Resistin Expression Research Articles

Correlation between LRG1 and Adipokines in Psoriasis

Background and Objective. Patients with psoriasis may exhibit abnormal changes in serum adipokine levels, which are often related to disease severity of the disease. Leucine‐rich alpha‐2‐glycoprotein 1 (LRG1) is an acute‐phase inflammatory protein that may be linked to adipokines in psoriasis. In this study, we evaluated the differences in the expression of adipokines and LRG1 between patients with psoriasis and healthy individuals, analyzed the correlation between the expression of LRG1 and adipokines, and explored their relationship with psoriatic lesions. Methods. In this cross‐sectional study, patients with psoriasis (n = 54) and healthy controls (n = 26) were enrolled, and their clinical characteristics were recorded. Fasting venous blood samples were collected from each participant. The serum concentrations of leptin, resistin, adiponectin, and LRG1 in each sample were measured using the enzyme‐linked immunosorbent assay. Results. The study included 54 patients with psoriasis vulgaris and 26 healthy controls. The serum levels of LRG1, leptin, and resistin were significantly higher in patients with psoriasis than in healthy controls. Conversely, adiponectin levels were significantly lower in patients with psoriasis. The study showed that LRG1 expression was positively correlated with leptin and resistin expression but negatively correlated with adiponectin expression. Interestingly, only leptin, resistin, and LRG1 expression showed a linear correlation with the Psoriasis Area and Severity Index (PASI). When we categorized patients with psoriasis based on their LRG1 levels, we observed that the group with high LRG1 levels showed a higher PASI. Conclusions. We observed a significant correlation between LRG1 and adipokine expression in patients with psoriasis. In addition, the expression levels of LRG1, leptin, and resistin were observed to be correlated with the severity of psoriasis. We believe that the occurrence and development of psoriasis are collectively influenced by LRG1 and leptin/resistin expression.

Mechanistic Insights of Rutin against Metabolic Disorders

Rutin, a quercetin glycoside comes under the class flavonol. The aglycone part of rutin is known as quercetin. It is found in numerous fruits and plants, especially apricots, buckwheat, cherries, grapefruit, grapes, oranges, and plums. Rutin shows cardioprotective, neuroprotective, and nephroprotective effects mediated via its antioxidant mechanism. The neuroprotective effect of rutin is utilized in the treatment of Parkinson’s disease. It has been documented in the scientific literature that rutin improves obesity through brown fat activation, modulates DNA damage signaling in cancer cells, reduces inflammation by inhibiting eicosanoid biosynthesis, lipoxygenase, cyclooxygenase, and phospholipase A2 activities, enhances insulin release as well as decreases the expression of resistin along with increases the expression of PPAR γ in diabetic patients, increases total cholesterol, high-density lipoprotein and very low-density lipoprotein levels, whereas low-density lipoprotein level decreases resulting into antilipidemic activity, inhibits diabetic liver injury and diabetic cardiomyopathy. Repurposing of rutin was also done against SARS-CoV-2. Our study aims to survey the most recent progress with emphasis on how rutin adapts intracellular signaling cascades to treat different metabolic disorders. However, the precise cellular and molecular mechanisms of rutin are known and more clinical studies are required to provide a novel therapeutic approach for the treatment of metabolic disorders.

Antiresistin Neutralizing Antibody Alleviates Doxorubicin-Induced Cardiac Injury in Mice.

Resistin is closely related to cardiovascular diseases, and this study is aimed at examining the role of resistin in doxorubicin- (DOX-) induced cardiac injury. First, 48 mice were divided into 2 groups and treated with saline or DOX, and the expression of resistin at different time points was examined (N = 24). A total of 40 mice were pretreated with the antiresistin neutralizing antibody (nAb) or isotype IgG for 1 hour and further administered DOX or saline for 5 days. The mice were divided into 4 groups: saline-IgG, saline-nAb, DOX-IgG, and DOX-nAb (N = 10). Cardiac injury, cardiomyocyte apoptosis, inflammatory factors, and the biomarkers of M1 and M2 macrophages in each group were analyzed. DOX administration increased the expression of resistin. DOX treatment exacerbated the loss of body and heart weight and cardiac vacuolation in mice. The antiresistin nAb reversed these conditions, downregulated the expression of myocardial injury markers, and decreased apoptosis. In addition, the antiresistin nAb decreased p65 pathway activation, decreased M1 macrophage differentiation and the expression of related inflammatory factors, and increased M2 macrophage differentiation and the expression of related inflammatory factors. The antiresistin nAb protected against DOX-induced cardiac injury by reducing cardiac inflammation and may be a promising target to relieve DOX-related cardiac injury.

ADSCs stimulated by resistin promote breast cancer cell malignancy via CXCL5 in a breast cancer coculture model

The tumor microenvironment represents one of the main obstacles in breast cancer treatment owing to the presence of heterogeneous stromal cells, such as adipose-derived stem cells (ADSCs), that may interact with breast cancer cells and promote cancer development. Resistin is an adipocytokine associated with adverse breast cancer progression; however, its underlying mechanisms in the context of the breast tumor microenvironment remain largely unidentified. Here, we utilized a transwell co-culture model containing patient-derived ADSCs and breast cancer cell lines to investigate their potential interaction, and observed that breast cancer cells co-cultured with resistin-treated ADSCs (R-ADSCs) showed enhanced cancer cell growth and metastatic ability. Screening by proteome arrays revealed that C-X-C motif chemokine ligand 5 (CXCL5) was released in the conditioned medium of the co-culture system, and phosphorylated ERK was increased in breast cancer cells after co-culture with R-ADSCs. Breast cancer cells treated with the recombinant proteins of CXCL5 showed similarly enhanced cell migration and invasion ability as occurred in the co-culture model, whereas application of neutralizing antibodies against CXCL5 reversed these phenomena. The orthotopic xenograft in mice by breast cancer cells after co-culture with R-ADSCs had a larger tumor growth and more CXCL5 expression than control. In addition, clinical analysis revealed a positive correlation between the expression of resistin and CXCL5 in both tumor tissues and serum specimens of breast cancer patients. The current study suggests that resistin-stimulated ADSCs may interact with breast cancer cells in the tumor microenvironment via CXCL5 secretion, leading to breast cancer cell malignancy.

Angiotensin II type 1 receptor (AT1) blockade by Telmisartan attenuates hepatic steatosis in high-fat fed mice reducing Resistin, TRL4, and Myd88 expression

BackgroundTelmisartan is a non-peptide angiotensin II receptor antagonist which acts by ACE/AngII/AT1 axis blockade (ARB). In the last years increasing evidence of its metabolic benefits pointed out this drug as the most promising ARB for nonalcoholic fatty liver disease (NAFLD) treatment. The aim of the present study was to investigate the Telmisartan effect on treating NAFLD in mice fed with a high-fat diet evaluating liver gene modulation. Twenty-four male mice were divided into four groups and fed for 60 days with a standard diet (ST), standard diet plus TEL (ST+TEL 5 mg/kg/day by gavage for 4 weeks), high-fat diet (HFD), or high-fat diet plus TEL (HFD+TEL 5 mg/kg/day by gavage for 4 weeks). Body weight, lipid profile, insulin, alanine transaminase, and aspartate aminotransferase were evaluated. Liver histology was analyzed. US imaging was performed to access liver dimension and echogenicity and also epididymal fat pad thickness. The expression of proinflammatory resistin/TRL4/MYD88 pathway was analyzed.ResultsThe main findings showed that TEL reduced the resistin, TRL4, and Myd88 liver expression in the HFD + TEL group when compared to the obese control group (HFD). Decreased hepatic steatosis in the HFD + TEL group demonstrated by US measurements of the liver longitudinal axis and echogenicity were observed. In addition, TEL reduced epididymal adipose pad thickness, body weight, transaminases, and improved glucose tolerance test and HDL cholesterol.ConclusionsWe observed that Telmisartan treatment improved metabolism, decreasing NAFLD.Graphical Telmisartan improves metabolic and lipid profile and liver steatosis of obese mice

Effect of short-term high fat diet on resistin levels and expression of autophagy-related genes in the cartilage of male rats

Obesity is a significant risk factor for the development of knee osteoarthritis (KOA). However, the precise molecular mechanisms linking obesity to OA remain unclear. In the present study, we investigated the effect of short-term high-fat diet (HFD) on the development of OA and the possible role of the adipokine resistin and autophagy-related genes in mediating this effect. Thirty adult male Wistar rats were equally divided into 2 groups: control and obese groups. Body mass index (BMI), levels of lipid profile, glucose, insulin and HOMA-IR index were significantly higher in the obese group compared with control. Our results revealed significantly higher serum and cartilage resistin levels with a significant increase in the mRNA expressions of toll-like receptor 4 (TLR4), matrix metalloproteinase-9 (MMP-9) and interleukin-1β (IL-1β) as well as protein levels of IL-1β, matrix metalloproteinase-13 (MMP-13), ADAMTS 5 (aggrecanase-2) and caspase-3 in the cartilage of obese rats. The HFD induced a significant upregulation of autophagy related 5 (ATG5), beclin-1 and light chain 3 (LC3) mRNA expressions and a significant downregulation of mammalian target of rapamycin (mTOR) expression in cartilage. The protein levels of cartilage ATG5 were also significantly elevated in HFD-fed group. In conclusion, we suggested that increased levels of resistin and expression of autophagy-related genes may contribute in part, to OA development in HFD-fed rats. This provides a novel insight into the early molecular changes in the cartilage associated with obesity.

Resistin Expression Is Associated With Interstitial Lung Disease in Dermatomyositis.

ObjectiveIn the current study, we aimed to assess resistin mRNA levels in the peripheral blood mononuclear cells (PBMCs) of dermatomyositis patients with interstitial lung disease (DM-ILD) and their correlation with disease activity.MethodsWe detected resistin mRNA levels in the PBMCs of 37 DM-ILD, 8 DM patients without ILD, and 19 healthy control (HC) subjects by performing quantitative reverse transcription real-time polymerase chain reaction analysis. Associations between resistin expression levels and major clinical manifestations, laboratory examinations, and disease activity were also analyzed. In addition, resistin expression in lung specimens from patients with DM-ILD was examined via immunohistochemistry and immunofluorescence.ResultsResistin mRNA levels in PBMCs were significantly higher in DM-ILD than that in DM patients without ILD and HCs (p = 0.043, 0.014, respectively). Among these DM-ILD patients, the resistin levels were significantly elevated in those with rapidly progressive ILD than in those with chronic ILD (p = 0.012). The resistin mRNA levels in DM-ILD positively correlated with serum alanine aminotransferase (r = 0.476, p = 0.003), aspartate aminotransferase (r = 0.488, p = 0.002), lactate dehydrogenase (r = 0.397, p = 0.014), C-reactive protein (r = 0.423, p = 0.008), ferritin (r = 0.468, p = 0.003), carcinoembryonic antigen (r = 0.416, p = 0.011), carbohydrate antigen 125 (r = 0.332, p = 0.047), interleukin-18 (r = 0.600, p < 0.001), and lung visual analog scale values (r = 0.326, p = 0.048), but negatively correlated with the diffusing capacity of carbon monoxide (DLco)% (r = −0.447, p = 0.041). Immunohistochemical analysis of resistin showed its elevated expression in the macrophages, alveolar epithelial cells, and weak fibrotic lesions from patients with DM-ILD. Immunofluorescence staining confirmed CD68+ macrophages co-express resistin.ConclusionsResistin levels were increased in patients with DM-ILD and associated with disease activity and ILD severity. Therefore, resistin may participate in the pathogenesis of DM-ILD and may act as a useful biomarker.

The Role of the Adipokine Resistin in the Pathogenesis and Progression of Epithelial Ovarian Cancer.

Obesity is a civilization disease associated with an increased risk of developing cardiovascular diseases, diabetes, and some malignancies. The results concerning the relationship between obesity and epithelial ovarian cancer (EOC) are inconclusive. The higher incidence of neoplasms in obese subjects has led to the development of the adipokine hypothesis. Omental adipocyte cells interact with cancer cells, promoting their migration and metastasis via the secretion of adipokines, growth factors, and hormones. One of the adipokines is resistin. It was shown in vitro that resistin stimulates the growth and differentiation of ovarian cancer cells. Moreover, it increases the level of angiogenesis factors, e.g., matrix metalloproteinase 2 (MMP-2) and vascular epithelial growth factor (VEGF). Additionally, resistin induces epithelial–mesenchymal transition (EMT) and stemness in EOC cell lines. A positive correlation has been shown between a higher level of resistin expression and the stage of histological differentiation of EOC or the occurrence of lymph node metastases. In addition, the overexpression of resistin has been found to act as an independent factor determining disease-free survival as well as overall survival in EOC patients. Growing evidence supports the finding that resistin plays an important role in some mechanisms leading to the progression of EOC, though this issue still requires further research.

The regulation of adipokines related to obesity and diabetes is sensitive to BDNF levels and adipose tissue location.

The role of BDNF in adipose tissue metabolism is poorly understood. We investigated the effects of decreased levels of BDNF on the expression of major adipokines in different fat depots (e.g., subcutaneous and epididymal) of mouse groups fed three different diet protocols. BDNF heterozygous (+ / -) mice were used to evaluate the effect of reduced BDNF levels. Six groups of C57BL/6J breed wild type (WT) and BDNF (+ / -) mice were formed. These groups were fed, respectively, a control diet (CD), a high-fat diet (HFD), and a high-sucrose diet (HSD) for 4months. Serum samples and adipose tissues were used for biochemical assays. The serum concentrations and tissue expression levels of leptin, adiponectin, and resistin were measured. Compared to the CD-fed WT group (control group), serum leptin and leptin expression levels were found to be higher in all experimental groups. Serum adiponectin levels were lower in the BDNF (+ / -) groups and HFD-fed WT group than in the control group. Epididymal adiponectin expression was found to be lower in the HFD-fed BDNF (+ / -) group and higher in HSD-fed groups than in the control group. Compared to the control group, adiponectin expression increased in the WT groups in subcutaneous adipose tissue. Serum resistin levels were elevated in the HFD-fed groups. Resistin expression in epididymal adipose tissue was lower in the CD-fed and HFD-fed groups than in the control group. BDNF levels and diet differentially affect the expression of adipokines in different fat tissues in the body. BDNF may play a protective role in obesity and diabetes.

Resistin production does not affect outcomes in a mouse model of acute surgical sepsis.

Because of the strong correlation between the blood concentration of circulating resistin and the illness severity of septic patients, resistin has been proposed as a mediator of sepsis pathophysiology. In vitro data indicate that human resistin directly impairs neutrophil migration and intracellular bacterial killing, although the significance of these findings in vivo remain unclear. The objectives of the present study were: (1) to validate the expression of human resistin in a clinically relevant, murine model of surgical sepsis, (2) to assess how sepsis-induced changes in resistin correlate with markers of infection and organ dysfunction, and (3) to investigate whether the expression of human resistin alters immune function or disease outcomes in vivo. 107 male, C57BL/6 mice transgenic for the human resistin gene and its promoter elements (Retn+/-/-, or Retn+) were generated on a Retn-/- (mouse resistin knockout, or Rko) background. Outcomes were compared between age-matched transgenic and knockout mice. Acute sepsis was defined as the initial 24 h following cecal ligation and puncture (CLP). Physiologic and laboratory parameters correlating to the human Sequential Organ Failure Assessment (SOFA) Score were measured in mice, and innate immune cell number/function in the blood and peritoneal cavity were assessed. CLP significantly increased circulating levels of human resistin. The severity of sepsis-induced leukopenia was comparable between Retn+ and Rko mice. Resistin was associated with increased production of neutrophil reactive oxygen species, a decrease in circulating neutrophils at 6 h and an increase in peritoneal Ly6Chi monocytes at 6 h and 24 h post-sepsis. However, intraperitoneal bacterial growth, organ dysfunction and mouse survival did not differ with resistin production in septic mice. Ex vivo resistin-induced impairment of neutrophil function do not appear to translate to increased sepsis severity or poorer outcomes in vivo following CLP.

The effect of Psidium guajava hydroalcoholic extract on reducing the expression of Resistin and TNF-α genes in articular chondrocytes of patients with knee osteoarthritis.

Knee osteoarthritis is the most common joint disease and the most important cause of disability in elderly patients. Due to the side effects of nonsteroidal anti-inflammatory drugs (NSAIDs) in the treatment of osteoarthritis, the use of herbs is recommended as an alternative treatment. The guava fruit can be considered as a natural medicine due to its antioxidant and anti-inflammatory properties. In this study, the effect of Psidium guajava hydroalcoholic extract was considered on reducing the expression of the resistin gene and TNF-α gene in articular chondrocytes of patients with knee osteoarthritis. For this purpose, cartilage chondrocytes of 10 Chinese patients with knee osteoarthritis, who were indicated for arthroplasty, were used for evaluating the effect of guava fruit on the expression of these genes. Articular chondrocytes were cultured under appropriate conditions and their viability was assessed by MTT assay. To increase the level of cytokines, cells were treated with lipopolysaccharide (LPS). They were kept in an incubator with 90% humidity at 37°C for the next steps. Then, the expression of the resistin gene and TNF-α gene was investigated by RNA isolation and cDNA preparation. The results showed that the expression of the resistin gene and TNF-α gene were reduced to 56.59% and 51.86%, respectively, by hydroalcoholic extract of guava fruit. Therefore, according to the results of this study and previous researches, the hydroalcoholic extract of guava fruit (Psidium guajava) can be considered as an effective complementary and alternative treatment for osteoarthritis of the knee.

Exosomal MALAT1 Derived from High Glucose-Treated Macrophages Up-Regulates Resistin Expression via miR-150-5p Downregulation.

Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays a crucial role in the pathophysiological process associated with diabetes-related complications. The effect of high glucose levels on macrophage-derived exosomal MALAT1 is unknown. Therefore, we investigated the molecular regulatory mechanisms controlling exosomal MALAT1 in macrophages under high glucose treatment and the therapeutic target of macrophage-derived exosomal MALAT1 using a balloon injury model of vascular disease in diabetic rats. High glucose (25 mM) significantly increased MALAT1 expression in macrophage-derived exosomes. MALAT1 suppressed miR-150-5p expression in macrophage-derived exosomes under high-glucose conditions. Silencing MALAT1 using MALAT1 siRNA significantly reversed miR-150-5p expression induced by macrophage-derived exosomes. Macrophage-derived exosomes under high-glucose treatment significantly increased resistin expression in macrophages. Silencing MALAT1 and overexpression of miR-150-5p significantly decreased resistin expression induced by macrophage-derived exosomes. Overexpression of miR-150-5p significantly decreased resistin luciferase activity induced by macrophage-derived exosomes. Macrophage-derived exosome significantly decreased glucose uptake in macrophages and silencing MALAT1, resistin or overexpression of miR-150-5p significantly reversed glucose uptake. Balloon injury to the carotid artery significantly increased MALAT1 and resistin expression and significantly decreased miR-150-5p expression in arterial tissue. Silencing MALAT1 significantly reversed miR-150-5p expression in arterial tissue after balloon injury. Silencing MALAT1 or overexpression of miR-150-5p significantly reduced resistin expression after balloon injury. In conclusion, high glucose up-regulates MALAT1 to suppress miR-150-5p expression and counteracts the inhibitory effect of miR-150-5p on resistin expression in macrophages to promote vascular disease. Macrophage-derived exosomes containing MALAT1 may serve as a novel cell-free approach for the treatment of vascular disease in diabetes mellitus.

Evaluation of Resistin and Fascin-1 Expression and their Correlation with Recurrence in the Patients of Oral Squamous Cell Carcinoma

Introduction: Squamous cell carcinoma is the most common epithelial malignancy of the oral cavity. The five years survival rate is approximately 50% and is even lower i.e, 30% in the patients with recurrence of this disease. Since recurrence has a major influence on five years survival, it becomes imperative to identify the molecular elements responsible for recurrence of oral squamous cell carcinoma. Aim: To evaluate the expression of resistin and fascin-1 and their correlation with recurrence in the patients of oral squamous cell carcinoma. Materials and Methods: A cohort study will be conducted in the Department of Oral Pathology, Sharad Pawar Dental College and Hospital, Wardha, Maharashtra, India. The duration of the study will be 24 months. A 4 μm thick section from paraffin embedded blocks of formalin fixed biopsy tissues of 60 cases having primary oral squamous cell carcinoma will be processed and stained for mouse monoclonal resistin (clone C-10) and mouse monoclonal fascin-1 (clone 55k-2) antibodies. Results: The results will be analysed by the correlation tests, Pearson and Spearman correlation coefficient. Conclusion: Local recurrence is influenced by site of tumour, depth of invasion, resection margins and lymphovascular spread. As recurrence is directly related to the poor prognosis and survival rate in the patients of oral squamous cell carcinoma, so it is essential to identify molecular markers indicative of recurrence. Fascin and resistin markers could be used to identify a subset of oral squamous cell carcinoma patients which are prone to recurrence.

Down Regulation of Chemerin and Resistin in Type II Diabetic Rats Treated With Silver Nanoparticles Synthetized Using Eryngium thyrsoideum Boiss Extract

Introduction: Diabetes is related to the higher production of inflammatory markers such as chemerin and resistin. Hypoglycemic influences of Eryngium thyrsoideum Boiss and silver nanoparticles (SNPs) have been established. The present study investigated the impacts of chemically or biologically synthesized SNPs using E. thyrsoideum extract on chemerin and resistin gene expressions in type II diabetic rats. Methods: Twenty male Wistar rats weighing 180-200 g were used. Type 2 diabetes was induced by nicotinamide and streptozotocin. Saline and 2.5 mg/kg chemically or biologically synthesized SNPs were injected to diabetic rats for two weeks. Five healthy rats received saline for two weeks. One day after the last injection, fasting blood samples were collected. Mean serum concentrations of glucose, creatinine, urea, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were measured by spectrophotometry. The gene expression of chemerin and resistin was determined by real-time polymerase chain reaction (PCR). Results: Mean serum concentrations of glucose, urea, ALT, AST, and mean relative gene expression of chemerin and resistin remarkably decreased in the diabetic group receiving SNPs prepared by either the chemical method or using Eryngium extract compared to the diabetic control group. Serum creatinine concentration did not change significantly in the control diabetic or diabetic groups receiving SNPs prepared either chemically or using the Eryngium extract. Conclusion: Chemically or green synthesized SNPs prevent liver hepatocyte damage. They reduced inflammatory factors via exerting hypoglycemic effects.

P38 MAPK pathway regulates the expression of resistin in porcine alveolar macrophages via Ets2 during Haemophilus parasuis stimulation

Haemophilus parasuis is a widespread bacterial pathogen causing acute systemic inflammation and leading to the sudden death of piglets. Resistin, a multifunctional peptide hormone previously demonstrated to influence the inflammation in porcine, was extremely increased in H. parasuis-infected tissues. However, the mechanism of resistin expression regulation in porcine, especially during pathogen infection, remains unclear. In the present study, we explored for the first time the transcription factor and signaling pathway mediating the expression of pig resistin during H. parasuis stimulation. We found that H. parasuis induced the expression of pig resistin in a time- and dose-dependent manner via the transcription factor Ets2 in porcine alveolar macrophages during H. parasuis stimulation. Moreover, the expression of Ets2 was mediated by the activation of the p38 MAPK pathway induced by H. parasuis, thus promoting resistin production. These results revealed a novel view of the molecular mechanism of pig resistin production during acute inflammation induced by pathogenic bacteria.

Dietary supplementation of inulin alleviates metabolism disorders in gestational diabetes mellitus mice via RENT/AKT/IRS/GLUT4 pathway

BackgroundGestational diabetes mellitus (GDM) has significant short and long-term health consequences for both the mother and child. There is limited but suggestive evidence that inulin could improve glucose tolerance during pregnancy. This study assessed the effect of inulin on glucose homeostasis and elucidated the molecular mechanisms underlying the inulin-induced antidiabetic effects during pregnancy.MethodFemale C57BL/6 mice were randomized to receive either no treatment, high-dose inulin and low-dose inulin for 7 weeks with measurement of biochemical profiles. A real-time2 (RT2) profiler polymerase chain reaction (PCR) array involved in glycolipid metabolism was measured.ResultsInulin treatment facilitated glucose homeostasis in a dose-dependent manner by decreasing fasting blood glucose, advanced glycation end products and total cholesterol, and improving glucose tolerance. Suppressing resistin (RETN) expression was observed in the inulin treatment group and the expression was significantly correlated with fasting blood glucose levels. The ratios of p-IRS to IRS and p-Akt to Akt in liver tissue and the ratio of p-Akt to Akt in adipose tissue as well as the expression level of GLUT4 increased significantly after inulin treatment.ConclusionsOur findings indicated improvement of glucose and lipid metabolism by inulin was to activate glucose transport through the translocation of GLUT4 which was mediated by insulin signaling pathway repairment due to decreased expression of RETN and enhanced phosphorylation of IRS and Akt in GDM mice.

Evaluation of Resistin Levels in Gingival Crevicular Fluid in Diabetic Patients with And without Chronic Periodontitis

Background: Resisting, a newly identified adipocyte secreted hormone may hold a value as an inflammatory mediator, associated with insulin resistance and periodontitis. The aim of the study was to determine the resistin levels in diabetic patients with and without chronic periodontitis. Materials and Methods: A total of 80 patients (both Male and Female) participated in the study. Subjects were categorized into four groups (20 each); the group I (healthy), group II (generalized chronic periodontitis), group III (generalized chronic periodontitis without diabetes mellitus), and group IV (generalized chronic periodontitis with Diabetes Mellitus). The clinical parameters, which included plaque index (PI), gingival index (GI), probing pocket depth (PPD) and clinical attachment level (CAL), random blood sugar level (RBS), glycated haemoglobin (HbA1c) were recorded. All the assessments were performed at baseline. GCF samples were collected. Resistin was examined by utilizing a monetarily accessible ELISA unit. Contrasts among groups were statistically analysed. Results: The expression of resisting was significantly increased between the diseased subjects when compared to healthy subjects and was statistically significant (p&lt; 0.001). When all the samples were analyzed together, a significant positive correlation (p &lt;0.001) was observed between GCF resistin expression, clinical parameters (GI, PI, PPD, CAL) &amp; biochemical parameters (RBS and HbA1c). Conclusion: Resisting levels are increased in CP and T2DM. Hence, GCF resistin levels may be considered as a potential inflammatory marker for periodontitis with T2DM

Resistin levels in the gingival crevicular fluid among diabetic and non-diabetic chronic periodontitis patients

It is of interest to document theresistin levels in chronic periodontitis patients (CP) with or without type 2 diabetes mellitus (T2DM) in the gingival crevicular fluid (GCF).The expression of resistin was significantly higher in chronic periodontitis when compared to the periodontally healthy groups. Resistin levels were high in CP and T2DM. Therefore, GCF resistin levels is of interest as a potential incendiary marker for periodontitis with T2DM.

Resistin levels in the gingival crevicular fluid among diabetic and non-diabetic chronic periodontitis patients

It is of interest to document theresistin levels in chronic periodontitis patients (CP) with or without type 2 diabetes mellitus (T2DM) in the gingival crevicular fluid (GCF).The expression of resistin was significantly higher in chronic periodontitis when compared to the periodontally healthy groups. Resistin levels were high in CP and T2DM. Therefore, GCF resistin levels is of interest as a potential incendiary marker for periodontitis with T2DM.

Expression and role of resistin on steroid secretion in the porcine corpus luteum

Resistin plays an important role in adipogenesis, obesity, insulin resistance, and reproduction. Previous studies showed resistin action on ovarian follicular cells; however, whether resistin regulates steroid secretion in luteal cells is still unknown. Our aim was first to determine the expression of resistin and its potential receptors (tyrosine kinase-like orphan receptor 1 (ROR1) and toll-like receptor 4 (TLR4)) in the porcine corpus luteum (CL), regulation of its expression, effect on kinases phosphorylation, and luteal steroidogenesis. Our results showed that the expression of resistin and its receptors was dependent on the luteal phase and this was higher at the mRNA level in the late compared with the early and middle luteal phase. At the opposite, resistin protein expression was higher in the middle and late compared with the early luteal phase, while ROR1 and TLR4 expression was highest in the early luteal phase. Additionally, we observed cytoplasmic localisation of resistin, ROR1, and TLR4 in small and large luteal cells. We found that luteinising hormone, progesterone (P4), insulin, and insulin-like growth factor 1 regulated the protein level of resistin, ROR1, and TLR4. Resistin decreased P4 and increased oestradiol (E2) secretion via changes in steroidogenic enzymes expression and via the activation of protein kinase A (PKA) and mitogen-activated protein kinase (MAP3/1), increased the expression of receptors LHCGR and ESR2 and decreased the expression of PGR. Moreover, resistin decreased PKA phosphorylation and enhanced MAP3/1 phosphorylation. Taken together, resistin could act directly on steroid synthesis and serve as an important factor in in vivo luteal cell function.