Resistin Gene Research Articles

Association between the RETN -420C/G polymorphism and type 2 diabetes mellitus susceptibility: A meta-analysis of 23 studies.

The published findings on the link between the resistin (RETN) gene polymorphism and type 2 diabetes mellitus (T2DM) risk are still contradictory. Here, through a meta-analysis, we summarized a more precise evaluation of their connection by synthesizing existing research. PubMed, Google Scholar, and Web of Science were electronically searched, and all cited sources were manually searched. The heterogeneity of effects was tested and all statistical analyses were performed in Stata 12.0. A total of 23 studies with 10,651 cases and 14,366 controls on RETN -420C/G polymorphism were included. The overall results showed that the association of RETN -420C/G polymorphism and T2DM susceptibility was not significant [for the allelic model: odds ratio (OR) = 0.98, 95% confidence interval (CI) = 0.87-1.10, pheterogeneity <.001; I 2 = 84.6%; for the dominant model: OR = 0.96, 95% CI = 0.80-1.15, pheterogeneity <.001; I 2 = 87.1%; and for the recessive model: OR = 0.96, 95% CI = 0.82-1.12, pheterogeneity <.001; I 2 = 56.9%] but with high heterogeneity across studies (p <.0001). Meta-regression found that the median age of T2DM participants (using age 50 as the cutoff) could be a factor in the observed variation. The RETN -420C/G polymorphism seems to be linked to an increased risk of T2DM in younger individuals [for dominant: OR = 0.84 (95% CI, 0.72-0.98; pheterogeneity <.001; I 2 = 80.9%)] and decreased risk in older people [for dominant: OR = 3.14 (95% CI, 2.35-4.19; pheterogeneity = .98; I 2 = 0.0%)]. Current results found no evidence that the RETN -420C/G variant was linked to T2DM susceptibility, but the patient's age appears to be a potential factor that contributed to high heterogeneity across studies. Additional high-quality and well-designed investigations are required to confirm these results.

RESISTIN GENE POLYMORPHISM AND NONALCOHOLIC FATTY LIVER DISEASE RISK.

Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease and one of the main global health issues in which liver fat surpasses 5% of hepatocytes without the secondary causes of lipid accumulation or excessive alcohol consumption. Owing to the link between NAFLD and insulin resistance (IR) and obesity and the role of resistin in theses metabolic disorders, we explored the possible association between resistin gene (RETN) variant and NAFLD. A total of 308 unrelated subjects, including 152 patients with biopsy-proven NAFLD and 156 controls were enrolled and genotyped for the RETN gene rs3745367 variant using PCR-RFLP method. NAFLD patients had higher liver enzymes, systolic blood pressure (SBP), and diastolic blood pressure (DBP) than the controls (P<0.001). However, we observed no significant difference in genotype and allele frequencies between the cases with NAFLD and the controls for the RETN rs3745367 polymorphism either before or after adjustment for confounding factors including age, BMI, sex, smoking status, SBP, and DBP. To our knowledge, this study is the first one that investigated the association between RETN gene rs3745367 variant and biopsy-proven NAFLD. Our findings do not support a role for this gene polymorphism in NAFLD risk in Iranian population; nonetheless, they need to be further investigated in other populations.

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.

Modulating effects of steviol and steviol glycosides on adipogenesis, lipogenesis, glucose uptake and insulin resistance in 3T3-L1 adipocyte model

• Stevia-derived compounds modulate adipogenic and lipogenic gene expression. • Steviol decreases lipid accumulation in mature 3T3-L1 adipocytes. • Steviol and stevioside improve glucose uptake and mitigate insulin resistance. Stevia rebaudiana Bertoni is famous for sweetness due to the content of steviol glycosides (SG). This study aimed to determine the effect of SG (stevioside, rebaudioside A) and steviol on adipogenesis and lipogenesis in the 3T3-L1 model. Test compounds were also analysed for their ability to affect glucose uptake in hypertrophied insulin-resistant 3T3-L1 adipocytes. The most active compound in modulating adipogenesis, lipogenesis and insulin resistance was steviol, SG metabolism product. Steviol (10 μM, 100 μM) significantly down-regulated the expression of adipogenic transcription factors (PPARγ, C/EBPα, SREBP1) and lipogenic genes (FAS, aP2, LPL), which caused decreased lipid accumulation and triglyceride content in adipocytes. Treatment of insulin-resistant adipocytes with steviol (1 μM) and stevioside (1 μM, 10 μM) increased GLUT-4 transcript level and improved glucose uptake. Steviol also lowered resistin gene expression, which may mitigate insulin resistance in hypertrophied adipocytes. This study promotes SG as potential health-promoting ingredients in low-calorie functional foods.

The Effects of Resistin Gene Polymorphism on Pain Thresholds and Postoperative Sufentanil Consumption in Gastric Cancer Patients.

PurposeAs an adipocyte-secreted hormone, resistin is linked to inflammation, insulin resistance and atherosclerosis. Currently, resistin is proposed as a novel biomarker for postoperative pain intensity. However, due to the various types of surgery and limited numbers of studies, previous conclusions should be validated. This study aimed to explore the effect of resistin polymorphism (rs3745367) on pain thresholds and sufentanil consumption in gastric cancer patients.Patients and MethodsA total of 148 gastric cancer patients enrolled in this study had their pain thresholds measured before surgery. After the exclusion of 16 patients, the characteristics of demography and clinic, numerical rating scale (NRS) and sufentanil consumption of 132 patients were recorded. Rs3745367 of resistin was identified by Sanger sequencing. Multivariate linear regression analysis was performed for sufentanil consumption and mechanical pain threshold.ResultsThe distributions of the GG, AG, and AA genotypes of rs3745367 among the participants were 54 (40.9%), 65 (49.2%), and 13 (9.9%), respectively. The mechanical pain threshold (P=0.04) and postoperative sufentanil consumption in the 1st 24 h (P=0.03) were significantly different among GG, AG, and AA genotype carriers. There was no significant difference among the three genotypes for the heat pain threshold and cold pain threshold. Regarding the NRS, no statistically significant difference among the three different genotypes was found 24 h postoperatively.ConclusionRs3745367 of resistin is associated with the mechanical pain threshold and postoperative sufentanil consumption in gastric cancer patients. Patients with the AA genotype of rs3745367 present an increased mechanical pain threshold and decreased postoperative sufentanil consumption.

RETN Gene Single Nucleotide Polymorphism Profile on Triglyceride-Glucose Index as Insulin Resistance Proxy Among Cohort Population of Non-Communicable Diseases in Bogor

Genetic factors such as single nucleotide polymorphisms (SNPs) are thought to contribute to the increasing incidence of diabetes mellitus (DM) through insulin resistance. SNPs in the RETN (resistin) gene encoding the resistin protein have been reported to play a role in causing abnormalities in blood glucose and lipid metabolism. Still, studies related to this have rarely been explored in cohort population models. This study aimed to evaluate the relationship of resistin gene SNPs to the trend of the triglyceride-glucose index (TyG) as a proxy for insulin resistance. The data were obtained from the results of the biomedical laboratory examination among participants of a cohort study in the Kebon Kalapa subdistrict, Bogor, every odd year period between 2015-2021 and from RETN genotyping (rs3745367). The generalized linear model (GLM) repeated measurement technique was used with the TyG index value as the dependent variable. The results of the GLM analysis showed that although there was a significant difference in the trend of the TyG index between the observation periods [F(2,87, 1671,1)=41,10, p-value &lt;0.001], that’s not the case for RETN gene SNP [F(5,73, 1671,1) = 1.09, p-value = 0.367]. However, the multivariate test results suggested the association of these SNPs with age and DM status [F(4, 583)=2.48, p-value = 0.043]. In conclusion, RETN gene SNPs may require interaction with other factors or genes to induce insulin resistance or act by indirect glucose–fatty acid metabolic cycle mechanisms.

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.

Positive association of -420C > G single nucleotide polymorphism in resistin gene promoter with insulin resistance indices in diabetic type 2 patients

IntroductionResistin is considered as an important adipocytokine that may have an association with obesity and insulin resistance. The association of resistin gene polymorphism with type 2 diabetes has been proved. In this study, we aim to investigate the association between polymorphism (rs1862513 RETN) of the promoter resistin gene and susceptibility to type 2 diabetes in Zanjan province of Iran. Methods and materialsOne hundred seventy five patients with type 2 diabetes and 175 non-diabetic individuals were participated in this case-control study. The DNA was extracted from the whole blood. Genotyping was performed using Restriction Fragment Length Polymorphism (RFLP)-PCR method technique for all individuals. The relationship between genotypes, clinical and biochemical variables such as age, fasting blood sugar and blood pressure (BP) were evaluated by automatic enzymatic method. ResultsThe current study showed that the genotype distribution of resistin gene promoter variant was different between diabetic and nondiabetic groups. The frequency of GG genotype in diabetes patients and non-diabetic subjects was 17.1% and 9.7%, respectively which considered this genotype as significant (OR = 2.168, CI = 1.106–4.252 and P = 0.024). The present study showed this polymorphism may contribute to diabetes susceptibility. ConclusionMultivariate Logistic regression models by considering confounding showed that variables such as high-density lipoprotein, Body mass index (BMI), sex and age has greater predictive validity than GG genotype. In addition, more studies with greater sample sizes is required to confirm our results.

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.

Role of the rs10401670 variant in the resistin gene on the metabolic response after weight loss secondary to a high-fat hypocaloric diet with a Mediterranean pattern.

The single nucleotide polymorphism (SNP) (rs10401670) of the RETN gene has been associated with metabolic disorder in obese subjects and has scarcely been evaluated after dietary interventions. The present study aimed to analyse the effects of the rs10401670 RETN gene polymorphism on metabolic changes secondary to weight loss and secondary to a high-fat hypocaloric diet with a Mediterranean dietary pattern. A Caucasian population comprising 284 obese patients without diabetes mellitus was analysed. Before and after 3 months of a high-fat hypocaloric diet with a Mediterranean pattern, an anthropometric evaluation, an assessment of nutritional intake and a biochemical analysis were performed. A statistical analysis was conducted for the combined CT and TT as a group and for wild-type CC as a second group. Decreases in weight, body mass index (BMI), fat mass, systolic blood pressure and waist circumference were similar in both genotypes groups. In T allele carriers, insulin, homeostatic model assessment for insulin resistance (HOMA-IR), triglycerides and C-reactive protein levels were decreased. The decrease in these parameters was statistically significant for triglycerides (-22.3 ± 9.3 mgdl-1 : p = 0.03), C-reactive protein (-2.8 ± 0.5 mgdl-1 : p = 0.03), insulin (-7.4 ± 2.9 mUIL-1 : p = 0.03) and HOMA-IR (-2.4 ± 1.0: p = 0.02). Leptin levels were decreased in both genotypes groups after the hypocaloric diet, as well as the anthropometric parameters BMI, weight, waist circumference and fat mass. Resistin and adiponectin levels remained unchanged in both groups. In the present study, we have detected a significant association between the T allele of this SNP and a better response of insulin resistance, triglycerides and C-reactive protein compared to non T allele carriers after weight loss with a high-fat hypocaloric diet and a Mediterranean diet.

Vertebral osteomyelitis is characterised by increased RANK/OPG and RANKL/OPG expression ratios in vertebral bodies and intervertebral discs.

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

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.

Effects of rosuvastatin and metformin on resistin levels in subcutaneous, epicardial and perivascular adipose tissues of patients with ischemic heart disease

Abstract The aim of the study was to assess the level of resistin in local fat depots and the possibility of correcting the level of resistin using rosuvastatin and metformin. Methods This study was performed at the Federal State Budgetary Institution's Research Institute for Complex Issues of Cardiovascular Diseases. The study included 84 patients with ischemic heart disease (IHD), who were planned to undergo coronary artery bypass grafting (CABG). The average age of the patients was 63.8 (50.1; 68.6) years. Patients were included in the study after they provided written informed consent. In order to study the combined effect of atorvastatin and metformin on the functional activity of adipocytes in the SAT, EAT, and PVAT, isolated adipocytes were cultured for 24 hours with the addition of drugs at different concentrations: 1 μmol/L atorvastatin (SigmaAldrich, China) + 1 mmol/L metformin (USP, Norway); 5 μmol/L atorvastatin + 10 mmol/L metformin. Then, the expression of mRNA resistin genes (RSTN) was assessed. Statistical analysis was performed using GraphPad Prism 6 (GraphPad Software), nonparametric tests, and multivariate statistics methods. Results The level of RSTN expression in the EAT was the highest compared to the SAT (2.6 times, p=0.0014) and the PVAT (1.9 times, p=0.0017). The level of secretion of the resistin in the culture medium of adipocytes corresponded to the expression of the resistin gene. Cultivation of adipocytes with rosuvastatin showed that low concentrations (1 μmol/L) did not have a significant effect on the functional activity of adipocytes. At the same time, 5 μmol/L rosuvastatin reduced the level of RSTN expression and protein secretion, but only in subcutaneous adipocytes in compared with control. Culturing adipocytes with metformin at a concentration of 10 mmol/L reduced the level of RSTN expression and protein secretion in the culture medium in all three adipose tissues. At the same time, 1 mmol/L metformin did not have a significant effect. The use of a combination of the drugs rosuvastatin and metformin at various concentrations led to a decrease in the RSTN expression in the SAT, EAT, and PVAT, but only when 5 μmol/L rosuvastatin + 10 mmol/L metformin were used. Conclusion Thus, the level of resistin in adipocytes of adipose tissue of patients with IHD is influenced only by rosuvastatin at a concentration of 5 μmol/L and only on adipocytes of adipose tissue, reducing the level of RSTN expression and protein secretion in the culture medium. Metformin was more effective than rosuvastatin and at high concentrations (10 mmol/L) reduced RSTN expression and protein secretion in the culture medium regardless of the localization of adipocytes. The combined use of high concentrations of rosuvastatin (5 μmol/L) and metformin (10 mmol/L) of patients with IHD had a comparable effect with metformin at a concentration of 10 mmol/L. Funding Acknowledgement Type of funding sources: None.

Serum resistin levels and resistin gene polymorphism in patients with acne vulgaris: does it correlate with disease severity?

Acne vulgaris is a disease that inflames the sebaceous gland with multiple etiologies. Many proinflammatory adipokines contribute to this pathogenesis. Resistin is a proinflammatory mediator that activates kappa B, a nuclear factor, and c-Jun N-terminal kinases pathways inducing toll-like receptor-2, interleukin-1, 6, and tumor necrosis factor alpha. Resistin gene affects the promoter and intron regions' polymorphisms' expression levels. We aimed to study the association of resistin gene polymorphisms (RETN -420 C/G) and the development of acne vulgaris and whether it is associated with serum resistin levels and disease severity. Resistin (RETN) gene (rs1862513) genotypes were identified using restriction fragment length polymorphism (RFLP), and serum resistin presence was assessed by enzyme-linked immunosorbent assay in 40 patients with acne vulgaris and 40 age- and sex-matched healthy controls as a cross-reference. Patients were divided into mild, moderate, and severe groups. Global Acne Grading System (GAGS) was used to assess the severity of acne vulgaris. CG and GG genotypes were present in cases (P = 0.006) odds ratio (OR)1 = 4.43; 95% confidence interval (CI) (1.53, 12.7) and OR2 = 5.47; 95% CI (0.99, 30.1); G-allele statistically dominated in the patient group where P = 0.001 and OR = 3.57; 95% CI (1.63, 7.80). A positive significant relationship between RETN genotypes and serum resistin levels and GAGS score was present. RETN genes rs1862513 GG and G allele are correlated to acne vulgaris development and severity in a sample of the Egyptian population. This study comprised a small sample size. The cases may not accurately represent the general population; only one clinic was enrolled in the study.

Association between resistin gene (-420 C>G) polymorphism and acne vulgaris.

Acne vulgaris (AV) is the most prevalent inflammatory skin disease and develops on the face and upper trunk. Resistin, a member of the cysteine-rich secretory proteins family, is an adipokine expressed primarily in macrophages and monocytes; it has a role to play in the inflammatory period. This study's purpose was to detect whether known resistin gene (-420 C>G) polymorphism plays a role in the pathogenesis of AV. Patients with AV (n=94) and healthy controls (n=94) were enrolled in this investigation. Resistin gene (-420 C>G) polymorphism was decided by PCR-RFLP procedure. The distribution of genotype frequencies of resistin gene (-420 C>G) polymorphism was significantly different between the AV and healthy controls (p=0.002). We found that the resistin gene (-420 C>G) CG genotype exhibited a significant association with decreased acne vulgaris risk. Our study is the first report investigating the relationship between the risk of AV and resistin gene (-420 C>G) polymorphism in the Turkish population. Resistin gene (-420 C>G) polymorphism is related to AV pathogenesis. CG genotype has a protective role and may be linked to a reduced risk of AV development. Furthermore, studies are needed to verify these findings in other populations.

4-Thiazolidinone-based derivatives do not affect differentiation of mouse embryo fibroblasts (3T3-L1 cell line) into adipocytes

Nowadays, diabetes mellitus type 2 (T2DM) is a serious problem in western European societies and in the United States. Thiazolidinediones (TZDs) are a broad group of compounds used to decrease insulin resistance in TDM2. To date, it has been believed that TZDs act mainly through activation of peroxisome proliferator-activated receptor gamma (PPARγ). The PPARγ receptor is important in differentiation of preadipocytes into mature adipocytes. Therefore, given the potential of structurally related thiopyrano[2,3-d]thiazoles Les-2194 and Les-3377 and 4-thiazolidinone derivative Les-3640 to interact with the PPARγ receptor, the aim of the present study was to evaluate the impact of the 4-thiazolidinone-based derivatives mentioned above on the process of 3T3-L1 cell line differentiation into adipocytes. In the first part of our study, we prove that Les-2194, Les-3377, and Les-3640 are cytotoxic to 3T3-L1 cells. In the next stage, we determine that Les-2194, Les-3377, and Les-3640 stimulate lipid accumulation (using the ORO staining method) and induce specific gene expression (Dlk1, Fabp4, Vegfa, Pai-1, Resistin, Adiponectin, and Pparγ). Our data show that rosiglitazone, pioglitazone, Les-2194, and Les-3640 at a concentration of 2 μM do not affect 3T3-L1 cell viability and do not activate the apoptotic process. Only Les-3377 decreased the number and metabolism of the cells. Although all the studied compounds influenced the expression of Dlk1, Fabp4, Vegfa, Pai-1, Resistin, Adiponectin, and Pparγ genes, none of them caused gene expression similar to that induced by rosiglitazone or pioglitazone. The ORO staining showed that rosiglitazone and pioglitazone induced lipid accumulation in the 3T3-L1 cell line, which is a marker of mature adipocytes. Only rosiglitazone increased Pparγ protein expression after 14 days of differentiation.

Adipokine signatures of subcutaneous and visceral abdominal fat in normal-weight and obese women with different metabolic profiles.

IntroductionMetabolic syndrome arises from abnormal adipose function accompanied by insulin resistance. As early factors reflecting/impacting lipid storage dysfunction of adipose tissues, we sought to determine adipokine levels in subcutaneous and visceral adipose tissues (SAT and VAT).Material and methodsGene and protein expression levels of leptin, adiponectin, and resistin were analysed in SAT and VAT of normal-weight and overweight/obese women, subclassified according to insulin resistance index, triglyceride, total, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol levels into metabolically healthy and “at risk” groups.ResultsCompared with normal-weight women, obese women had higher serum leptin levels (p < 0.05), as well as increased leptin gene and protein expression in VAT. Conversely, expression levels of leptin were lower in SAT of obese women, and minor in the SAT of “at risk” groups of women, compared with weight-matched healthy groups. In addition, lower adiponectin levels were detected in SAT of metabolically healthy obese women (p < 0.01), and lower in SAT and VAT (p < 0.05) of “at risk” obese women compared to healthy, obese women. Significant differences in resistin levels were only observed in obese women; resistin gene expression was higher in VAT and SAT of obese, compared to normal-weight women. However, higher gene expression was not consistent with protein expression of resistin.ConclusionsLow adiponectin in both examined adipose tissues and inappropriate leptin expression levels in SAT appear to be important characteristics of obesity-related metabolic syndrome. Intriguingly, this adipokine dysregulation is primary seen in SAT, suggesting that endocrine dysfunction in this abdominal depot may be an early risk sign of metabolic syndrome.

Resistin -420 C&gt;G Polymorphism in Female Patients of Acne in Pakistan

Acne vulgaris is an inflammatory skin disorder of pilosebaceaous units. The clinical characteristics are seborrhea, sebaceous glands, non inflammatory lesions, inflammatory lesions and severe scaring. Propionibacterium acnes are the main pathophysiological factor influencing the acne development. Resistin gene is a novel proinflammatory cytokine involved in the initiation of inflammatory disorders like cardiovascular diseases, obesity and atherosclerosis. Various SNPs have been discovered in human RETN gene which is involved in different inflammatory disorders. Purpose of this study was to analyze RETN -420 C&gt;G polymorphism in female acne patients of Pakistani population. About 58 control female subjects and 76 acne female patients were recruited for this study. In order to examine the RETN -420 C&gt;G polymorphism in the promoter region, PCR and RFLP techniques were used. Statistically significant P value &lt;0.05 for the RETN -420 C&gt;G polymorphism was obtained in genotype/alleles frequencies between acne patients and control female subjects. Significant association between genotype frequencies, disease severity and acne scars distribution among female patients was also observed. It is concluded that RETN -420 promoter polymorphism was not associated with family history and skin types; however it was significantly associated with acne pathopysiology

Hypothyroidism and Obesity: Resistin May Inversely be Associated with Thyroid Function

Resistin plays an important role in the body’s metabolic system and its devastation is associated with obesity. Thyroid hormones also play a role in regulating the body’s overall metabolism. So in this experimental study, we tried to investigate the relationship between the resistin gene expression and thyroid hormones in Wistar rat. For experiments, 24 Wistar rats, were used to develop obesity (obese group, n=8) or hypothyroidism (hypothyroid group, n=8); also 8 rats were used as control. To cause obesity in obese rats, they were kept for 60 d and fed with a high fat diet. Propylthiouracil was used to induce hypothyroidism. Resistin messenger ribonucleic acid expression was evaluated by real time polymerase chain reaction in all rats. Data were compared between the groups of study by statistical package for the social sciences. The results showed that the obese group had a significantly higher weight than the two hypothyroid and control groups (p 0.05). The results of the study of the relative expression of resistin gene in the three study groups did not show a significant difference (p>0.05). However, the control group had less expression than the two obese and hypothyroid groups. Separating animals to 2 groups of high resistin and low resistin expression revealed higher triiodothyronine and thyroxine in a group of animals expressing low resistin (p<0.05). There were so many controversies between studies and this disagreement could be because of serum resistin. The short half-life of resistin cannot be considered for the study of resistin and as well as the human studies should also assess its expression.