Resistin Concentrations Research Articles

Leptin Does Not Influence TSH Levels in Obese Short Children.

IntroductionGrowth hormone (GH) and thyroid hormones are important for children growing. In some obese children a slightly elevated TSH concentration is observed. This may be an adaptive mechanism: stimulation of pro-TRH biosynthesis in the hypothalamus in response to elevated leptin. The increased TSH may also reflect the necessity of maintaining the resting energy expenditure or may be a result of inappropriate, low FT4 concentration. Thus, we evaluated serum TSH and FT4 concentrations in idiopathic short stature (ISS) children (non GH-deficient) and examined the effect of children’s nutritional status and levels of selected adipocytokines on thyroid function, searching for the presence of various forms of subclinical hypothyroidism, which may be the cause of the slow growth rate.MethodsThe study group included 115 children (50 girls and 65 boys) with ISS, aged (mean ± SD) 10.4 ± 3.34 years. In each child, lipids, TSH, FT4, IGF-1, maxGH during the stimulation tests, leptin, adiponectin and resistin concentrations were determined. Based on BMI SDS, 3 subgroups: slim (n=26), obese (n=21) and normal weight (n=68) were distinguished.ResultsThere was no correlation between leptin level and TSH, FT4 levels. The levels of leptin, total cholesterol and LDL-cholesterol in obese short children were significantly higher than in children from other subgroups. In turn, the levels of adiponectin, resistin, TSH and FT4 did not differ between subgroups. In 7% of children, an elevated TSH level was found (but less than 10 mIU/L), with a similar frequency across subgroups. The higher the leptin, the lower maxGH in clonidine stimulation test was recorded.ConclusionsIt seems that in obese children with idiopathic short stature leptin does not increase TSH secretion. This may be related to a disruption of the effect of leptin on TSH production and could indicate wide ranging disturbances of hypothalamic signals, and consequently be the cause of inappropriate GH secretion.

Dietary Supplementation With Fine-Grinding Wheat Bran Improves Lipid Metabolism and Inflammatory Response via Modulating the Gut Microbiota Structure in Pregnant Sow.

This study investigated the effects of fine-grinding wheat bran on pregnant sow body condition, lipid metabolism, inflammatory response, and gut microbiota. In this study, wheat bran was crushed into three particle sizes. A total of 60 Landrace × Yorkshire second parity sows were allotted to two groups: CWB (a diet containing coarse wheat bran with particle size of 605 μm) and FWB (a diet containing fine wheat bran with particle size of 438 μm). Fine-grinding wheat bran had higher soluble dietary fiber concentration, swelling capacity, water-holding capacity, and fermentability than coarse wheat bran. Pregnant sows fed FWB throughout pregnancy had lower body weight and fat deposition than sows fed CWB. And the piglet body weight at birth of the FWB group was remarkably increased. Serum concentrations of lipids (triglycerides, total cholesterol, and free fatty acid), interleukin 6, leptin, and resistin were decreased on day 90 of pregnancy by fine wheat bran supplementation. Feeding FWB significantly decreased abundance of Firmicutes and dramatically increased the abundance of Bacteroidetes at phylum level. At genus level, the abundance of Terrisporobacter was decreased in FWB feeding sows, but the abundance of Parabacteroides was increased. Fecal total short-chain fatty acids, propionate, and butyrate contents were markedly increased in the FWB group. The results suggested that the physicochemical properties of finely ground wheat bran had been improved. Dietary supplementation with fine wheat bran changed the gut microbiota structure and enhanced the short-chain fatty acids level, which improved the maternal body condition, metabolic and inflammatory status, and reproductive performance in sows.

Omentin inhibits the resistin-induced hypertrophy of H9c2 cardiomyoblasts by inhibiting the TLR4/MyD88/NF-κB signaling pathway.

The recently identified adipocytokine omentin was previously found to be expressed mainly in human omental and visceral adipose tissues. As such, reduced plasma concentrations of omentin were revealed to be associated with increased risks of cardiovascular diseases. Omentin has also been previously demonstrated to exert anti-inflammatory effects. By contrast, resistin is a protein that has been associated with obesity and type-2 diabetes mellitus, and the serum concentration of resistin is increased significantly in these populations. Resistin is involved in mediating inflammation development, where they can promote cardiac hypertrophy in humans through toll-like receptor 4 (TLR4)-related signaling. In the present study, the potential effects of omentin on resistin-induced hypertrophy in H9c2 cardiomyoblasts were investigated. In the absence/presence of omentin, H9c2 cardiomyoblasts were treated with resistin. Omentin was found to significantly inhibit resistin-induced increases in the surface area of H9c2 cardiomyoblasts as determined by immunofluorescence. In addition, omentin significantly inhibited resistin-induced increases in the mRNA expression of atrial natriuretic factor, brain natriuretic peptide, β-myosin heavy chain (which is a characteristic feature of cardiac hypertrophy) and TLR4, which was determined using reverse-transcription-quantitative PCR. According to western blotting results, omentin significantly inhibited resistin-induced ERK phosphorylation, which is an important mediator of cardiomyoblast hypertrophy. Furthermore, omentin significantly inhibited resistin-induced protein expression of TLR4, myeloid differentiation factor 88 (MyD88) and NF-κB phosphorylation, both of which are important members of inflammatory signaling. To conclude, data from the present study suggest that omentin can inhibit resistin-induced H9c2 cardiomyoblast hypertrophy through inhibition of the TLR4/MyD88/NF-κB signaling pathway. Therefore, omentin serve as an attractive therapeutic target against resistin-induced cardiac hypertrophy.

Changes in adipokine levels and metabolic profiles following bariatric surgery

BackgroundBariatric surgery is considered to be the most effective treatment option for weight reduction in obese patients. Abdominal obesity is frequently accompanied by metabolic syndrome (MS). Adipokines are cell signaling proteins that have direct impact upon the metabolic homeostasis. The purpose of this analysis was to evaluate the effect of bariatric surgery, including laparoscopic sleeve gastrectomy (LSG) and laparoscopic gastric bypass (LRYGB) on the adipokine levels and metabolic profile as well as MS and status of type 2 diabetes (T2D).MethodsWe analyzed anthropometric parameters, blood levels of adipokines, vitamins, lipids and inflammatory markers in 30 bariatric surgery patients with obesity of class II or III 1 month before and 1 year after surgery as well as in 60 obese patients from general practice (GP) and 15 patients with normal body mass (control).ResultsThe BMI was significantly higher among patients before surgery and GP patients in comparison to control and post-surgery patients. The levels of glucose, cholesterol and LDL-cholesterol, triglyceride and hs-CRP were the highest in patients before surgery but decreased significantly after surgery, while the level of HDL-cholesterol increased after surgery.The levels of adiponectin increased and that of leptin decreased after surgery. The significant difference in the concentration of resistin was revealed between LSG and LRYGB methods. The relationship between resistin and vitamin D was also found. The patients with MS and T2D displayed significantly greater reduction in lipid markers and adipokine levels than the rest of patients.ConclusionRemarkable changes in levels of adipokines after bariatric surgery appear like increase in adiponectin and decrease in leptin levels. Significant improvement in anthropometric parameters, metabolic and inflammatory markers occurs, suggesting high potential for reduction of metabolic syndrome and risk for type 2 diabetes. We have shown for the first time ever that level of vitamin D may be involved in resistin regulation.

Roles of plasma leptin and resistin in novel subgroups of type 2 diabetes driven by cluster analysis

BackgroundA novel classification has been introduced to promote precision medicine in diabetes. The current study aimed to investigate the relationship between leptin and resistin levels with novel refined subgroups in patients with type 2 diabetes mellitus (T2DM).MethodsThe k-means analysis was conducted to cluster 541 T2DM patients into the following four subgroups: mild obesity-related diabetes (MOD), severe insulin-deficient diabetes (SIDD), severe insulin-resistant diabetes (SIRD) and mild age-related diabetes (MARD). Individuals meeting the exclusion criteria were eliminated, the data for 285 patients were analyzed. Characteristics were determined using various clinical parameters. Both the leptin and resistin levels were determined using enzyme-linked immunosorbent assay.ResultsThe highest levels of plasma leptin were in the MOD group with relatively lower levels in the SIDD and SIRD groups (P < 0.001). The SIRD group had a higher resistin concentration than the MARD group (P = 0.024) while no statistical significance in resistin levels was found between the SIDD and MOD groups. Logistic regression demonstrated that plasma resistin was associated with a higher risk of diabetic nephropathy (odds ratios (OR) = 2.255, P = 0.001). According to receiver operating characteristic (ROC) curves, the area under the curve (AUC) of resistin (0.748, 95% CI 0.610–0.887) was significantly greater than that of HOMA2-IR (0.447, 95% CI 0.280–0.614) (P < 0.05) for diabetic nephropathy in the SIRD group.ConclusionsLeptin levels were different in four subgroups of T2DM and were highest in the MOD group. Resistin was elevated in the SIRD group and was closely related to diabetic nephropathy.

Measurement of Plasma Resistin Concentrations in Horses with Metabolic and Inflammatory Disorders.

Simple SummaryObesity and its associated complications, such as metabolic syndrome, are an increasing problem in both humans and horses in the developed world. Adipose tissue is a key endocrine organ that communicates with other organs by multiple endocrine substances called adipokines. There is evidence to suggest that adipokines may contribute to the regulation of biological processes, such as metabolism, immunity, and inflammation. The aim of this study was to investigate the usefulness of one of these adipokines in horses, resistin, and its relationship with insulin dysregulation (ID) and inflammation. Seventy-two horses, included in one of the four following groups, were studied: healthy controls, horses with inflammatory conditions, horses with mild, and horses with severe ID. Plasma resistin concentrations were significantly different between groups, and the highest values were recorded in the inflammatory and severe ID groups. The lack of correlation of resistin with basal insulin concentration and the significant correlation of resistin with the inflammatory marker serum amyloid A suggest that, as is the case in humans, plasma resistin concentrations in horses are predominantly related to inflammatory conditions and not to ID.Obesity and its associated complications, such as metabolic syndrome, are an increasing problem in both humans and horses in the developed world. The expression patterns of resistin differ considerably between species. In rodents, resistin is expressed by adipocytes and is related to obesity and ID. In humans, resistin is predominantly produced by inflammatory cells, and resistin concentrations do not reflect the degree of obesity, although they may predict cardiovascular outcomes. The aim of this study was to investigate the usefulness of resistin and its relationship with ID and selected indicators of inflammation in horses. Seventy-two horses, included in one of the four following groups, were studied: healthy controls (C, n = 14), horses with inflammatory conditions (I, n = 21), horses with mild ID (ID1, n = 18), and horses with severe ID (ID2, n = 19). Plasma resistin concentrations were significantly different between groups and the higher values were recorded in the I and ID2 groups (C: 2.38 ± 1.69 ng/mL; I: 6.85 ± 8.38 ng/mL; ID1: 2.41 ± 2.70 ng/mL; ID2: 4.49 ± 3.08 ng/mL). Plasma resistin was not correlated with basal insulin concentrations. A significant (r = 0.336, p = 0.002) correlation was found between resistin and serum amyloid A. Our results show that, as is the case in humans, plasma resistin concentrations in horses are predominantly related to inflammatory conditions and not to ID. Horses with severe ID showed an elevation in resistin that may be secondary to the inflammatory status associated with metabolic syndrome.

Study of serum ghrelin and resistin levels and their correlation with zinc and magnesium in men with type 2 diabetes

Introduction: The objectives of our work were to compare the serum concentrations of lipid parameters,insulin, resistin, ghrelin, zinc and magnesium between two groups of men with obese type 2 diabetes and a control group and to study possible correlations between these differentparameters. Material and methods: This was a monocentric case-control study during the period 19 October 2015 to 18 November 2015. It included biological parameters from two separate samples: a group of 41 male, obese, type 2 diabetic patients and a group of 34 diabetes-free controls. Results: Mean plasma ghrelin concentrations were significantly lower in patients with type 2 diabetes compared to those in the control group: (14.05 ± 2.35 pg/mL) versus (45.45 ± 13.59 pg/mL). Mean resistance was significantly higher in diabetics (10.09 ± 2.63 ng/mL) compared to healthy subjects (2.22 ± 0.58 ng/mL). In multivariate analysis, body mass index (BMI) and insulin levels were factors that could influence zincemia variability, while BMI and ghrelinaemia appeared to be predictors of magnesium variability. Discussion: Most correlation studies are based on serum zinc concentration. The different possible correlations between resistin, zinc, magnesium and ghrelin require an increase in the size of the study population, as well as an increase in nutritional surveys during the different stages of type 2 diabetes and obesity. Conclusion: It would be interesting to evaluate, according to the stages of obesity, serum levels of magnesium and ghrelin, on the one hand, and serum levels of zinc and insulin, on the other hand.

Adipocyte related peptides - galanin and resistin in endometrioid type endometrium cancer.

The aim of (this) study was to investigate concentrations of galanin and resistin in patients with endometrioid type endometrium cancer. A total of 85 patients (52 Endometrioid type Endometrium Cancer patients and 33 healthy controls) were included in the study. Serum galanin and resistin levels were measured by an enzyme-linked immunosorbent assay (ELISA). It was found that the sensitivity and specificity of galanin at the cut off level of 0,37 ng/mL, was 82.96% and 68.78% respectively (AUC = 0.795, CI:0.691-0.898, p < 0.001). Sensitivity and specificity of resistin at the 0.27 ng/mL cut off level, was found to be 82.95% and 59.12% respectively (AUC = 0.705, CI:0.588-0.822, p < 0.001) for prediction of endometrioid type endometrium cancer diagnosis. Bivariate logistic regression analysis showed that, increased galanin concentration, greater than 0.37 ng/mL, increased the risk of having endometrioid type endometrium cancer 10.2 times (95% CI: 3.425-30.881, p < 0.001) and resistin concentration > 0.27 ng/mL, increased the risk of having endometrioid type endometrium cancer 5.6 fold (95% CI: 1.939-16.282, p = 0.001). On the other hand, according to adjusted Odds Ratio results of the multiple logistic regression analysis, effect of interaction between galanin and resistin on having endometrioid type endometrium cancer was statistically significant. Increased galanin concentration > 0.37 ng/mL with increased resistin concentration > 0.27 ng/mL had adjusted Odds Ratio = 27.182 times greater risk of having endometrioid type endometrium cancer (95% CI: 6.653 to 111.109, p < 0.001). Increased galanin and resistin levels, either separately or together with, seemed to increase the risk of endometrioid type endometrium cancer other than different risk factors.

THE ROLE OF RESISTIN IN THE PROGRESSION OF NON-ALCOHOLIC FATTY LIVER DISEASE

The aim of the research was to study the relationship between plasma concentrations of resistin and indicators of enzyme and pigment metabolism in patients with non-alcoholic fatty liver disease (NAFLD) and its combination with type 2 diabetes mellitus (DM-2). Materials and methods. On the base of Kharkiv Regional Hospital a total of 90 patients were examined, including patients with NAFLD (n = 20) and its combination with DM-2 with normal body weight (n = 20) and obesity (n = 50), as well as 20 healthy volunteers. A complex of clinical, laboratory and instrumental (including liver biopsy in 9 patients) examinations of patients was performed. Results. A direct relationship was established between the level of resistin and indicators of enzyme and pigment exchange in groups of patients with combined pathology. A significant increase of resistin plasma level, as well as disorders of the liver function were determined in all groups of patients in comparison with the controls. The most marked changes were revealed in patients with combination of NAFLD, DM-2 and obesity. Conclusions. The established relationship between the level of resistin and the indicators of the liver functional state suggests that an increase of resistin level may reflect the presence of impaired liver function in patients with NAFLD in combination with DM-2, predicting the progression of NAFLD. In order to detect the disorders of liver function in patients with DM-2, it is recommended to determine the level of resistin in patients with NAFLD, especially when concomitant obesity is present. Patients with resistin level (&gt; 8.06 ± 0.23 ng/ml) should be considered at risk of NAFLD progression.

Association of circulating leptin, adiponectin, and resistin concentrations with long-term breast cancer prognosis in a German patient cohort

Adipokines including leptin, adiponectin and resistin have been linked to risk of obesity-related cancers potentially through low-grade chronic inflammation pathways. We aimed to assess the role of post-diagnosis circulating adipokines on long-term prognosis in a prospective breast cancer cohort. Adipokines were measured in blood collected at baseline shortly after diagnosis (2002–2005) and at follow-up (2009) from 3112 breast cancer patients enrolled in the population-based MARIE study. Half of the patients had measurements at both time-points. All-cause mortality, breast cancer specific mortality and recurrences were ascertained up to June 2015 (11 years median follow-up). Associations with time-varying adipokine concentrations overall and stratified by estrogen and progesterone receptor (ERPR) were evaluated using adjusted proportional hazard regression. At baseline (n = 2700) and follow-up (n = 2027), median concentrations for leptin, adiponectin and resistin were 4.6 and 2.7 ng/ml, 24.4 and 30.0 mg/l, 15.4 and 26.2 ng/ml, respectively. After adjustment, there was no evidence for associations between adipokines and any outcome overall. In ERPR negative tumors, highest vs. lowest quintile of adiponectin was significantly associated with increased breast cancer specific mortality (HR 2.51, 95%CI 1.07–5.92). Overall, post-diagnosis adipokines were not associated with long-term outcomes after breast cancer. In patients with ERPR negative tumors, higher concentrations of adiponectin may be associated with increased breast cancer specific mortality and warrant further investigation.

Evaluation of the frequency of RETN c.62G&gt;A and RETN c.-180C&gt;G polymorphisms in the resistin coding gene in girls with anorexia nervosa

Anorexia nervosa (AN) is a serious psychosomatic syndrome, classified as an eating disorder. AN patients strive to lose weight below the normal limits defined for a specific age and height, achieving their goal even at the expense of extreme emaciation. AN has a multifactorial aetiology. Genetic factors are believed to be significant in the predisposition to the development of AN. In girls suffering from AN significantly lower levels of resistin (RES) in blood serum are observed as compared to healthy girls. These differences may lead to a thesis that functional genetic polymorphisms in RES coding genes can be responsible for this phenomenon. In our pilot study we demonstrated significant differences in the distribution of genotypes in the locus RETN c.-180C>G of the RES gene in 67 girls with AN and 38 healthy girls. It seems reasonable to compare the frequency of polymorphisms of RETN c.62G>A and RETN c.-180C>G in the RES gene in girls with AN and in healthy subjects in a bigger cohort and to analyse correlations between individual variants of the polymorphisms referred to above and the RES levels in blood plasma. The study covered 308 girls with the restrictive form of AN (AN) and 164 healthy girls (C) (aged 11-19 years). The RES levels in blood serum were determined by means of the ELISA method on a Bio-Vendor machine from LLC (Asheville, North Carolina, USA). The DNA isolation was carried out by means of Genomic Mini AX BLOOD (SPIN). The PCR reaction was carried out on a ThermoCycle T100 thermocycler. 80-150 ng of the studied DNA and relevant F and R starters were added to the reaction mixture. The reaction products were subjected to digestion by restriction enzymes and separated on agarose gels (RFLP). The average RES level in blood serum in the AN group was significantly lower (p < 0.0001) than in the C group. The distribution of genotypes in the locus RETN c.62 of the RES gene was similar in both groups. A significant difference was demonstrated in the distribution of genotypes in the polymorphic site RETN c.-180 of the RES gene between AN and C (p = 0.0145) and in the distribution of the C and G alleles in the locus RETN c.-180 (p < 0.0001). The C allele occurred significantly more frequently than the G allele in the C group as compared to the AN group. In all the study subjects jointly (AN and C) a significant positive correlation between the blood RES levels on one hand and the body mass (r = 0.42; p < 0.0001) and BMI (r = 0.61; p< 0.0001) on the other was observed. There was no correlation between the concentration of RES in blood serum and the distribution of genotypes in the loci of the resistin gene referred to above. The CG genotype in the locus RETN c.-180 C>G of the RES gene may constitute one of the factors predisposing to the development of AN in girls. The genotype in the loci RETN c.62 G>A and RETN c.-180 C>G of the resistin gene has no influence on the levels of this hormone in blood in AN patients.

Odnos serumskih nivoa adiponektina i rezistina kod pacijenata sa hroničnim hepatitisom B i teškom fibrozom jetre

BackgroundRecent 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.MethodsThe 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.ResultsThere 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 (p<0.001). There was no significant difference between mean serum adiponectin levels according to the values of FIB-4 and APRI scores.ConclusionsProgression 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.

FTO and PLAG1 Genes Expression and FTO Methylation Predict Changes in Circulating Levels of Adipokines and Gastrointestinal Peptides in Children.

Adipokines and gastrointestinal tract hormones are important metabolic parameters, and both epigenetic factors and differential gene expression patterns may be associated with the alterations in their concentrations in children. The function of the FTO gene (FTO alpha-ketoglutarate dependent dioxygenase) in the regulation of the global metabolic rate is well described, whereas the influence of protooncogene PLAG1 (PLAG1 zinc finger) is still not fully understood. A cross-sectional study on a group of 26 children with various BMI values (15.3–41.7; median 28) was carried out. The aim was to evaluate the dependencies between the level of methylation and expression of aforementioned genes with the concentration of selected gastrointestinal tract hormones and adipokines in children. Expression and methylation were measured in peripheral blood mononuclear DNA by a microarray technique and a restriction enzyme method, respectively. All peptide concentrations were determined using the enzyme immunoassay method. The expression level of both FTO and PLAG1 genes was statistically significantly related to the concentration of adipokines: negatively for apelin and leptin receptor, and positively for leptin. Furthermore, both FTO methylation and expression negatively correlated with the concentration of resistin and visfatin. Cholecystokinin was negatively correlated, whereas fibroblast growth factor 21 positively correlated with methylation and expression of the FTO gene, while FTO and PLAG1 expression was negatively associated with the level of cholecystokinin and glucagon-like peptide-1. The PLAG1 gene expression predicts an increase in leptin and decrease in ghrelin levels. Our results indicate that the FTO gene correlates with the concentration of hormones produced by the adipose tissue and gastrointestinal tract, and PLAG1 gene may be involved in adiposity pathogenesis. However, the exact molecular mechanisms still need to be clarified.

Type 1 Diabetic Patients After Simultaneous Pancreas and Kidney Transplantation Have Less Intense Periodontal Inflammation Compared to Kidney Recipients Treated with Insulin.

BackgroundLong-term diabetes predisposes to pathological changes in periodontal tissues. Improvement in this respect can be expected in patients after pancreas transplantation.The aim of this study was to assess and compare the intensity of periodontium pathological lesions and inflammation markers concentration in gingival crevicular fluid (GCF) in patients with type 1 diabetes (T1D) after kidney (KTx) or simultaneous pancreas and kidney transplantation (SPK).Material/MethodsThe study included 20 T1D patients after SPK and 16 after KTx, and 15 non-diabetic kidney recipients (control). Periodontal clinical parameters and concentration of selected biochemical markers of inflammation in GCF were assessed. The following tests were used in statistical data analysis: Shapiro-Wilk test, the t test, the Mann-Whitney U tests, one-way ANOVA with Tukey’s post hoc test, and χ2 test (also with Yate’s correction). Moreover, linear regression and Pearson or Spearman correlation coefficient was used.ResultsThere were no differences in modified Sulcus Bleeding Index (mSBI) and GCF volume between the SPK group and control group, whereas values of these parameters in the KTx group were higher than in the SPK and control groups. Maximal clinical attachment loss and pocket depth and Periotest values were higher in diabetic recipients compared to controls, and did not differ between SPK and KTx.The concentration of IL-1β, MMP-8, resistin, TNFα, and YKL40 in the GCF in the KTx group was higher than in the SPK and control groups.In the combined group of T1D patients, there was a correlation between blood HbA1c and mSBI, GCF volume, and resistin, TNF-α and YKL40 concentrations, and between resistin concentration and mSBI.ConclusionsT1D patients after SPK show lower levels of inflammatory markers in GCF and present reduced intensity of periodontitis compared to kidney recipients treated with insulin.The severity of morphological changes in periodontium in T1D patients after KTx or SPK is higher than in non-diabetic kidney recipients.

Higher Physical Activity Level Improves Leptin Concentrations in Spinal Cord Injury Subjects

The present study was designed to compare the body composition and indicators of chronic inflammatory grade, such as leptin, adiponectin, and resistin concentrations in irregularly active and active SCI subjects. Thirty-two male subjects participated in this study. They were divided into three groups: able-bodied control irregularly active (control, n = 11), irregularly active with SCI (SCI-IA, n = 8), and physically active with SCI (SCI-PA, n = 13). The enzyme-linked immunosorbent assay (ELISA) assessed serum concentrations of leptin, adiponectin, and resistin. All volunteers performed the maximum oxygen uptake (VO2max) test, 24 h total energy expenditure (TEE), and body composition by skinfold thicknesses. Leptin concentrations were higher in the SCI-IA group when compared to the other groups, while no significant differences were found between the SCI-PA and control cohorts. In addition, no significant differences were found among groups for serum adiponectin and resistin concentrations either. The SCI-PA group showed significantly higher values for TEE and VO2max when compared to the other groups. Percentages of body fat and circumference were decreased in the control and SCI-PA groups when compared to the SCI-IA cohort. Associations between leptin and cardiorespiratory capacity and anthropometric markers were also observed. Our findings highlight that the lack of physical activity in the SCI subjects leads to poor general physical fitness and higher levels of body adiposity, which may induce hyperleptinemia, an essential marker for cardiometabolic disorders.

Association of Adiponectin, Leptin and Resistin Plasma Concentrations with Echocardiographic Parameters in Patients with Coronary Artery Disease.

The imbalanced network of adipokines may contribute to the development of systemic low-grade inflammation, metabolic diseases and coronary artery disease (CAD). In the last decade, three classic adipokines—adiponectin, leptin and resistin—have been of particular interest in studies of patients with CAD due to their numerous properties in relation to the cardiovascular system. This has directed our attention to the association of adipokines with cardiac structure and function and the development of heart failure (HF), a common end effect of CAD. Thus, the purpose of this study was to analyse the associations of plasma concentrations of adiponectin, leptin and resistin with parameters assessed in the echocardiographic examinations of CAD patients. The presented study enrolled 167 Caucasian patients (133 male; 34 female) with CAD. Anthropometric, echocardiographic and basic biochemical measurements, together with plasma concentrations of adiponectin, leptin and resistin assays, were performed in each patient. Adiponectin concentrations were negatively associated with left ventricular ejection fraction (LVEF) and shortening fraction (LVSF), and positively associated with mitral valve E/A ratio (E/A), left ventricular end-diastolic volume (LVEDV), left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter LVESD, and left atrium diameter (LAD). Resistin concentrations were negatively associated with E/A. Leptin concentrations, although correlated with HF severity assessed by the New York Heart Association (NYHA) Functional Classification, were not independently associated with the echocardiographic parameters of cardiac structure or function. In conclusion, adiponectin and resistin, but not leptin, are associated with the echocardiographic parameters of cardiac remodelling and dysfunction. These associations suggest that adiponectin and resistin might be involved in mechanisms of cardiac remodelling or compensative response. We also suggest the possible benefits of adiponectin and resistin level measurements in the monitoring of patients with CAD.

The role of resistin and its relation to other pathogenetic factors of the chronic kidney disease development

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 &amp;lt; 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.

Metabolomic Profiling Demonstrates Postprandial Changes in Fatty Acids and Glycerophospholipids Are Associated with Fasting Inflammation in Guatemalan Adults

BackgroundMetabolic flexibility is the responsiveness to heterogeneous physiological conditions, such as food ingestion. A key unresolved question is how inflammation affects metabolic flexibility. ObjectivesOur study objective was to compare metabolic flexibility, specifically the metabolomic response to a standardized meal, by fasting inflammation status. MethodsParticipants in Guatemala (n = 302, median age 44 y, 43.7% men) received a standardized, mixed-macronutrient liquid meal. Plasma samples (fasting, 2 h postmeal) were assayed by dual-column LC [reverse phase (C18) and hydrophilic interaction LC (HILIC)] with ultra-high-resolution MS, for concentrations of 6 inflammation biomarkers: high-sensitivity C-reactive protein (hsCRP), leptin, resistin, IL-10, adiponectin, and soluble TNF receptor II (TNFsR). We summed the individual inflammation biomarker z-scores, after reverse-coding of anti-inflammation biomarkers. We identified features with peak areas that differed between fasting and postmeal (false discovery rate–adjusted q <0.05) and compared median log2 postprandial/fasting peak area ratios by inflammation indicators. ResultsWe found 1397 C18 and 974 HILIC features with significant postprandial/fasting feature ratios (q <0.05). Overall inflammation z-score was directly associated with the postprandial/fasting feature ratios of arachidic acid, and inversely associated with the feature ratio of lysophosphatidic acid (LPA), adjusting for age and sex (all P < 0.05). The postprandial/fasting ratio of arachidic acid was negatively correlated with resistin, IL-10, adiponectin, and TNFsR concentrations (all P < 0.05). Feature ratios of several fatty acids—myristic acid [m/z 227.2018, retention time (RT) 229], heptadecanoic acid (m/z 269.2491, RT 276), linoleic acid (m/z 280.2358, RT 236)—were negatively correlated with fasting plasma concentrations of leptin (nanograms per milliliter) and adiponectin (micrograms per milliliter), respectively (all P < 0.05). The postprandial/fasting ratio of LPA was positively correlated with IL-10 and adiponectin (both P < 0.05); and the ratio of phosphatidylinositol was positively correlated with hsCRP (P < 0.05). ConclusionsPostprandial responses of fatty acids and glycerophospholipids are associated with fasting inflammation status in adults in Guatemala.

Resistin levels in perivascular adipose tissue and mid-term mortality in patients undergoing coronary artery bypass grafting.

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.

Disease-Modifying Potential of Metformin and Alendronate in an Experimental Mouse Model of Osteoarthritis.

Osteoarthritis (OA) is the most common degenerative joint disease causing progressive damages of the cartilage and subchondral bone, synovial inflammation, and severe pain. Despite the complex pathomorphological changes that occur in OA, the approach to different forms of OA is standardized. The global results from pharmacological treatment are not satisfactory. Hence, this study aimed to explore the effects of metformin, alendronate, and their combination on OA development and progression in mice with collagenase-induced osteoarthritis (CIOA). Female ICR (CD-2) mice were randomized to five groups: control group, CIOA untreated, CIOA + metformin, CIOA + alendronate, and CIOA + metformin + alendronate. OA was induced by the intra-articular (i.a.) injection of collagenase. OA phenotype was analyzed by flow cytometry (bone marrow cell differentiation), ELISA (serum levels of the adipokines leptin and resistin), and histology (pathological changes of the knee joint). Treatment with metformin, alendronate, or their combination inhibited the expression of RANK and RANKL on osteoblasts and osteoclasts obtained by ex vivo cultivation of bone marrow cells in mineralization or osteoclastogenic media. In addition, metformin treatment was effective for the attenuation of fibroblast differentiation, but not of mesenchymal stem cells (MSCs), while alendronate had an opposite effect. The combination of metformin and alendronate had a suppressive effect on both MSCs and fibroblasts differentiation. Treatment with metformin, alendronate, and their combination decreased serum concentrations of leptin and resistin in the chronic phase of arthritis. The histopathological examination showed that compared with the untreated CIOA group (OA score 9), the groups treated with metformin (OA score 4) or alendronate (OA score 6) had lower scores for cartilage changes. Metformin combined with alendronate significantly decreased the degree of cartilage degeneration (OA score 2), suggesting that this combination might be a useful approach for the treatment of OA patients.