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

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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]

Irisin is a myokine with a potential role in cardiometabolic diseases, but previous studies have described inconsistencies between serum irisin and physical activity (PA). Our aim was to analyze the relationship between serum irisin and leisure-time PA (LTPA) in a large sample of the general adult population, and secondarily, to evaluate its relationship with two PA-related biomarkers (HDL cholesterol and resistin). A cross-sectional study was nested in the "CDC of the Canary Islands" cohort participants (n = 3827, 18–75 years, 60% women). PA was collected by administering the Minnesota leisure-time physical activity questionnaire, and physical examination and blood tests (irisin, resistin, HDL-cholesterol) were performed. Irisin inversely correlated with BMI (p < 0.001 in women) and resistin (p = 0.038 in women, p = 0.004 in men), and directly with HDL cholesterol (p < 0.001in women). There was a direct association of irisin with leisure-time and energy expenditure in light, moderate and vigorous LTPA, which was stronger in women than men. The distribution of leisure-time and PA variables across irisin quintiles showed a significant trend, except for light LPTA in men. Adjusting for age, sex and BMI, the association of irisin with leisure-time and LTPA variables was stronger than the association of these variables with resistin and HDL cholesterol, reaching the strongest association for irisin with the 80th percentile of time of LTPA (OR = 2.57; 95% CI = 2.00–3.31). There is a direct and independent association between serum irisin levels and LTPA in the general adult population, which is stronger than other biomarkers of PA. Findings on exercise-related irisin support the possibility of irisin health benefits. [ABSTRACT FROM AUTHOR]

To investigate the blood levels of adipokines in obese patients with endometrial cancer who have and have not undergone omentectomy. Between September 2017 and September 2019, the study recruited 54 patients with endometrial cancer. Measurements were taken of blood levels of human leptin, perilipin-1, adiponectin, adipolin, resistin, visfatin, and estrone preoperatively and postoperatively before adjuvant therapy or at the end of one month. The serum samples were separated by centrifugation for 10 mins at 3,000 revolutions/min, then stored at −80 °C until assay. In this prospective study, a total of 54 endometrial cancer patients were analyzed in two separate groups according to the omentectomy status. Comprehensive staging surgery with omentectomy and without omentectomy was performed in 26 patients and 28 patients, respectively. The age, body mass index, body fat index, waist circumference, and skin thickness values of the patients with and without omentectomy were found to be similar. No statistically significant difference was determined between the patients with and without omentectomy in respect of the blood level of the adipokines measured preoperatively. A strong statistically significant correlation was determined between the pre and postoperative levels of Human Leptin (p = 0.002), perilipin-1(p = 0.001), adipolin (p < 0.001), adiponectin (p < 0.001), resistin (p = 0.001), visfatin (p < 0.001), and estrone (p = 0.004) (r = −0.43, −0.47, 0.75, 0.84, −0.47, - 0.58, −0.41, respectively) Omentectomy affected the postoperative blood levels of adipokines in obese patients with endometrial cancer. As omentectomy may have some positive effects on metabolism in these patients, it may be considered during endometrial cancer surgery due to the possible positive metabolic effects. • The coexistence of endometrial cancer with obesity is common. • Omentectomy changed blood levels of adipokines. • Adipokines have a critical role on the metabolism of glucose or lipid [ABSTRACT FROM AUTHOR]

Aims: Although overweight and obesity are associated with increased risk of atrial fibrillation (AF), the underlying mechanisms are not well characterised. Recent data suggest that this link may be partly due to abnormal adipose tissue-derived cytokines or adipokines. However, this relationship is not well clarified. To evaluate the association between adipokines and AF in a systematic review and meta-analysis.Data Synthesis: PubMed, Embase, and Web of Science Core Collection were searched from inception through 1st March 2021. Studies were included if they reported any adipokine and AF, with their quality assessed using the Newcastle-Ottawa scale. Data were independently abstracted, with unadjusted and multivariable adjusted estimates pooled in a random-effects meta-analysis. Data are presented for overall prevalent or incident AF and AF subtypes (paroxysmal, persistent, or non-paroxysmal AF). A total of 34 studies, with 31,479 patients, were included. The following adipokines were significantly associated with AF in the pooled univariate data - apelin (risk ratio for prevalent AF: 0.05 [0.00-0.50], p = 0.01; recurrent AF: 0.21 [0.11-0.42], p < 0.01) and resistin (incident AF: 2.05 [1.02-4.1], p = 0.04; prevalent AF: 2.62 [1.78-3.85], p < 0.01). Pooled analysis of multivariable adjusted effect size estimates showed adiponectin as the sole independent predictor of AF incidence (1.14 [1.02-1.27], p = 0.02). Moreover, adiponectin was associated with non-paroxysmal AF (persistent AF: 1.45 [1.08-1.94, p = 0.01; non-paroxysmal versus paroxysmal AF: 3.14 [1.87-5.27, p < 0.01).Conclusions: Adipokines, principally adiponectin, apelin, and resistin, are associated with the risk of atrial fibrillation. However, the association is not seen after multivariate adjustment, likely reflecting the lack of statistical power. Future research should investigate these relationships in larger prospective cohorts and how they can refine AF monitoring strategies.Prospero Id: CRD42020208879. [ABSTRACT FROM AUTHOR]

Wnt1 inducible protein-1 signaling pathway (WISP-1) is a relatively new adipokine involved in many cellular processes, including epithelial mucosa healing. The aim of the study was to compare circulating levels of WISP-1 and other selected adipokines [adiponectin, resistin and retinol-binding protein 4 (RBP-4)] in children with inflammatory bowel disease (IBD) with healthy controls and to investigate possible differences between Crohn's disease patients. (CD) or ulcerative colitis (UC). The study was performed as a case-control study. In addition to adipokines, anthropometric, lipid parameters, markers of inflammation or disease activity were evaluated in all participants. Compared to healthy controls (n=20), significantly lower levels of adiponectin and higher levels of resistin and WISP-1 were found in patients with IBD (n=58). Elevation of WISP-1 was detected only in the CD group (n=31). There were no differences in RBP-4 levels between the groups. Adiponectin, WISP-1 and RBP-4 were independently associated with body mass index only, resistin levels were associated with C-reactive protein levels and leukocyte counts. Adverse adipokines production reflects presence of dysfunctional fat tissue in IBD patients. Higher levels of WISP-1 in CD compared to patients with UC may indicate a specific role for mesenteric adipose tissue in WISP-1 production. [ABSTRACT FROM AUTHOR]

Autoimmune thyroiditis (AIT) and type 2 diabetes mellitus (DM2) are the most common endocrinological diseases worldwide. Relation between these diseases explains several hypotheses. One of them is influence of some adipocytokines. This study evaluated association between three adipocytokines (adiponectin, resistin and visfatin) and thyroid and glycid status in patients with DM2 and AIT compared to the control group (CG). The group consisted of four subgroups: patients with DM2 without thyreopathies, patients with AIT on substitution therapy without diabetes and prediabetes, patients with DM2 and AIT on substitution therapy and healthy subjects as the CG. We investigated parameters of thyroid and glucose metabolism and serum levels of three adipocytokines. The mean level of resistin in the group of patients with diabetes and thyroiditis was significantly higher than in patients with thyroiditis without diabetes and than in the CG. We found a weak negative correlation between visfatin and fasting glucose levels in patients with thyroiditis without diabetes. We detected a weak negative correlation between resistin and glycated hemoglobin and a weak negative correlation between visfatin and thyroid gland volume in patients with diabetes without thyroiditis. In the CG we determined a weak positive correlation between visfatin and free thyroxin. Our results are consistent with several studies, which confirmed association between AIT and adipocytokines. [ABSTRACT FROM AUTHOR]

Kaempferol (KPF) is a dietary polyphenol reported to have various beneficial effects on human health. However, its molecular mechanisms in regulating lipid and glucose metabolism are not fully understood. This study examined the effects of KPF on obesity, dyslipidemia, and diabetes in Tsumura, Suzuki, Obese Diabetes mice. The 6-week administration of KPF decreased fat weight, serum total cholesterol, and low-density lipoproteins (LDLs); increased high-density lipoproteins (HDLs); and improved glucose tolerance. Additionally, KPF increased LDL receptor (LDLR) and apolipoprotein A1 (ApoA1) gene expression and decreased serum resistin levels. These findings suggest that the decrease in LDL and the increase in HDL caused by KPF may be due to increases in hepatic LDLR and ApoA1 expression, respectively. Furthermore, it is possible that the improvement in glucose tolerance by KPF may occur via resistin reduction. These mechanisms may be parts of complex mechanism by which KPF improves metabolic syndrome. [ABSTRACT FROM AUTHOR]

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. 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. 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 < 0.001) and the high-density lipoprotein (HDL) decreased (p < 0.001). The mean CIMT was significantly increased in cases (0.62 ± 0.16 mm) compared to control (0.51 ± 0.11 mm)(p = 0.006). Serum resistin significantly correlated with hs-CRP, HDL and anti-nuclear antibody (p = 0.027, p < 0.001,p = 0.013 respectively). There was no significant correlation between resistin and markers of insulin resistance, SLEDAI-2 k and CIMT. Resistin expression in the serum of patients with SLE was not significantly higher than controls. Although resistin was correlated with two cardiovascular risk factors (HDL-C, hs-CRP), it did not correlate significantly with insulin resistance, disease activity, damage index and CIMT in SLE patients. [ABSTRACT FROM AUTHOR]

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 <0.001). Patients who died had a higher SYNTAX score, higher EuroSCORE II, and lower resistin levels in PVAT than survivors (p <0.001, p=0.004, and p=0.041, respectively). A stepwise regression analysis revealed that survival was related to resistin concentrations above the median value (hazard ratio [HR], 4.67, 95 % CI, 1.02-21.4, p=0.048) and EuroSCORE II (used as continuous variable, HR, 1.55, 95 % CI, 1.16-2.07, p=0.003). The mid-term mortality in patients with advanced CAD is associated with low resistin concentrations in PVAT surrounding the LMCA. [ABSTRACT FROM AUTHOR]

Metabolic syndrome is a clustering of metabolic disorder with unclear molecular mechanism. Increasing studies have found that the pathogenesis and progression of metabolic syndrome are closely related to inflammation. Here, we report celastrol, a traditional Chinese medicine, can improve high fat diet-induced metabolic syndrome through suppressing resistin-induced inflammation. Mechanistically, celastrol binds to adenylyl cyclase associated protein 1 (CAP1) and inhibits the interaction between CAP1 and resistin, which restrains the cyclic adenylate monophosphate (cAMP)–protein kinase A (PKA)–nuclear factor kappa-B (NF- κ B) signaling pathway and ameliorates high fat diet-induced murine metabolic syndrome. Knockdown of CAP1 in macrophages abrogated the resistin-mediated inflammatory activity. In contrast, overexpression of CAP1 in macrophages aggravated inflammation. Taken together, our study identifies celastrol, which directly targets CAP1 in macrophages, might be a promising drug candidate for the treatment of inflammatory metabolic diseases, such as metabolic syndrome. In obesity, adipose tissue generates resistin, which binds to CAP1 on macrophages and activates the cAMP–PKA–NF- κ B signaling pathway and promotes proinflammatory cytokines expression. These factors further aggravate inflammation, insulin resistance, and hepatic steatosis. Celastrol ameliorates metabolic syndrome via binding to CAP1 and inhibiting its interaction with resistin. [Display omitted] [ABSTRACT FROM AUTHOR]

To explore the effect of diabetic status on the proinflammatory chemokine profile and levels of advanced glycation end products (AGEs) in gingival crevicular fluid (GCF) derived from patients with type 2 diabetes mellitus (T2DM) undergoing fixed orthodontic treatment. Two groups, nondiabetic and T2DM, were included. Their demographics, biochemical parameters including hemoglobin A1c, fasting blood glucose, body mass index, and oral hygiene status were recorded. GCF sampling was performed after 2 months of placement of stainless steel archwires and chemokines (primary outcome) were quantified using Human Magnetic Luminex multiplex assay. Secondary outcomes were assessment of clinical periodontal status, unstimulated whole saliva flow rate, and GCF flow rate. Twenty participants each in the nondiabetic (mean age: 26.4 years) and T2DM (mean age: 27.2 years) groups gave consent to participate. Biochemical analysis showed significantly increased values for hemoglobin A1c (P <.001), fasting blood glucose (P <.0001), body mass index(P =.047), and unstimulated whole saliva flow rate (P =.041) for the T2DM group. Bleeding on probing was significantly higher in participants with T2DM than nondiabetic participants (P =.039). Resistin (P =.034) and AGEs (P =.017) showed significantly higher values in participants with T2DM than nondiabetic participants. Pearson correlation analysis indicated a significant positive correlation between resistin (r = 0.1372; P =.022) and AGEs (r = 0.0194; P =.0186) against bleeding on probing in participants with T2DM. The biochemical profile of GCF samples from participants with T2DM after alignment demonstrated higher levels of resistin and AGEs. The data suggest the presence of a proinflammatory response in patients with T2DM undergoing fixed orthodontic treatment. [ABSTRACT FROM AUTHOR]

Background and Aims: Pediatric obesity associates with both low-grade inflammation and cardiometabolic risk on the population level. Yet on an individual patient level, overweight/obesity does not always equal increased cardiometabolic risk. In this study, we examine whether low-grade inflammation associates with cardiometabolic risk in Danish children, independent of degree of adiposity. We further assess the value of integrating multiple inflammation markers to identify children with very-high cardiometabolic risk profiles.Method and Results: We studied 2192 children and adolescents aged 6-18 years from an obesity clinic cohort and a population-based cohort, in a cross-sectional study design. Anthropometry, blood pressure, pubertal stage and body composition by dual-energy X-ray absorptiometry were assessed, and biomarkers including fasting serum high sensitivity C-reactive protein (hsCRP), white blood cells (WBC), resistin, lipid profile and glucose metabolism were measured. Adjusted correlation analysis and odds ratios were calculated. We found that, independent of degree of adiposity, having high-normal inflammation marker concentrations associated with increased cardiometabolic risk: for girls, hsCRP >0.57-9.98 mg/L (mid/upper tertile) associated with ~2-fold higher odds of dyslipidemia and hepatic steatosis (vs. lower tertile). For both sexes, WBC >7.0-12.4 109/L (upper tertile) associated with 2.5-fold higher odds of insulin resistance. Lastly, children with multiple inflammation markers in the high-normal range exhibited the most severe cardiometabolic risk profile.Conclusion: Low-grade inflammation associates with cardiometabolic risk in children independent of degree of adiposity. The associations vary with sex and inflammation marker measured. Finally, integrating multiple low-grade inflammation markers identifies a very-high-risk subgroup of children with overweight/obesity and may have clinical value. [ABSTRACT FROM AUTHOR]

The aim was to investigate: changes of inflammatory, stress and cardiac response in patients undergoing open heart surgeries up to five days after the procedure; the association between inflammatory, stress and cardiac response and whether changes in a certain marker can predict short-term patient outcome. Ninety patients were divided into three groups, 30 participants each (on-pump, off-pump revascularization and valve replacement group). The following markers were measured: complete blood count, CRP, IL-6, IL-10, leptin, resistin, monocyte chemoattractant protein-1 (MCP-1), cortisol, CK and hsTnT in 5 points. Resistin increased in all three groups. Lower IL-10 levels were found after the surgery and higher levels of leptin and MCP- 1 in the off-pump than in the on-pump group. Off-pump group had higher values of IL-6, IL-10, leptin, resistin and MCP-1 and lower levels of CK and hsTnT 24 after surgery than the on-pump group. We found significant correlation between MCP-1 and resistin. The difference between resistin at time points 2 and 3 significantly predicted transfusion needs; while the difference between CRP and resistin before and at the end of the surgery together with the difference between leukocytes at the end and 24 hours after the surgery predicted the use of inotropic agents/vasopressors. Cardiac surgeries cause an increase of inflammatory, stress and cardiac markers. Only resistin correlated with MCP-1 which confirms the link between resistin secreted form infiltrated macrophages and enhanced release of MCP-1. [ABSTRACT FROM AUTHOR]

Regular physical activity (PA) has been associated with decreased risk of many chronic diseases and increased longevity among older adults. In addition, ageing has been associated with higher levels of different inflammatory biomarkers while the association between inflammatory biomarkers and PA has remained controversial. The aim of the current investigation was to examine the association between blood biomarkers and objectively assessed PA among a sample of healthy older women with different levels of PA engagement. A total of 81 healthy women were recruited. Study participants were allocated to three groups according to accelerometer-obtained PA data. Body composition was assessed with dual-energy X-ray absorptiometry. Fasting blood samples were collected for the measurement of resistin, leptin, tumour necrosis factor alpha (TNFα) and C-reactive protein (CRP) concentrations. There were no significant differences between groups for resistin, leptin, TNFα and for CRP concentrations; however, higher moderate-to-vigorous physical activity (MVPA) groups tended to have lower level of blood biomarker concentrations. There was a significant negative relationship between resistin and steps per day. Inverse association between leptin and MVPA was significant after controlling for age. In multivariate stepwise linear regression analysis, steps per day were the strongest independent predictor for resistin, whereas for leptin, TNFα and CRP the strongest independent predictor was whole body fat mass. In conclusion, this study demonstrated negative association between resistin concentration and steps per day. Sedentary time and light PA had no relationship with resistin, leptin, TNFα or CRP concentrations. [ABSTRACT FROM AUTHOR]

We monitored changes in serum leptin, adiponectin, and resistin concentrations in obese cats during weight loss. Six naturally developed obese cats were fed low-fat, high-fiber dry food during a 9-week experimental period. Serum leptin, adiponectin, and resistin concentrations were measured at week 0, 4, 8, and 9. Body weight became significantly lower week 4 onward than that at week 0 (P<0.05 or 0.01). At week 9, serum leptin concentrations were significantly lower than those at week 0 (P<0.05). Contrarily, serum adiponectin and resistin concentrations did not significantly differ within the 9 weeks. While serum leptin levels were strongly positively correlated with body weight (r=0.923, P<0.001), serum adiponectin levels were moderately negatively correlated with it (r=−0.529, P<0.01), with serum resistin having a no correlation with body weight. Serum leptin levels might be more closely related with pathogenesis of adiposity than serum adiponectin or resistin in cats. [ABSTRACT FROM AUTHOR]

As the inflammatory regulators, Resistin-like molecule β (RELMβ) and Resistin might be potential biomarkers of necrotizing enterocolitis (NEC), while thrombocytopenia is often related to the severity of NEC, clinical observation suggests that thrombocytopenia might be an early biomarker of NEC. The aim of this study was to evaluate whether RELMβ, Resistin and thrombocytopenia could be biomarkers for early diagnosis of NEC in preterm infants. From January 2016 to March 2018, twenty-nine NEC preterm infants who were diagnosed with NEC (Bell's stage ≥Ⅱ) by two independent neonatologists and twenty-nine non NEC preterm infants at neonatal intensive care unit in our hospital were enrolled in this case-control study. Preterm infants with a history of serious infections (sepsis, pneumonia), asphyxia, and congenital malformations were excluded from the study. The plasma RELMβ and Resistin were evaluated by enzyme linked immunosorbent assay (ELISA) and serum platelet levels were measured directly by ordinary light microscope at the diagnosis of NEC (Bell's stage ≥Ⅱ). Plasma RELMβ levels in NEC group were significantly higher than control group (P < 0.05). The optimal cut-off value of RELMβ determined by receiver operating characteristic curve (ROC) was 378.3 ng/L. The overall estimates for sensitivity and specificity of high RELMβ concentrations in the detection of neonatal NEC were 71.4% and 91.7%, respectively. No significant difference was found in plasma Resistin levels between two groups (P > 0.05). If platelet level was less than 157 × 109/L, the sensitivity and specificity were 69.34% and 82.87%, respectively. Interestingly, the combination of RELMβ and thrombocytopenia increased sensitivity and specificity to 82.89% and 93.21%, respectively. The combination of RELMβ and thrombocytopenia was a reliable biomarker for the early diagnosis of NEC in this study with 82.89% sensitivity and 93.21% specificity, respectively. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases (CVDs) are major causes of morbidity and mortality in systemic lupus erythematosus (SLE) patients. Resistin is an inflammatory adipocytokine associated with insulin resistance and an increased risk of CVD. To study the possible role of resistin (RETN) +299A>G and +62G˃A gene polymorphisms in the development of CVDs among Egyptian SLE patients and their impact on cardio metabolic risk and disease activity. +299A>G and +62G˃A genes polymorphisms were assessed in 140 patients and 100 controls by polymerase chain reaction (PCR). The carotid intima-media thickness (CIMT) was measured. SLE disease activity index (SLEDAI) was assessed. Serum resistin, homeostasis model assessments (HOMA-IR and HOMA-β), fibrinogen and homocysteine were measured. The mean age of patients was 31.1 ± 7.6 years and disease duration 5.4 ± 2.5 years. Serum resistin was significantly increased in patients (4.9 ± 0.2 ng/ml) compared to control (3.02 ± 0.9 ng/ml) (p < 0.001). Serum resistin significantly correlated with uric acid (p < 0.001), homocysteine (p < 0.001), fibrinogen (<0.001) and SLEDAI (p < 0.001). AA genotypes and A allele +299G>A were significantly higher in patients than control (37.9% vs 10% and 63.6% vs 33.5%; p < 0.001). Serum resistin, CIMT, uric acid, fibrinogen and homocysteine was significantly higher in +299G>A GA and AA patients compared to GG (p < 0.001) and HOMA-β decreased (p < 0.001). HOMA-β, fibrinogen and uric acid were independently correlated with resistin (p < 0.001). Resistin +299G/A gene polymorphisms especially the AA genotype and A allele may play an important role in pathogenesis and activity of SLE as well as susceptibility to develop CVD in Egyptian population. [ABSTRACT FROM AUTHOR]

Metabolic syndrome (MetS) is characterized as a cluster of metabolic disorder including increased blood pressure, elevated blood glucose level, high cholesterol level and visceral fat obesity. Polypeptide hormones such as adiponectin and resistin play a significant role in glucose and lipids metabolism, liver and pancreas function. This study aimed to investigate the relationship between serum adiponectin and resistin with MetS criteria among Temiar subtribe in Kuala Betis. This cross sectional study involved 123 subjects from Temiar subtribe in Kuala Betis, Gua Musang, Kelantan. MetS criteria were measured according to standard protocol by modified National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guideline. Anthropometric and biochemical measurements were performed including serum adiponectin and resistin for every study subjects. Serum adiponectin was significantly lower in MetS subjects (7.98 ± 5.65 ng/ml) but serum resistin was found to be significantly higher in MetS subjects (11.22 ± 6.34 ng/ml) compared to non-MetS subjects with p < 0.001 and p = 0.002 respectively. Serum adiponectin was negatively correlated with most of the cardio-metabolic risk factors; BMI, waist circumference, systolic and diastolic blood pressure, fasting blood glucose, triglyceride and total cholesterol. Serum resistin was found to be positively correlated with BMI, waist circumference, fasting blood glucose and total cholesterol. The difference in serum adiponectin and resistin level among MetS individuals indicated the potential of serum adiponectin and resistin to be used as a biomarker for the diagnosis of MetS among Temiar subtribe. [ABSTRACT FROM AUTHOR]

• Phytochemical characterization of ethanolic extract of the leaves from Mangifera indica. • Analyzes with extract of M. indica and its isolated majority compound (mangiferin). • Cytotoxic and anti-inflammatory evaluation of M. indica and mangiferin in vitro. • Post and co-treatment in vivo evaluated with M. indica and mangiferin. • Activity differences between extracts of M. indica and mangiferin. This study aimed phytochemical characterization (UPLC-DAD-MS/MS) of ethanolic extract of the leaves from Mangifera indica (EMI) and Mangiferin (MAN), analysis of the cytotoxic (MTT) and anti-inflammatory potential (expression of TNF-α) of EMI and MAN in vitro. In addition, was evaluate the effect on the mRNA expression of genes (CB1, PPARγ, adiponectin, resistin and leptin) associated with adipogenesis in adipose tissue of rats fed a cafeteria diet. Thus, wistar rats were treated by gavage with EMI and MAN for several days (according to the post and co-treatments). The adipose tissue was weighed and checked the expression of different markers by RT-PCR. The presence of MAN as major compound in EMI was verified. Both EMI and MAN were not cytotoxic, with lower EMI expression of TNF-α. Furthermore, EMI and MAN had proadipogenic action on post-treatment, while in the co-treatment, EMI attenuated the effect of adipogenesis and MAN increased the adipogenic process. [ABSTRACT FROM AUTHOR]

Background: We sought to clarify the role of testosterone substitution in terms of insulin resistance and metabolic profile dysregulation in hypogonadism. Methods: Twenty-nine male Wistar rats aged 11–12 weeks were divided in three groups: control (C, n = 10), sham operation; orchiectomy (ORX, n = 9); and orchiectomy + testosterone substitution (ORX+T, n = 10). Blood samples were obtained at day 1 (operation), after 10 days (intramuscular T injection 100 μg/100 g b.w.), 25 days (second T injection) and 40 days (sacrifice). Results: Hormonal replacement significantly attenuated the negative effect of orchiectomy on insulin resistance as indicated by the successive changes in both insulin levels (1.44 ± 2.94 vs. 4.10 ± 2.47 vs. 1.78 ± 0.68 ng/mL, for D1, D10 and D40, respectively; p = 0.028 and p = 0.022, respectively) and HOMA-IR index (1.36 ± 2.75 vs. 3.68 ± 1.87 vs. 1.74 ± 0.69 ng/mL, for D1, D10 and D40, respectively; p = 0.024 and p = 0.026, respectively) in the ORX+T group. Irisin levels peaked at the 10th postoperative day and were decreased at the end of the experiment (0.27 ± 0.11 vs. 0.85 ± 0.54 vs. 0.02 ± 0.07 ng/mL for D1, D10 and D40, respectively; p = 0.028 in both cases), whereas resistin levels did not differ. Experimental hypogonadism results in an unfavorable lipid profile and insulin resistance, which is not observed when the ORX animals are substituted for T. [ABSTRACT FROM AUTHOR]

Type-II Endometrial Cancer (EMC) is one of the most common types of gynaecological cancer affecting more than 2.7 million people worldwide. Clinical evidence shows that adipokines levels are abnormally altered in Type-II EMC and reported to be one of the major responsible factor for uncontrolled proliferation and metastasis in Type-II EMC. Reversing the altered adipokine levels, therefore, help to control Type-II EMC proliferation and metastasis. In the present hypothesis we focus on the possible role of Thiazolidinediones in favourably altering the adipokine levels to benefit in the management of Type-II EMC. [ABSTRACT FROM AUTHOR]

Abstract Continuously rising trends in obesity-related malignancies render this disease spectrum a public health priority. Worldwide, the burden of cancer attributable to obesity, expressed as population attributable fraction, is 11.9% in men and 13.1% in women. There is convincing evidence that excess body weight is associated with an increased risk for cancer of at least 13 anatomic sites, including endometrial, esophageal, renal and pancreatic adenocarcinomas; hepatocellular carcinoma; gastric cardia cancer; meningioma; multiple myeloma; colorectal, postmenopausal breast, ovarian, gallbladder and thyroid cancers. We first synopsize current epidemiologic evidence; the obesity paradox in cancer risk and mortality; the role of weight gain and weight loss in the modulation of cancer risk; reliable somatometric indicators for obesity and cancer research; and gender differences in obesity related cancers. We critically summarize emerging biological mechanisms linking obesity to cancer encompassing insulin resistance and abnormalities of the IGF-I system and signaling; sex hormones biosynthesis and pathway; subclinical chronic low-grade inflammation and oxidative stress; alterations in adipokine pathophysiology; factors deriving from ectopic fat deposition; microenvironment and cellular perturbations including vascular perturbations, epithelial-mesenchymal transition, endoplasmic reticulum stress and migrating adipose progenitor cells; disruption of circadian rhythms; dietary nutrients; factors with potential significance such as the altered intestinal microbiome; and mechanic factors in obesity and cancer. Future perspectives regarding prevention, diagnosis and therapeutics are discussed. The aim of this review is to investigate how the interplay of these main potential mechanisms and risk factors, exerts their effects on target tissues provoking them to acquire a cancerous phenotype. Highlights • Excess body weight is associated with an increased risk for a range of malignancies. • The triad of obesity, insulin resistance and adipokine aberrations is linked to cancer. • Subclinical chronic low-grade inflammation and oxidative stress is another mechanism. • Altered gut microbiome contributes to inflammation and release of carcinogenic products. • Microenvironmental perturbations and circadian rhythm disruption are additional mechanisms. [ABSTRACT FROM AUTHOR]

Summary Adipokines are biologically active cytokines that are mainly produced in adipose tissue. There is evidence, in man and mice, that some adipokines may be secreted in other tissues including the vascular endothelium, epithelia and sebaceous glands. Moreover, modified serum levels of adipokines have been detected in people with acne vulgaris or psoriasis; it is suspected that adipokines could contribute to local and systemic inflammatory conditions. We aimed to evaluate the expression of three adipokines (i.e. leptin, adiponectin and resistin) in normal canine skin. Formalin-fixed, paraffin wax-embedded punch biopsy samples were obtained from the sparsely-haired skin of the caudal ventral abdomen of a single clinically healthy dog with no history of skin disease. Immunohistochemistry was applied, using rabbit polyclonal primary antibodies specific for leptin, adiponectin and resistin. Adipokines were not expressed in normal canine dermis or hypodermis. In contrast, they were detected in the keratinocytes of all epidermal layers and hair follicle segments, sebocytes, apocrine gland cells and in the vascular endothelium. This is the first report on the expression of adipokines in normal canine skin, a first step in studying their role in the skin physiology and inflammatory skin diseases of dogs. [ABSTRACT FROM AUTHOR]

Abstract Objective Resistin is a hormone that has been associated with metabolic syndrome and cardiovascular disease. The role of resistin in patients with peripheral artery disease (PAD) has not been fully explored. This study seeks to understand the relationship between serum resistin, vascular function, and cardiovascular outcomes in patients with PAD. Methods There were 106 patients with PAD who were recruited between 2011 and 2016. Patients attended a baseline visit during which a comprehensive vascular physiology assessment including medical and surgical history, radial artery tonometry, and flow mediated-vasodilation (FMD) was completed. A blood sample was drawn, and serum resistin was assayed using enzyme-linked immunosorbent assay kits. Using the time of study enrollment as the time of origin, incident major adverse cardiac events (MACEs) were identified by subsequent chart review and defined as a composite end point of myocardial infarction, coronary revascularization, transient ischemic attack, stroke, or death from a cardiac cause. Results Patients had a mean age of 68 ± 8 years, were largely white (75%), and had comorbidities commonly associated with PAD including hypertension (92%), hyperlipidemia (87%), coronary artery disease (37%), and diabetes mellitus (38%). After stratification by resistin quartile, higher resistin quartiles were significantly associated with an older age, a greater number of pack-years smoked, and a lower estimated glomerular filtration rate. Despite similar comorbidities and medication use, endothelial function, as measured by FMD, was significantly lower with increasing resistin quartile (I, 9.1% ± 3.3%; II, 7.1% ± 3.5%; III, 5.8% ± 4.0%; IV, 5.6% ± 3.5%; P =.002). In multivariable linear regression, higher resistin quartiles (III and IV) were associated with lower FMD relative to quartile I after adjusting for several patient characteristics, medications, and comorbidities (III, −2.26 [95% confidence interval (CI), −4.51 to −0.01; P =.05]; IV, −2.53 [95% CI, −4.87 to −0.20; P =.03]). During a median follow-up period of 36 months (interquartile range, 29-45 months), 21 patients experienced the primary end point. In a Cox proportional hazards model adjusted for smoking status, coronary artery disease, and age, each 1 ng/mL increase in resistin was associated with a 10% increased risk of MACEs (hazard ratio, 1.10; 95% CI, 1.00-1.20; P =.04). Conclusions In patients with PAD, higher levels of resistin were associated with impaired endothelial function and an increased rate of MACEs. These results suggest that resistin may be a marker or effector of impaired vascular physiology and adverse cardiac outcomes in patients with PAD. Further research is needed to determine the potential mechanisms by which resistin may impair endothelial function and increase MACEs in this population. [ABSTRACT FROM AUTHOR]

Background: Psoriasis is frequently associated with obesity and cardiovascular diseases. Adipocytokines have been implicated in the pathogenesis of psoriasis and its cardiometabolic comorbidities. Objectives: The aim of this study was to assess the roles of leptin, resistin, and high-molecular-weight (HMW) adiponectin in psoriasis as well as their relationship with Psoriasis Area and Severity Index (PASI), obesity, and insulin resistance. Materials and Methods: Forty-six psoriasis patients and equivalent age-, sex-, and body mass index (BMI)-matched controls were recruited in this study. PASI, waist and hip circumferences, and waist/hip ratio (WHR) were recorded, and total body fat mass (TBFM) values were measured using a bioimpedance body composition analyzer. Fasting serum leptin, resistin, and HMW adiponectin levels were measured, and homeostasis model assessment values for insulin resistance (HOMA-IR) were calculated. Results: After the adjustment for anthropometric variables, leptin levels did not differ significantly between the groups (P = 0.736). The patient group showed significantly elevated resistin and lower HMW adiponectin levels (P = 0.007, P= 0.010, respectively). The correlation of serum leptin, resistin, and HMW adiponectin with PASI was not significant (r = −0.100, P= 0.506; r = −0.053, P= 0.726; r = −0.103, P= 0.494, respectively). HOMA-IR positively correlated with leptin and negatively correlated with HMW adiponectin (r = 0.426, P < 0.001; r = −0.393, P < 0.001, respectively). The correlation of leptin and resistin with BMI was direct while that of HMW adiponectin with BMI was inverse (r = 0.532, P < 0.001; r = 0.240, P= 0.021; r = −0.408, P < 0.001, respectively). No significant differences were detected regarding TBFM, and waist and hip circumferences (P = 0.187, P = 0.090, P= 0.543, respectively). However, WHR was significantly higher in the patient group (P = 0.015). Conclusion: Altered adipocytokine levels in psoriasis patients suggest a possible role of adipocytokines in the relationship between psoriasis and its metabolic comorbidities. Fat distribution is also different from the healthy population with similar TBFM values, and abdominal obesity, which is an independent cardiovascular risk factor, is more prevalent in psoriasis patients. [ABSTRACT FROM AUTHOR]

The renin-angiotensin-system (RAS), endothelial dysfunction and sympathetic nervous system are mechanistic risk factors of hypertension. The study sought to elucidate the interplay of adipokines in the pathogenesis of essential hypertension. This comparative cross-sectional study recruited 200 confirmed hypertensive patients from the KATH and 50 age-matched normotensives. Participants’ blood pressures, anthropometric and socio-demographic information were voluntarily obtained. Serum levels of adiponectin, leptin and resistin of the participants were quantified using the ELISA. Renal function, lipid profile and glycemic status of all subjects were also analyzed. Hypertensive patients showed a significantly higher anthropometric indices of adiposity compared to normotensives, CI (p < 0.0001), BAI (p < 0.0001) and AVI (p = 0.002). Adiponectin levels (p < 0.0001) were significantly lower in the hypertensive relative to the normotensives. Furthermore, significantly higher concentrations of serum leptin (p = 0.016) and the leptin-adiponectin ratio (p = 0.001) were observed among the hypertensive compared to the normotensives. The study further observed a direct association between serum leptin and weight (r = 0.111, p = 0.022), BMI (r = 0.129, p = 0.009) and WHtR (r = 0.098, p = 0.045) but inverse relationship with height (r = −0.134, p = 0.006) among the hypertensive. Serum leptin has a significant negative correlation with HDL-C among the hypertensive (r = −0.174, p = 0.013). The fully aOR for hypertension as predicted by resistin and adiponectin were 1.12 (95% Cl, 1.02–1.25); p = 0.019) and 0.93 (95% Cl, 0.91–0.95); p = 0.0001) respectively. We found that elevations in serum levels of leptin and resistin, and low levels of adiponectin may play a role in the pathogenesis of essential hypertension. Therefore, adipokines may offer themselves as potential indices for early and accurate detection of high blood pressure. At the same time our present results also confirm the conclusions with respect to correlation of leptin and obesity. Further longitudinal studies in a larger population are warranted to investigate the physiological and pathological functions of adipokines in hypertension. [ABSTRACT FROM AUTHOR]

Highlights • Intermuscular adipose tissue may contribute to the chronic inflammation associated with obesity and increased risk of cardiometabolic disease. • Intermuscular adipose tissue may contribute to the chronic inflammation associated with increased risk of cardiometabolic disease. Abstract Objective This study examined the associations between abdominal IMAT area and density with inflammatory markers associated with cardiometabolic disease. Methods 1897 participants enrolled in the Multi-Ethnic Study of Atherosclerosis underwent computed tomography to quantify body composition and measurements of adiponectin, leptin, interleukin-6 (IL-6), C-reactive protein (CRP), and resistin. Results The mean age and body mass index of participants was 65 years and 28 kg/m2, respectively, and 50% were female. After adjustment for age, sex, and race/ethnicity, as IMAT area increased and density decreased from the first to fourth quartile, markers of inflammation increased linearly (p < 0.01). Using linear regression, and with adjustment for demographics, cardiovascular disease risk factors, and abdominal muscle area and density, a 1-standard deviation (SD) increase in total abdominal IMAT area was associated with a 21%, 36% and 20% higher IL-6, leptin, and CRP, respectively, and 19% lower adiponectin (p < 0.001). With similar adjustment, a 1-SD decrease in total abdominal IMAT density was associated with a 14%, 32%, and 15% higher IL-6, leptin, and CRP, respectively, and 22% lower adiponectin (p < 0.001). These associations were attenuated with the addition of visceral fat (p > 0.05). Conclusions Abdominal IMAT area and density are associated with inflammatory markers, with these associations attenuated by central adiposity. [ABSTRACT FROM AUTHOR]

Background: Our recent research showed that resistin has a neuroprotective effect against stroke-induced injury through suppressing apoptosis and oxidative stress. However, the molecular mechanism of neuroprotection of resistin is unclear. This work was designed to examine the effect of mouse recombinant resistin on mRNA expression of Tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β), Interleukin-10 (IL-10), Transforming growth factor-β1 (TGF- β1), and Heat shock protein-70 (HSP-70) in mouse model of stroke.Materials and Methods: Transient focal cerebral ischemia was induced by the middle cerebral artery occlusion (MCAO) in mice. TNF-α, IL-1β, IL-10, TGF-β1, and HSP-70 mRNA were detected at sham (0 hour), 3 hours, 6 hours, 12 hours, and 24 hours after MCAO using real-time QRT-PCR method. Moreover, animals were treated with resistin at the dose of 400ng/mouse at the commencement of MCAO, and mRNA expression of the cytokines and HSP-70 was measured 24 hours after MCAO.Results: Tumor necrosis factor-α and IL-1β mRNA expression markedly increased at 12-hour time point and then returned to the basal level at 24 hours after MCAO; but HSP-70 mRNA expression increased at 24-hour time point. Furthermore, resistin (400 ng/mouse) significantly increased TGF-β1 and IL-10 and decreased HSP-70 gene expression at 24 hours after MCAO.Conclusions: Our findings revealed that a molecular mechanism of attenuating ischemic damage by resistin administration probably is increased mRNA expression of anti-inflammatory cytokines. However, applying resistin in the clinical settings for the treatment of stroke deserves further researches in the future. [ABSTRACT FROM AUTHOR]