Resistin Gene Expression Research Articles

Resistin Pathway as Novel Mechanism of Post-lung Transplantation Bronchial Stenosis.

Bronchial stenosis remains a significant source of morbidity among lung transplant recipients. Though infection and anastomotic ischemia have been proposed etiologies of the development of bronchial stenosis, the pathophysiologic mechanism has not been well elucidated. In this single-centered prospective study, from January 2013 through September 2015, we prospectively collected bronchoalveolar lavage (BAL) and endobronchial epithelial brushings from the direct anastomotic site of bronchial stenosis of bilateral lung transplant recipients who developed unilateral post-transplant bronchial stenosis. Endobronchial epithelial brushings from the contralateral anastomotic site without bronchial stenosis and BAL from bilateral lung transplant recipients who did not develop post-transplant bronchial stenosis were used as controls. Total RNA was isolated from the endobronchial brushings and real-time polymerase chain reaction reactions were performed. Electrochemiluminescence biomarker assay was used to measure 10 cytokines from the BAL. Out of 60 bilateral lung transplant recipients, 9 were found to have developed bronchial stenosis with 17 samples adequate for analysis. We observed a 1.56 to 70.8 mean-fold increase in human resistin gene expression in the anastomotic bronchial stenosis epithelial cells compared with nonstenotic airways. Furthermore, IL-1β (21.76±10.96pg/mL; control 0.86±0.44pg/mL; P <0.01) and IL-8 levels (990.56±326.60pg/mL; control 20.33±1.17pg/mL; P <0.01) were significantly elevated in the BAL of the lung transplant patients who developed anastomotic bronchial stenosis. Our data suggest that the development of postlung transplantation bronchial stenosis may be in part mediated through the human resistin pathway by IL-1β induced transcription factor nuclear factor-κβ activation and downstream upregulation of IL-8 in alveolar macrophages. Further study is needed in the larger patient cohorts and to determine its potential therapeutic role in the management of post-transplant bronchial stenosis.

Effect of Aerobic Training and Cinnamon on Expression of Resistin Gene in Adipose Tissue of Male Rats Fed with a High-Fat Diet

Background: The pathogenesis of obesity is very complex, and a number of factors are involved in its occurrence. To treat or control obesity and diabetes, various treatment methods, such as the use of natural and synthetic drugs or lifestyle modifications, are recommended for obese people. Exercise is an active lifestyle that can have beneficial effects on obese people. Due to people's concerns about the side effects of chemical drugs, including drug resistance, today in medicine, the use of herbal compounds with different properties, including cinnamon, has been considered by everyone. Objectives: In the current work, simultaneous application of cinnamon extract (CE) and aerobic practices were studied on the expression of the resistin gene (RG) in adipose tissue of male rats on a high-fat diet. Methods: The influence of 5 days a week of aerobic exercise for 6 weeks, along with a simultaneous high-fat diet (as an emulsion with the rate of 150 mL in excess of the routine diet) and consumption of CE (200 mg/kg), were studied. The expression of the RG in adipose tissue of male rats that received a high-fat diet in their daily food was assessed. Independent variables of the present study included performing 6 weeks of aerobic exercise, consumption of CE, and high-fat diet as the underlying variables. The mRNA expression of the proteins was evaluated using real-time PCR. The effect of variables on between-group and within-group changes was assessed using a one-way analysis of variance and the Bonferroni test. Results: Different patterns, including high-fat diet, cinnamon, and combinations of high-fat diet/cinnamon, high-fat diet/aerobic exercise, and high-fat diet/aerobic exercise, were significant on resistin in adipose tissue. Conclusions: The best results in terms of mitigating the adverse effects of diet on the expression of RG were observed for a combination of six weeks of exercise and CE. Therefore, the simultaneous utilization of aerobic exercise and CE is recommended.

Dry heat whole Sorghum BRS 305 flour modulate satiety and improves antioxidant response in brain of Wistar rats fed with high-fat high-fructose diet

Sorghum BRS 305 (Sorghum bicolor L. Moench) is a cereal with high tannins and anthocyanins content and keep better the resistant starch when submitted to dry heat treatment. Our objective was to investigate the effects of BRS 305 dry heat treatment whole sorghum flour on satiety and antioxidant response in brain and adipose tissue of Wistar rats fed with a high fat high fructose diet (HFHF). Male Wistar rats were divided in two groups: control (n = 8) and HFHF (n = 16) for eight weeks. After, animals of HFHF group were divided: HFHF (n = 8) and HFHF + BRS 305 sorghum whole flour (n = 8), for 10 weeks. Sorghum consumption reduced gene expression of leptin, resistin, and endocannabinoid receptor 1 type (CB1) in adipose and brain tissues compared to HFHF group. In brain, sorghum consumption also promotes reduction in neuropeptide Y (NPY) gene expression. BRS305 sorghum consumption improved gene expression of sirtuin-1 (SIRT1) in adipose tissue, and in the brain increased heat shock protein 72 (HSP72), erythroid-derived nuclear factor 2 (NRF2), peroxisome proliferator-activated receptor alpha (PPARα), superoxide dismutase (SOD) and catalase activity compared to HFHF. In silicoanalysis showed interaction with PPARα, CB1, and leptin receptors. Advanced glycation end products (AGEs) concentrations in group HFHF + sorghum did not differ from HFHF group. Advanced glycation end products receptors (RAGEs) concentrations did not differ among experimental groups. Then, BRS 305 sorghum submitted to dry treatment was able to modulate gene expression of markers related to satiety and improve antioxidant capacity of rats fed with HFHF diet.

Upregulation of peripheral blood mononuclear cells resistin gene expression in severe obstructive sleep apnea and obstructive sleep apnea with coexisting type 2 diabetes mellitus.

Obstructive sleep apnea (OSA) is characterised by increased systemic inflammation, and is often accompanied with type 2 diabetes mellitus (T2DM) and cardiovascular disease. The aim of this investigation was to evaluate gene expression of resistin, its receptor CAP1 and CD36 as the indicators of the inflammatory changes in PBMCs in relation to the severity of OSA, and the presence of type 2 diabetes mellitus (T2DM) in OSA. Severity of OSA was defined by the apnea/hypopnea index (AHI): AHI < 30: mild to moderate OSA (MM-OSA), AHI ≥ 30: severe OSA (S-OSA). Presence of T2DM was captured: OSA with T2DM (OSA + T2DM), OSA without T2DM (OSA-T2DM). PBMC resistin, CAP1, and CD36 mRNA were determined by real-time PCR. Resistin mRNA was significantly upregulated in S-OSA(N = 54) compared to the MM-OSA (N = 52,P = 0.043); CAP1 and CD36 mRNA levels did not differ between the groups (P = 0.302; P = 0.166, respectively). Resistin mRNA was significantly upregulated in OSA + T2DM (N = 29)compared to the OSA-T2DM (N = 77,P = 0.029); CAP1 and CD36 mRNA levels did not differ between the groups (P = 0.662; P = 0.108, respectively). AHI and T2DM were independent predictors of resistin mRNA above the 75th percentile (OR = 3.717[1.152-11.991]; OR = 3.261[1.000-10.630], P = 0.042 respectively). Resistin gene upregulation in S-OSA indicates its possible contribution to increased inflammation in S-OSA and makes it a possible marker of the disease severity. Resistin gene upregulation in OSA + T2DM suggests that ajoint effect of these two comorbidities may have a major contribution to increased inflammation and complications that arise from this state.

Resistin gene expression: Novel study in dromedary camel (Camelus dromedarius)

Resistin, an adipocyte-specific hormone involved in insulin resistance and adipocyte differentiation, was initially identified in adipose tissue and macrophages. The physiological role of this molecule in camels remains largely unexplored. This study analysed for the first time blood and tissue levels of resistin as well as expression of resistin gene by real time PCR in adipose tissue (hump, visceral &amp; epididymal) and different muscles (gastrocnemius, heart and caecum) in dromedary camels. The results revealed that resistin concentration was significantly (P&lt;0.01) higher in epididymal adipose tissue as compared to other tissues and the lowest concentration was detected in serum. Additionally, the differential mRNA expression levels of resistin gene showed the highest expression level in epididymal adipose tissue as compared to other tissues. In conclusion, the results demonstrated for the first time that resistin was expressed in different tissues of dromedary camels. These data underscore an important facet of the physiological role of resistin as a factor involved in insulin resistance and glucose metabolism in camels.

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.

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.

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.

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.

Increased gene expression of resistin and CD36 in peripheral blood mononuclear cells is associated with hypercholesterolemia in patients with obstructive sleep apnea

Background and Aims: Obstructive sleep apnea (OSA) is associated with increased risk of cardiovascular disease. Resistin is recognized as a potent proinflammatory cytokine that is able to influence atherosclerotic plaque progression through several mechanisms. Resistin facilitates formation of foam cells through upregulation of CD36 scavenger receptor and increased uptake of oxidized low density lipoprotein. Its proinflammatory effects are mainly exerted via adenylate cyclase-associated protein 1 (CAP1). The aim of this study was to investigate if resistin, CAP1 and CD36 mRNA levels in peripheral blood mononuclear cells (PBMCs) are associated with hypercholesterolemia in patients with obstructive sleep apnea.

Influence of prenatal stress on metabolic abnormalities induced by postnatal intake of a high-fat diet in BALB/c mice.

Prenatal insults during fetal development result in increased likelihood of developing chronic disease. Obesity, the biggest risk factor for the development of metabolic disease, is affected by several genetic and environmental factors. High-fat diet (HFD) consumption is usually linked with the development of obesity. The main goal of this study was to analyze the impact of the exposure to a HFD in prenatally stressed animals. For this purpose, we subjected pregnant BALB/c mice to restraint stress for 2 h a day between gestational day (GD) 14 and GD 21. Prenatally stressed and control offspring of both sexes were postnatally exposed to a HFD for 24 weeks. We found that prenatal stress (PS) per se produced disturbances in males such as increased total blood cholesterol and triglycerides, with a decrease in mRNA expression of sirtuin-1. When these animals were fed a HFD, we observed a rise in glucose and insulin levels and an increase in visceral adipose tissue gene expression of leptin, resistin, and interleukin-1 beta. Although females proved to be more resilient to PS consequences, when they were fed a HFD, they showed significant metabolic impairment. In addition to the changes observed in males, females also presented an increase in body weight and adiposity and a rise in cholesterol levels.

Gene expression of the immunoinflammatory and immunological status of obese dogs before and after weight loss.

Obesity is characterized by a low degree of chronic inflammation state that, along with metabolic modifications, promotes important changes in the animal’s organism. Adipose tissue actively participates in inflammation and immunity, and several defense cells of the organism may, therefore, be involved in the diversity found between obese and ideal weight individuals. Studies regarding this subject have shown immune cell changes in humans and rats, however, the literature is scarce in relation to dogs. Thus, the present study aimed to evaluate the gene expression profile of immunoinflammatory response and the lymphoproliferation of obese dogs before and after weight loss. Eight female dogs, neutered, of different breeds, aged between 1 and 8 years (4.74±3.19), obese, with body condition score (BCS) of 9 out of a 9-point scale and body composition determined by the deuterium isotope dilution method were included. The obese dogs were enrolled in a weight loss program and after losing 20% of their initial weight became a second experimental group. A third experimental group consisted of eight female dogs, neutered, aged between 1 and 8 years (3.11±0.78) and with ideal BCS (5 out of a 9-point scale). Gene expression of immunoinflammatory cytokines (resistin, leptin, adiponectin, TNF-α, IL-6, IL-8, and IL-10) was assessed by qRT-PCR and immunity was assessed by lymphoproliferative response using the flow cytometry technique. The data that presented normal distribution was evaluated by analysis of variance by the PROC MIXED of the SAS and when differences were detected, these were compared by the Tukey test. Regarding the gene expression data, the procedure PROC GLIMMIX was adopted and the methodology of generalized linear model was used, in which the Gama distribution proved to be adequate. Values of p<0.05 were considered significant. The mean weight loss period of the animals included in the study was 194.25 ± 28.31 days and the mean weekly weight loss rate was 1.02 ± 0.82%. The average fat mass, both in percentage (P<0.001) and in kilograms (P = 0.012), was higher in the obese group (40.88%; 8.91kg), returning to normal and without difference between the control group (19.16%; 3.01kg) and after weight loss (22.10%; 4.11kg). The weight loss program resulted in an increase in percentage of lean body mass (P = 0.001), 55.50% in obese animals vs 77.90% in obese dogs after weight loss, the latter with no difference when compared to the control group (80.84%). The obese group presented increased gene expression of resistin and IL-8 in relation to the weight loss group (P = 0.002). In adiponectin, the obese group presented increased mRNA gene expression when compared to the weight loss group (P = 0.003). The evaluation of lymphocyte proliferation showed differences between the group of obese animals before and after weight loss (P = 0.004). Weight loss resulted in an increase in the lymphoproliferation rate (18.48%) compared to obese dogs at the beginning of the study (10.71%). These results indicate that weight loss modulates the immunoinflammatory response of obese dogs and may present important benefits to health and longevity of dogs.

An increase in inflammation and islet dysfunction is a feature of prediabetes.

Type 2 diabetes (T2D) is a global health problem that will be diagnosed in almost 300 million people by 2025 according to the World Health Organization. Before being diagnosed with T2D, individuals may have glucose levels above normal but below the diabetic range. This condition is known as prediabetes. Studies showed that people with prediabetes had an increase in several pro-inflammatory cytokines in their serum and in their fasting glucose levels. The answer remains unclear when inflammation begins in the pancreas and islets, and what is the extent of this inflammation. Subjects with haemoglobin A1c levels from 5.7% to 6.4% were classified as pre-diabetic. Sections of pancreas and isolated islets from normal donors and donors with prediabetes were tested for markers of inflammation and glucose-stimulated insulin secretion (GSIS). Gene and protein expression of the inflammatory markers resistin, interleukin-1 beta, tumour necrosis factor-alpha, interleukin-6, and monocyte chemoattractant protein-1 increased in donors with prediabetes compared to normal donors. GSIS response was significantly decreased in pre-diabetic islets compared to normal islets. Donors with prediabetes also had decreased expression of CD163+ cells but not CD68+ cells. Based on our findings, inflammation and islet dysfunction may be more significant than originally thought in people with prediabetes. Rather than being in a normal state before diabetes occurs, it appears that subjects are already in an early diabetic condition resembling more closely T2D.

The Relevance of Single-nucleotide Polymorphism +62 G>A to the Expression of Resistin Gene Affecting Serum Resistin Levels in Metabolic Syndrome in the Egyptian Population.

Metabolic Syndrome (MS) is a clinical condition consisting of risk factors associated with type two diabetes and developing cardiovascular disease. It has been suggested that resistin is a linkage between obesity, inflammation and type two diabetes. This study aims to investigate whether Resistin Gene (RETN) polymorphism (+62G>A) is linked to MS and resistin levels among the Egyptian population. This study was performed with 310 Egyptian volunteers: 160 MS subjects and 150 controls. Anthropometric parameters and biochemical variables were determined. The RETN +62G>A polymorphism was genotyped by PCR-RFLP technique. The resistin levels of the MS group were significantly higher than those of the control group. Resistin levels were positively correlated with anthropometric parameters and liver biomarkers in the MS group. According to RETN +62G>A polymorphism, carriers with the A allele (GA/AA) had significantly increased resistin levels than subjects with the GG genotype, consequently, the RETN +62G >A polymorphism was found to be related to MS, biochemical parameters and anthropometric variables. These findings propose that the RETN +62G>A polymorphism has a great impact on the circulating resistin concentrations, and that resistin levels are strongly related to MS. Therefore, this RETN polymorphism is related to the risk of the prevalence of MS in the Egyptians.

Nicotinamide and its metabolite N1-Methylnicotinamide alleviate endocrine and metabolic abnormalities in adipose and ovarian tissues in rat model of Polycystic Ovary Syndrome

Polycystic Ovary Syndrome (PCOS), as a common endocrine disorder is accompanied by hyperandrogenism, insulin resistance, ovulation problems, and infertility. Various types of off-label drugs like metformin have been used for the management of targeted problems caused by PCOS such as insulin resistance and hyperandrogenism. Nicotinamide (NAM) acts as a substrate of visfatin and Nicotinamide N-Methyltransferase (NNMT) leading to the generation of Nicotinamide Adenine Dinucleotide (NAD) and N1-Methylnicotinamide (MNAM), respectively. MNAM is known as an anti-inflammatory, anti-thrombosis, and anti-diabetic agent. In this study, the effects of NAM and MNAM on metabolic and endocrine abnormalities were evaluated in the adipose and ovarian tissues of a letrozole-induced rat model of PCOS. Our results showed that MNAM and NAM reversed abnormal estrous cycle and reduced the serum testosterone levels and CYP17A1 gene expression. Furthermore, all therapeutic factors improved HOMA-IR after treatment and NAM significantly increased the expression of GLUT4 and decreased the gene expression of visfatin. Also, MNAM diminished the gene expression of visfatin and resistin. It is noteworthy that all the therapeutic factors successfully activated the AMPK. In summary, this study is the first study reported beneficial effects of NAM and MNAM on the treatment of PCOS. Additionally, the alleviative effects of our therapeutic factors may be partially mediated by the AMPK-dependent manner due to the contribution of the AMPK in the expression of CYP17A1, visfatin, resistin, and GLUT4. Although more studies are required to unravel the exact mode of actions of MNAM and NAM in the PCOS, the findings of the current study shed light on an urgent need for discovering novel therapeutic pharmaceuticals regarding the treatment of PCOS.

Molecular and expression characteristics of resistin (RETN) and its effects on the differentiation of intramuscular preadipocyte in goat

Resistin (RETN) is a hormone secreted by adipocytes, which plays an important role in glucose and lipid metabolism. The aim of this study is to clone and obtain the full length open reading frame (ORF) of goat RETN gene sequence, and to reveal its molecular and expression characteristics. Simultaneously, we explore its effect on the differentiation of intramuscular preadipocytes in goat. The full length ORF sequence of goat RETN gene was cloned by RT-PCR technique, and bioinformatics analysis was performed though relevant biological softwares. In this study, the expression of RETN mRNA in goat tissues and intramuscular preadipocytes during differentiation was detected by qPCR technique. Furthermore, RNA interference was used to explore the effects of RETN on intramuscular preadipocytes differentiation in goat. The results showed that the cloned goat RETN gene sequence was 428 bp in length, of which the ORF was 330 bp, encoding 109 amino acids. Sequence analysis revealed that it had 12 phosphorylation sites and an O-glycosylation site, and its protein contained a signal peptide sequence. Also, the RETN gene is expressed in goat various analyzed tissues, and the results showed that the expression of RETN gene in lung tissue was higher than that in other analyzed tissues of goat (p < .01). Moreover, the expression level of RETN gene in the goat's intramuscular preadipocytes decreased first and then increased, and reached the highest on the fifth day, which was significantly higher than that of undifferentiated intramuscular preadipocytes (p < .001). After transfecting intramuscular preadipocyte with siRNA, we found that the mRNA level of RETN was significantly down-regulated by 70% and 87% (p < .01). Oil red O staining results showed that the interference of RETN gene can promote the differentiation of intramuscular preadipocytes. After knockdown of RETN with siRNA, the PPARγ, AP2, C/EBPα, C/EBPβ and SREBP1 genes were significantly up-regulated (p < .01). Thus, it can be inferred that RETN inhibits the differentiation of goat intramuscular preadipocytes, probably through regulating the expression of C/EBPα, C/EBPβ, PPARγ, AP2 and SREBP-1 genes.

High-fat diet in pregnant rats and adverse fetal outcome

Background: Although pregestational obesity has been associated with increased risk of adverse fetal outcome, the mechanisms behind are not known. We aimed to investigate the influence of the maternal metabolic state on fetal outcome in rats exposed to either a high-fat diet (HFD) or a control diet (CD). We also investigated the impact of serum collected from HFD/CD pregnant rats on CD embryonic development in whole-embryo cultures.Material and methods: On gestational day 0, 9, 10, or 20 maternal plasma/serum samples were collected as pregnancies were terminated for the estimations of maternal metabolic state and embryo-fetal development. We measured embryonic gene expression of ROS scavenger enzymes as well as genes involved in inflammation in maternal adipose tissue.Results: In HFD maternal plasma/serum, concentrations of glucose, β-hydroxybutyrate, branched-chain amino acids, and leptin were increased, whereas those of triacylglycerol, cholesterol, and palmitic, oleic, linoleic, and α-linolenic acids were decreased. Gene expression of CuZnSOD, IL-6, IL-10, and resistin was increased in HFD maternal adipose tissue, whereas that of CuZnSOD and MnSOD was decreased in HFD-exposed embryos. HFD caused retention of most fatty acids in the maternal liver as well.Conclusion: HFD alters the maternal metabolic state, increases fetal resorptions in vivo, and increases the rate of fetal/embryonic malformations both in vivo and in vitro. These findings suggest that metabolic disturbances in HFD pregnant rats have profound adverse developmental effects in the offspring.

Effect of continuous aerobic training versus high intensity interval training on Resistin and insulin resistance in type 2 diabetic rats

Introduction: The adipose tissue produces and releases peptides that contributes to various processes in body, including insulin resistance. The aim of this study was to investigate the effect of eight weeks of continuous aerobic training versus high intensity interval training on Resistin and insulin levels and insulin resistance in type 2 diabetic male wistar rats. Methods: In this experimental research, twenty-four Wistar rats became diabetic in seven months. In next phase, after introducing the training environment, Wistar rats were randomly assigned into three equal groups of six each: control, continuous (20 minutes, 60% maximum speed) and intense interval (2 minutes of activity with 80% maximum speed, 2 minutes recovery with 30% maximum speed). The rats trained five times a week for eight weeks. Resistin gene expression and plasma insulin and glucose levels were measured before and after eight weeks. One-way ANOVA was carried out at P&lt;0.05 for statistical analysis using SPSS software version16. Results: Regardless the type of training, differences between pre and post training results was statistically significant for insulin (P=0.024), glucose (P=0.037), insulin resistance (P=0.001) and Resistin (P=0.009). Interval training leads to the significant changes in all factors except the Resistin gene expression (P&lt;0.05). There was a significant relationship between changes in insulin resistance and Resistin gene expression (P=0.005, r=0.63). Conclusion: The results of this study showed that training is an effective factor in insulin resistance process and related factors in diabetes, and Resistin also play a role in this process, but it seems that regular training is more important factor than its type to change the Expression of Resistin.

Eccentric resistance training and β-hydroxy-β-methylbutyrate free acid affects muscle PGC-1α expression and serum irisin, nesfatin-1 and resistin in rats.

The hypothalamus controls metabolism and feeding behaviour via several signals with other tissues. Exercise and supplements can change hypothalamic signalling pathways, so the present study investigated the influence of eccentric resistance training and β-hydroxy-β-methylbutyrate free acid supplementation on PGC-1α expression, serum irisin, nesfatin-1 and resistin concentrations. Thirty-two male rats (8 weeks old, 200±17 g body mass) were randomly allocated to control, β-hydroxy-β-methylbutyrate free acid supplementation (HMB), eccentric resistance training (ERT), and β-hydroxy-β-methylbutyrate free acid supplementation plus eccentric resistance training (HMB+ERT) groups. Training groups undertook eccentric resistance training (6 weeks, 3 times a week) and supplement groups consumed β-hydroxy-β-methylbutyrate free acid (HMB-FA) orally (76 mg kg-1day-1). Twenty-four hours after the last training session, serum and triceps brachii muscle samples were collected and sent to the laboratory for analysis. Two-way ANOVA and Pearson correlation were employed (significance level: P<0.05). The results showed that eccentric resistance training increases skeletal muscle PGC-1α gene expression, as well as serum levels of irisin and nesfatin-1 (P=0.001). Eccentric resistance training decreased the serum concentration of resistin (P=0.001). HMB-FA supplementation increased skeletal muscle PGC-1α gene expression (P=0.002), as well as the serum concentration of irisin and nesfatin-1 (P=0.001), but decreased the serum concentration of resistin (P=0.001). Significant correlations were observed between PGC-1α gene expression and serum concentrations of irisin, nesfatin-1 and resistin. HMB-FA supplementation with eccentric resistance training may induce crosstalk between peptide release from other tissues and increases maximal muscle strength. The combination of the two interventions had a more substantial effect than each in isolation.

Relevance of single-nucleotide polymorphism to the expression of resistin gene affecting serum and gingival crevicular fluid resistin levels in chronic periodontitis and type 2 diabetes mellitus: A randomized control clinical trial.

Aim:The present study is aimed to investigate whether single-nucleotide polymorphism (SNP) of resistin gene (RETN) at −420 and +299 sites, is associated with resistin levels in serum and gingival crevicular fluid (GCF) in periodontally healthy, chronic periodontitis (CP) with and without type 2 diabetes mellitus (T2DM) patients.Materials and Methods:Serum and GCF samples were procured from all the 60 patients (twenty in each group) of the three study groups i.e., periodontally healthy (Group I), CP (Group II) and CP with T2DM patients (Group III) to analyze resistin levels using enzyme-linked immunosorbent assay test and clinical parameters were assessed at baseline and at 3 months after scaling and root planing (SRP). RETN polymorphism at −420 and +299 was genotyped by polymerase chain reaction-restriction fragment length polymorphism technique.Results:Patients with SNP −420 and +299 were positively correlated with increased serum and GCF resistin levels in Group II and Group III patients. SRP led to substantial reduction in the serum and GCF resistin levels.Conclusion:These findings are suggestive of a biologic link between resistin, periodontal diseases, and periodontal diseases with T2DM and RETN SNP at −420 and +299 in imparting increased resistin levels in inflammatory and diabetic conditions.