone, and testosterone. In addition, it downregulated the mRNA expression levels of steroidogenic genes. The intratesticular levels of apelin, adiponectin, and irisin were elevated while chemerin, leptin, resistin, vaspin, and visfatin were declined following the administration of either omega-3 or omega-6. The testicular concentration of interleukin 10 was increased while interleukin 1 beta, interleukin 6, tumor necrosis factor α, and nuclear factor kappa B were decreased after consumption of omega-3 or omega-6. In the testes, the levels of superoxide dismutase, catalase, glutathione peroxidase 1, and the total antioxidant capacity were improved. In conclusion, the administration of omega-3 or omega-6 adversely affects the process of steroidogenesis but improves the antioxidant and anti-inflammatory status of the reproductive system via modulating the levels of testicular adipokines.

Background/aim Adipocytokine, an adipocyte-derived protein, well-known to be involved in the pathogenesis of breast cancer. We aimed to measure the mRNA expression of resistin, TNF-?, interleukin six and eight (IL-6, and IL-8), and estrogen receptor alpha (ER-?) in peripheral blood mononuclear cells (PBMCs) of women with and without breast cancer. Materials and methods Blood samples were obtained from 32 women with breast cancer and 18 women without breast cancer. The PBMCs were isolated from whole blood using density gradient centrifugation. Target genes mRNA expression was measured by reverse-transcription polymerase chain reaction (RT-PCR). Body mass index was calculated, and the clinicopathological characteristics of subjects were also determined by histopathological examination. Results Our results indicated that the mRNA expression of resistin and IL-6 in PBMCs of breast cancer patients was significantly increased (approximately 3.5-fold, and 15-fold respectively) compared to healthy controls. Resistin expression was significantly associated with inflammatory markers including TNF-?, IL-6, IL-8, but not with anthropometric indices. Logistic regression analysis revealed that these adipokines were not associated with breast cancer. Based on the ROC curve analysis the diagnostic performance of IL-6 was significant (0.825, 95% CI: 0.549-0.947), thus, it might be considered as a breast cancer biomarker that reflecting an advanced and inflammatory stage of the disease. Conclusion Breast cancer is associated with increased expression of adipocytokines in PBMCs. Our results suggested that a PBMC-based gene expression test may be developed to detect breast cancer early.

Objective To investigate the longitudinal associations of serum inflammatory markers and adipokines with joint symptoms and structures in participants with knee OA. Methods Two hundred participants (46.5% female, mean age 63.1 years, mean BMI 29.5 kg/m2) from Tasmania, part of the VIDEO (Vitamin D Effect on OA) study, were randomly selected in the current study. Serum levels of 19 biomarkers, scores of WOMAC and MRI-assessed knee structures were evaluated at baseline and month 24. The patterns of biomarkers were derived from principal component analysis and their association with knee symptoms and structures were examined using adjusted generalized estimating equations. Results Five components explained 78% of the total variance. IL-1β, -2, -4, -6, -8, -17 A, -17 F, -21, -22 and -23 loaded the highest on the first component, which was associated with increased bone marrow lesions (BMLs) and WOMAC dysfunction score. IL-10, -12 and GM-CSF loaded on the second component, which was associated with increased cartilage volume, and decreased effusion synovitis and WOMAC scores. Leptin, adipsin and CRP loaded on the third component, which was positively associated with WOMAC scores. Resistin loaded on the fourth component, which was associated with increased BMLs and cartilage defects. Apelin-36 and adiponectin loaded on the fifth component, which was associated with increased BMLs. Conclusion Various inflammatory and metabolic components were associated differently with joint symptoms and structural changes in knee OA, suggesting a complex inflammatory and metabolic interrelationship in the pathogenesis of knee OA.

To determine the role of resistin, IL-1β, IL-6 and ceruloplasmin in the development of NAFLD and cardiovascular complications in patients with type 2 diabetes, 82 patients with type 2 diabetes with NAFLD were examined. All patients were divided into groups depending on the degree of liver damage: group 1 (stage of steatosis) — included 22 patients, group 2 (stage of steatohepatitis, NASH) — 40 patients, group 3 (stage of fibrosis) — 20 patients. The control group included 7 patients with type 2 diabetes without liver damage.Based on the stusy results analysis, it can be stated that adipokin resistin should be considered as one of the factors in the pathogenesis of NAFLD in patients with type 2 diabetes, namely as a marker of inflammatory changes in the liver in this category of patients. Further development of the disease at the stage of fibrosis is characterized by a slight decrease in the serum resistin concentration, which may indicate a decrease in inflammatory processes against the background of the development of fibrotic changes. It is at the stage of fibrosis that resistin is unidirectionally correlated with some lipid fractions, which confirms its role in atherogenesis and in the risk of developing cardiovascular complications of diabetes. With the development of NAFLD in patients with type 2 diabetes, the level of pro-inflammatory interleukins IL-1β and IL-6 increasesalready at the stage of NAS. It reflects inflammatory changes in the liver of these patients. Further insignificant increase in the content of interleukins IL-1β and IL-6 in the serum of patients may indicate the preservation of a high level of inflammation both at the stage of steatohepatitis and in the future, in the formation of fibrosis.We found no significant differences between ceruloplasmin levels in patients with type 2 diabetes with various stages of NAFLD and in the absence of liver damage

This study was designed to investigate the possible protective role of kefir beverage on kidney structure biologically, histochemical and some biochemical parameters such as cholesterol level, MCP-1, and resistin in high-fat diet-fed streptozotocin-diabetic rats. 60 rats were divided into two experiments by six groups: experiment Ⅰ included 3 non-diabetic ones and experiment ⅠⅠ included three STZ- induced diabetes groups. The groups were fed as follows: group 1 received a standard diet and served as control. Group 2 was fed on a standard diet and kefir (0.7 ml/animal/day by gavage). Group 3 received a high-fat diet and kefir (0.7 ml/animal/day by gavage). The diabetic males of groups A, B, and C were fed on the high-fat diet. Group B received besides kefir (0.7 ml/animal/day by gavage), while group C was injected additionally with insulin (0.76 UI/200 mg BW/day). After 5 weeks, animals of all groups were sacrificed. From the cell biological, histochemical, and histopathological conceptions, both kefir and insulin have various effects on cellular activities and different chemical materials contents, such as DNA, RNA, total protein, collagen, polysaccharides, and lipoproteins, in the examined normal and diabetic renal tubule cells of the male rats. Overall, it seems like kefir beverage may, to some extent, completely repair the diabetic pathological side effects such as kidney dysfunction regarding keeping the kidney tissue structurally almost normal with some changes in the histochemical components investigated, also there was an improvement in cholesterol level with a beneficial effect on lowering inflammatory markers. Finally, kefir highly reduces the collagen formation in the renal cells that prevent renal nephron from its function and we propose probably kefir treats kidney failure as a side effect of diabetes, by a mechanism that is opposite to the proposed mechanism, for the formation of this kidney failure induced by diabetes, via us in the present work.

Backgrounds The positive effects of reduction mammoplasty on metabolic profile have been shown in a limited number of studies. This study objective to reveal the effects of reduction mammoplasty on metabolic profile and anthropometric measurements. Subjects and Method The study was prospectively conducted on 42 patients who were operated between April 2019 and March 2020. Fasting plasma glucose, fasting plasma insulin, total cholesterol, triglyceride, high-density lipoprotein and low-density lipoprotein cholesterol, HgA1c, homeostasis model assessment scores, adiponectin, leptin, and resistin levels were evaluated. In addition, age, height, weight, body mass index; breast, chest, waist, hip circumference; waist-hip ratio, and bilateral breast resection tissue weights were recorded. Data and blood samples were collected one hour before the operation, 6 and 12 weeks after the operation. Result The patients' mean age was 43.14±10.24, and their average height was 159.42±4.96 cm. The excised bilateral dermo fatty tissue weight was 1435.85±721.16 g. At the postoperative 40th day a decrease in leptin (p = 0.001), resistin (p =0.008), glucose (p = 0.021) and insulin resistance values (p=0.013) stated. There was an increase in adiponectin (p < 0.001) and HDL (p = 0.013) levels at the postoperative 40th day. In the postoperative third month, these data returned to the previous levels that were measured before operations. However, an increase in hip circumference (p = 0.034) and a decrease in waist-hip ratio (p < 0.001) was detected in third month. Also, there was no difference in body mass index and weight compared to pre-operation. Conclusion After reduction mammoplasty, compensatory fat growth in the hip area, an increase in the hip circumference, and a decrease in the waist-hip ratio were observed in the postoperative third month. Level of Evidence This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266.

Chemerin and resistin are two adipocytokines involved in inflammatory processes that may paly a role in the development of endometriosis. The purpose of the current study was to examine the levels of chemerin and resistin in the follicular fluid (FF) of endometriosis patients and additionally, assess the association of FF chemerin and resistin with the severity of endometriosis and the number of mature oocyte and embryos. A total of 80 reproductive-aged women who underwent intracytoplasmic sperm injection and embryo transfer were evaluated in this study. FF samples were obtained from subjects with (n = 40) and without endometriosis (n = 40). The concentrations of chemerin and resistin were examined using ELISA. The Resistin FF level was significantly (p-value=.03) higher in women with endometriosis than women without endometriosis, while the effect size was medium (d = 0.47). There was no significant difference in Chemerin concentration between the two groups of this study. Results also showed a tendency towards the increase of FF values of resistin and chemerin in endometriosis patients with stage III-IV than stage I-II; however, this difference was not significant. No significant correlations were found between FF levels of resistin and chemerin with the number of mature oocyte and embryos. Thus, elevated FF resistin levels may be associated with endometriosis.IMPACT STATEMENTWhat is already known on this subject? To our knowledge, no studies have investigated chemerin levels in follicular fluid of infertile women with endometriosis undergoing ICSI. Although follicular fluid levels of resistin have been previously studied in endometriosis, it has not been studied yet whether its level is associated with the number of oocyte and embryos.What do the results of this study add? Our results indicate that significantly increased resistin levels in follicular fluid may be associated with the presence of endometriosis.What are the implications of these findings for clinical practice and/or further research? The findings are promising in that significantly increased resistin levels may add to the knowledge of the pathophysiology of endometriosis.

Alzheimer's disease (AD) is the fourth leading cause of death in the United States and the most common cause of adult-onset dementia. Recent results suggest an increased prevalence and severity in African Americans compared to Caucasians. Our understanding of the potential mechanism(s) underlying this ethnicity difference is limited. We previously described ethnicity-related differences in levels of neurodegenerative proteins and cytokines/chemokines in the BA21 region of African Americans and Caucasians with AD. Here, similar multiplex assays were used to examine those endpoints in patient postmortem cerebrospinal fluid (CSF). Additionally, we measured levels of C-peptide, ghrelin, gastric inhibitory polypeptide (GIP), glucagon-like peptide-1 (GLP-1), glucagon, insulin, leptin, PAI-1, resistin, and visfatin using a human diabetes 10-plex assay. The cytokine and chemokine assays revealed that levels of 26 chemokines or cytokines differed significantly with ethnicity, and three of those were significantly associated with gender. The neurodegenerative disease panel indicated that levels of soluble RAGE were significantly elevated in African Americans compared to Caucasians. All measures in the diabetes disease panel assay were significantly elevated in African Americans: ghrelin, GIP, GLP-1, glucagon, insulin, and visfatin. Through peripheral sample analysis, these results provide further evidence that ethnicity is critically involved in the manifestation of AD.

Background. There is evidence of the participation of adipose tissue hormones leptin, adiponectin and resistin in the formation of metabolic disorders in the retina, retinal neovascularization, and diabetic microangiopathy. The development of methods for the mathematical evaluation of the prognosis of diabetic retinopathy (DR) formation with the participation of adipokines is a relevant problem in modern diabetology. Aim. Elaboration of a mathematical model for assessing the prognostic significance of serum leptin, adiponectin and resistin to study the likelihood of deve­loping and progressing DR in patients with type 2 diabetes mellitus (DM). Materials and methods. An open observational single-center one-stage selective study was conducted among patients with type 2 DM and DR. The blood serum concentration of leptin, adiponectin and resistin, HbA1с, lipid metabolism findings were determined, the results of an instrumental examination of the fundus were analyzed. The diagnostic predictive value of serum leptin, adiponectin and resistin was assessed using discriminant analysis. Statistical analyses were conducted using Statistica 9.0 (StatSoft, Tulsa, OK, USA) software. The differences were considered statistically signifi­cant at p < 0.05. A model with linear combinations of the serum leptin, adiponectin and resistin, triglyceride (TG), HbA1с, type of antihyperglycemic therapy (oral anti-hyperglycemic medication or insulin therapy) were developed, and, subsequently, formulas for classification-relevant discriminant functions were derived. Results. Fifty-nine patients (107 eyes) with type 2 DM and DR (men and women; mean age, 58.20 ± 0.18 years; mean diabetes duration, 9.19 ± 0.46 years; mean HbA1с 9.10 ± 0.17 %) were assigned to the basic group and underwent the study. They were divided into three DR groups based on the stage of DR. When performing the ran­king of patients for discriminant analysis, the stage 2 DR group was aggregated with the stage 3 DR group for convenience to form the stage 2 + 3 DR group based on the pathognomonic sign (portents of proliferation or actual proliferation). Anti-diabetic therapy (ADT) included metformin, either alone (type 1 ADT) or in combination with oral anti-hyperglycemic medication (metformin + OAHGM, type 2 ADT) or insulin therapy (metformin + IT, type 3 ADT). Inclusion criteria were informed consent, age above 18 years, pre­sence of T2DM and DR. Exclusion criteria were endocrine or body system disorders leading to obesity (Cushing’s syndrome, hypothyroidism, hypogonadism, polycystic ovarian syndrome, or other endocrine disorders, including hereditary disorders, and hypothalamic obesity), type 1 DM, acute infectious disorders, history of or current cancer, decompensation of comorbidities, mental disorders, treatment with neuroleptics or antidepressants, proteinuria, clinically significant maculopathy, glaucoma or cataract. The study followed the ethical standards stated in the Declaration of Helsinki and was approved by the Local Ethics Committee. The formulas for classification-relevant discriminant functions were derived based on the results of physical examination, imaging and laboratory tests, and subsequent assessment of clinical signs of DM (HbA1с), DR stage and serum leptin, adiponectin, resistin, TG concentrations and taking into account the type of antihyperglycemic therapy. The classification functions (CF) computed based on the variables found from the above developed models provided the basis for predicting the development of DR. The formulas for CF from model are as follows: CF1 = 0.29 • TG + 1.55 • HbA1С + 1.81 • ADT_Type + 0.04 • Leptin + 0,34 • Adiponectin + 0,91 • Resistin – 13,82. CF2= 0.05 • TG + 1.36 • HbA1С + 3.01 • ADT_Type + 0.08 • Leptin + 0,35 • Adiponectin + 1,01 • Resistin – 15.95. A step-by-step approach to a diagnostic decision should be used. First, blood samples are tested for serum leptin, adiponectin and resistin, TG, blood HbA1c, and the patient is assigned a code for ADT Type (metformin only, 1; metformin + OAHGM, 2; or metformin + IT, 3). Second, CF1 and CF2 values are calculated based on clinical and laboratory data. Finally, the two values are compared to determine which is greater. The predictive decision is made by selecting the classification function with the greater value. Thus, if CF1 > CF2, the process can be stabilized at this stage given adequate glycemic control (through compensation of carbohydrate metabolism) and body mass control as well as patient compliance. If CF1 < CF2, the pathological process may progress to the next stage or even within stage 3, and there is an urgent need to reduce BMI, and to correct the ADT and the blood lipid profile. Conclusions. The informative value and statistical significance of the model were 71.4 % and p = 0.040, respectively. Using the formulas, one can determine the probability of progression of DR., Актуальність. Встановлені докази участі гормонів жирової тканини лептину, адипонектину і резистину в розвитку метаболічних порушень у сітківці ока, ретинальної неоваскуляризації, діабетичної мікроангіопатії. Розробка методів математичної оцінки прогнозу розвитку діабетичної ретинопатії (ДР) за участю адипокінів залишається актуальною проблемою сучасної діабетології. Мета: розробка математичної моделі оцінки прогностичної значущості лептину, адипонектину і резистину сироватки крові для вивчення ймовірності розвитку і прогресування діабетичної ретинопатії у хворих на цукровий діабет (ЦД) 2-го типу. Матеріали та методи. Проведено відкрите спостережне одноцентрове одномоментне вибіркове дослідження у хворих на ЦД 2-го типу з ДР. У сироватці крові пацієнтів визначали концентрацію лептину, адипонектину і резистину, глікованого гемоглобіну (HbA1с), показники ліпідного обміну, аналізували результати інструментального обстеження очного дна. Використовували дискримінантний аналіз. Статистично значущими вважали відмінності при p < 0,05. Була розроблена модель з лінійними комбінаціями досліджуваних показників, і згодом були отримані відповідні формули функцій класифікацій (ФК). Результати. Дослідження проведено у 59 пацієнтів (107 очей) (чоловіки і жінки) з ЦД 2-го типу та ДР: 27 чоловіків (45,76 %) і 32 жінки (54,24 %), середній вік — 58,20 ± 0,18 року, середня тривалість ЦД — 9,19 ± 0,46 року, середній рівень HbA1с — 9,10 ± 0,17 %. У хворих за даними об’єктивного, інструментального та лабораторного обстеження і подальшої оцінки клінічних ознак ЦД 2-го типу (HbA1с), ДР (стадія), даних ліпідограми (тригліцериди), концентрації лептину, адипонектину і резистину сироватки крові і з урахуванням особливостей цукрознижувальної терапії методом дискримінантного аналізу були розраховані формули ФК, на основі яких визначають можливість прогресування або стабілізації ДР. Висновки. Інформативність створеної математичної моделі оцінки прогностичної значущості гормонів жирової тканини в розвитку ДР у хворих на ЦД 2-го типу становить 71,4 %.

Type 2 diabetes mellitus (T2DM) results in compromised bone microstructure and quality, and subsequently increased risks of fractures. However, it still lacks safe and effective approaches resisting T2DM bone fragility. Pulsed electromagnetic fields (PEMFs) exposure has proven to be effective in accelerating fracture healing and attenuating osteopenia/osteoporosis induced by estrogen deficiency. Nevertheless, whether and how PEMFs resist T2DM-associated bone deterioration remain not fully identified. The KK-Ay mouse was used as the T2DM model. We found that PEMF stimulation with 2 h/day for 8 wk remarkably improved trabecular bone microarchitecture, decreased cortical bone porosity, and promoted trabecular and cortical bone material properties in KK-Ay mice. PEMF stimulated bone formation in KK-Ay mice, as evidenced by increased serum levels of bone formation (osteocalcin and P1NP), enhanced bone formation rate, and increased osteoblast number. PEMF significantly suppressed osteocytic apoptosis and sclerostin expression in KK-Ay mice. PEMF exerted beneficial effects on osteoblast- and osteocyte-related gene expression in the skeleton of KK-Ay mice. Nevertheless, PEMF exerted no effect on serum biomarkers of bone resorption (TRAcP5b and CTX-1), osteoclast number, or osteoclast-specific gene expression ( TRAP and cathepsin K). PEMF upregulated gene expression of canonical Wnt ligands (including Wnt1, Wnt3a, and Wnt10b), but not noncanonical Wnt5a. PEMF also upregulated skeletal protein expression of downstream p-GSK-3β and β-catenin in KK-Ay mice. Moreover, PEMF-induced improvement in bone microstructure, mechanical strength, and bone formation in KK-Ay mice was abolished after intragastric administration with the Wnt antagonist ETC-159. Together, our results suggest that PEMF can improve bone microarchitecture and quality by enhancing the biological activities of osteoblasts and osteocytes, which are associated with the activation of the Wnt/β-catenin signaling pathway. PEMF might become an effective countermeasure against T2DM-induced bone deterioration. NEW & NOTEWORTHY PEMF improved trabecular bone microarchitecture and suppressed cortical bone porosity in T2DM KK-Ay mice. It attenuated T2DM-induced detrimental consequence on trabecular and cortical bone material properties. PEMF resisted bone deterioration in KK-Ay mice by enhancing osteoblast-mediated bone formation. PEMF also significantly suppressed osteocytic apoptosis and sclerostin expression in KK-Ay mice. The therapeutic potential of PEMF on T2DM-induced bone deterioration was associated with the activation of Wnt/ß-catenin signaling.

The coronavirus disease 2019 (COVID-19) pandemic has put into evidence another pandemic – obesity. Currently, several studies have documented the association between obesity and COVID-19 severity. The mechanisms underlying the increased risk of complications and mortality in obese patients with COVID-19 are of diverse nature. Inflammation plays a central role in obesity. Metabolic alterations seen in obese patients are related to an inflammatory response, and several studies report elevated levels of circulating inflammatory cytokines in obese patients. Also, deregulated expression of adipokines, such as leptin and resistin, increase the expression of vascular adhesion molecule 1 and intercellular adhesion molecule 1 that contribute to increased vascular leukocyte adhesiveness and additional oxidative stress. Additionally, it is now recognized that the chronic impairment of systemic vascular endothelial function in patients with cardiovascular and metabolic disorders, including obesity, when intensified by the detrimental effects of SARS-CoV-2 over the endothelium, may explain their worse outcomes in COVID-19. In fact, vascular endothelial dysfunction may contribute to a unfavorable response of the endothelium to the infection by SARS-CoV-2, whereas alterations in cardiac structure and function and the prothrombotic environment in obesity may also provide a link to the increased cardiovascular events in these patients.