Increased Serum Resistin Levels Research Articles

Increased serum resistin levels associated with isolated coronary artery ectasia.

IntroductionCoronary artery ectasia (CAE) is localized or diffuse enlargement of the coronary artery more than 1.5 times in diameter in comparison with the adjacent normal coronary artery. The etiology and pathophysiology of CAE are not fully elucidated. Resistin is a newly identified adipocyte secreted hormone belonging to a cysteine-rich protein family. Recently it has been found to be relevant to inflammation-related disease and correlated with serum C-reactive protein (CRP). This research aimed to investigate whether the resistin level has a role in CAE etiopathogenesis.Material and methodsA hundred and three patients with diagnosis of CAE and 122 with normal coronary anatomy (NCA) were included. Details of baseline clinical characteristics and angiographic findings were recorded. Other necessary biochemical parameters were measured with an autoanalyzer. Blood was collected and stored for serum resistin level analysis.ResultsSerum resistin levels in CAE were higher than in the NCA group and were statistically significant (p = 0.001). Hypertension (OR = 1.006, 95% CI: 1.002–1.008, p = 0.025), tobacco use (OR = 1.089, 95% CI: 1.055–1.124, p < 0.001), serum resistin levels (OR = 2.431, 95% CI: 1.100–4.696, p = 0.01), hyperlipidemia (OR = 1.005, 95% CI: 1.000–1.014, p = 0.004), triglyceride (OR = 1.006, 95% CI: 1.001–1.010, p = 0.012) remained as independent factors for CAE. In the subgroup analysis of the CAE group, in patients with ectasia in three coronary arteries, resistin levels were significantly higher and statistically significant (p = 0.001). In ROC analysis, the sensitivity of serum resistin was 67.6% and specificity was 86.7% (AUC = 0.749, 95% CI: 0.621–0.877, p = 0.0001).ConclusionsSerum resistin level was significantly higher in CAE. In addition this study showed that serum resistin levels are directly proportional to the number of coronary arteries with ectasia. We think that this study will shed light on this subject and encourage further studies in this field.

High Serum Levels of Resistin is Associated With Acute Cerebral Infarction.

Background:The inflammatory process is involved in the pathogenesis of atherosclerosis and brain tissue injury following cerebral ischemia. Human resistin is a member of small cysteine-rich secreted proteins and has been implicated in inflammatory responses. This study investigated the association of serum resistin level with acute cerebral infarction (ACI). We also investigated its association with the short-term functional outcome.Methods:This study included 106 patients with ACI and 106 age-matched and sex-matched healthy control subjects. Serum resistin level was assessed by using enzyme-linked immunosorbent sandwich assay. The association of serum resistin levels with ACI was analyzed by logistic regression analysis.Results:The serum resistin level was significantly higher in patients with ACI than the control group [median (interquartile range), 35.7 ng/mL (13.0 to 70.5) ng/mL vs. 10.5 ng/ml (15.4 to 16.6), P<0.001]. Logistic regression analysis showed that serum resistin level was associated with an ACI (odds ratio=1.055, 95% confidence interval: 1.035-1.074, P<0.001). Among stroke subtypes, the serum resistin level was higher in the patients with large artery atherosclerosis than those with other subtypes (P=0.013). High resistin levels were also significantly associated with unfavorable functional outcome at discharge (odds ratio=1.043, 95% confidence interval: 1.024-1.063, P<0.001).Conclusions:This study suggests the potential association of resistin with stroke and cerebral atherosclerosis. Increased serum resistin levels were also associated with early unfavorable neurological outcome.

Increased serum resistin levels in metabolically unhealthy compared to metabolically healthy obese individuals; correlation with circulating white blood cell subpopulations

Increased serum resistin levels in metabolically unhealthy compared to metabolically healthy obese individuals; correlation with circulating white blood cell subpopulations

MiR-34a regulates mitochondrial content and fat ectopic deposition induced by resistin through the AMPK/PPARα pathway in HepG2 cells.

Resistin is an adipocyte-derived cytokine and was named for its role in the development of insulin resistance. Increased serum resistin levels are also associated with steatohepatitis and non-alcoholic fatty liver disease. In a previous study, resistin was observed to reduce mitochondrial content and upregulate miR-34a significantly in the liver. In this study, male C57BL/6 mice were injected with agomir-34a or control agomir, and HepG2 cells were transfected with miR-34a mimics or inhibitors to assess their role in resistin-induced fat deposition. The overexpression of miR-34a increased liver and HepG2 cell TAG content, decreased mitochondrial content, changed mitochondrial morphology and impaired mitochondrial function. In contrast, a miR-34a inhibitor significantly restored the TAG content and mitochondrial transmembrane potential. A study of transcriptional regulation revealed that C/EBPβ is essential for upregulating miR-34a by resistin. Furthermore, miR-34a inhibited the PPARα signaling pathway by binding to sites in the 3'UTR of AdipoR2 genes and the AMPK pathway. Consequently, this increased the fat content and decreased the mitochondrial content in HepG2 cells. This paper reveals a novel mechanism for mitochondrial regulation, which suggests that normal mitochondrial content and function is crucial for lipid metabolism in the liver.

The Association between Serum Resistin Levels and Major Adverse Cardiac Events

Resistin is a member of the family of cysteine-rich secretary proteins called resistin-like molecules (RELMs). It is suggested to be involved in inflammatory conditions and atherosclerosis. We have established a significant correlation between serum resistin levels and coronary artery disease (CAD) in a study was performed between 2011 and 2012 in our institute in two hundred fourteen patients (164 CAD patients and 50 controls). Then the CAD patients were followed up to investigate the relationship between increased serum resistin levels and major adverse cardiac events (MACE) between 2012 and 2016. One hundred fifty-five of 164 patients (95%) were followed up and 9 patients lost to follow up. There were 39 MACE (25%) in four years of follow-up. There were 16 in-hospital deaths due to cardiac causes, 8 revascularization procedures, and 15 re-hospitalization due to acute coronary syndrome (ACS) or heart failure (HF). The patients with MACE had similar serum resistin level (median: 71.37 pg/ml) compared to patients without MACE (median: 80.23 pg/ml) (p > 0.05).

Increased serum resistin levels correlate with psoriasis: a meta-analysis.

BackgroundRecent studies implicate adipokines in the pathogenesis of inflammatory diseases, including psoriasis. In this study we evaluated the significance of serum resistin levels in psoriasis patients using a meta-analysis approach.223MethodsRelevant articles were retrieved by searching the following English and Chinese databases: Cochrane Library, PubMed, Springer Link, Chinese Biomedical Database (CBM) and Chinese National Knowledge Infrastructure (CNKI). The retrieved studies were subjected to a thorough screening procedure to identify case–control studies that contained the required data. Data was extracted from each study and Version 12.0 STATA statistical software was employed for statistical analyses.ResultsNine case–control studies, containing 421 psoriasis patients and 348 healthy controls, were included in this study. The major result of the meta-analysis revealed a statistically significant association between serum resistin levels and psoriasis (SMD = 2.22, 95%CI: 1.14-3.29, P < 0.001). Subgroup analysis based on ethnicity showed that, compared to the healthy controls, serum resistin levels were markedly higher in psoriasis patients in both Asian and Caucasian populations (Asians: SMD = 3.27, 95%CI = 1.62 ~ 4.91, P < 0.001; Caucasians: SMD = 0.91, 95%CI = 0.28 ~ 1.54, P < 0.001).ConclusionsBased on our results, we conclude that serum resistin level in psoriasis patients is higher than healthy controls, and raises the possibility that elevated serum resistin levels may be a novel diagnostic marker in psoriasis and may predict the occurrence of co-morbidities in psoriasis patients.

Relationship Between Increased Serum Resistin Level and Severity of Coronary Artery Disease

Resistin, which is derived from the gene of RSTN, belongs to a family of cysteine-rich secretory proteins called resistin-like molecules (RELMs). Increased serum resistin levels are associated with coronary artery disease (CAD) and the risk of cardiovascular death. Patients (n = 214) with an initial diagnosis of stable angina pectoris, unstable angina pectoris, and myocardial infarction without ST-segment elevation and referred to catheter laboratory for coronary angiography were enrolled in the study. We aimed to investigate the relationship between increased serum resistin level and CAD. The severity of CAD was calculated by the Gensini scoring system. In conclusion, we established a significant correlation between serum resistin levels and CAD (P = .010). Also, serum resistin levels correlated with the Gensini score that represents the severity of CAD angiographically (P = .010).

Increased serum resistin levels in patients with coronary slow-flow phenomenon

Slow coronary flow (SCF) is an angiographic finding characterized by delayed opacification of the epicardial coronary arteries without obstructive coronary disease. Resistin, an adipocytokine, plays a major role besides low-grade inflammation in atherosclerotic vascular processes and may be of importance in other coronary pathologies such as SCF. The present study was cross-sectional and observational, consisting of 70individuals who underwent coronary angiography and had angiographically normal coronary arteries of varying coronary flow rates. The study included 50patients with isolated SCF and 20 control participants with normal coronary flow (NCF). There were no statistically significant differences between the SCF and NCF groups with respect to age, gender, presence of hypertension or diabetes mellitus, and smoking habit, except for increased creatinine levels (p = 0.014). The serum resistin level was significantly higher in the SCF group than in the NCF group (8.4 ± 7.2 vs. 5.4 ± 2.6ng/ml, p = 0.014). Ln-transformed resistin levels correlated positively with left anterior descending (LAD) coronary artery TIMI frame count (TFC) (r = 0.408, p < 0.001) as well as with glucose (r = 0.340, p = 0.004), creatinine (r = 0.248, p = 0.044), and C-reactive protein (CRP; r = 0.283, p = 0.023) levels, and negatively with LAD coronary flow velocity (r = - 0.314, p = 0.009). When multivariate analyses were performed, in linear regression analysis, ln-resistin was associated with a longer TFC [beta (standardized regression coefficient): 0.404, p = 0.001] and lower coronary flow velocity (beta: - 0.280, p = 0.035); in logistic regression analysis, ln-resistin was an independent predictor of the presence of SCF (OR: 6.692, 65 %CI: 1.117-40.1, p = 0.037). We demonstrated, for the first time, a significant increase in serum resistin levels in patients with SCF compared to subjects with NCF. We believe that further studies are needed to clarify the role of resistin in patients with SCF.

Porphyromonas gingivalis and Escherichia coli lipopolysaccharide causes resistin release from neutrophils

It was reported that periodontitis is associated with increased serum resistin levels. We examined whether there was a difference between the release of resistin from neutrophils incubated lipopolysaccharide (LPS) from Porphyromonas gingivalis and with LPS from Escherichia coli, and which cell-surface receptors and intracellular kinases were involved in this process. Several concentrations of P. gingivalis-LPS and E. coli-LPS were added to neutrophils, supernatant from cultured neutrophils was collected, and resistin levels were measured by ELISA. To examine signaling pathways, neutrophils were pretreated with monoclonal antibodies against CD14, CD18, TLR2, and TLR4, and specific inhibitors of PI3K and MAPKs. Resistin release from neutrophils was induced both by P. gingivalis-LPS and E. coli-LPS, but resistin release by P. gingivalis-LPS was weaker than E. coli-LPS in low concentrations. Resistin release was decreased by pretreatment with monoclonal antibodies against CD14, CD18, and TLR4, but not by TLR2. Moreover, it was decreased by inhibitors of PI3K, JNK, and p38 MAPK, but not by ERK1/2. Resistin release from neutrophils was induced by both P. gingivalis-LPS and E. coli-LPS. This was decreased by CD14, CD18, and TLR4 and was dependent on PI3K, JNK, and p38 MAPK, but not on ERK1/2 in intracellular pathways of neutrophils.

Inflammatory Induction of Human Resistin Causes Insulin Resistance in Endotoxemic Mice

OBJECTIVEAlthough adipocyte-derived murine resistin links insulin resistance to obesity, the role of human resistin, predominantly expressed in mononuclear cells and induced by inflammatory signals, remains unclear. Given the mounting evidence that obesity and type 2 diabetes are inflammatory diseases, we sought to determine the relationship between inflammatory increases in human resistin and insulin resistance.RESEARCH DESIGN AND METHODSTo investigate the role of human resistin on glucose homeostasis in inflammatory states, we generated mice lacking murine resistin but transgenic for a bacterial artificial chromosome containing human resistin (BAC-Retn), whose expression was similar to that in humans. The metabolic and molecular phenotypes of BAC-Retn mice were assessed after acute and chronic endotoxemia (i.e., exposure to inflammatory lipopolysaccharide).RESULTSWe found that BAC-Retn mice have circulating resistin levels within the normal human range, and similar to humans, lipopolysaccharide markedly increased serum resistin levels. Acute endotoxemia caused hypoglycemia in mice lacking murine resistin, and this was attenuated in BAC-Retn mice. In addition, BAC-Retn mice developed severe hepatic insulin resistance under chronic endotoxemia, accompanied by increased inflammatory responses in liver and skeletal muscle.CONCLUSIONSThese results strongly support the role of human resistin in the development of insulin resistance in inflammation. Thus, human resistin may link insulin resistance to inflammatory diseases such as obesity, type 2 diabetes, and atherosclerosis.

Association of circulating resistin with metabolic risk factors in Indian females having metabolic syndrome

Role of resistin in insulin sensitivity and metabolic syndrome (MetS) is controversial till date. Increased serum resistin levels are associated with MetS and insulin resistance. The aim of this study was to investigate the relationship between serum resistin levels with markers of the MetS in females. In a cross-sectional study, a total of 170 healthy female subjects were selected for the study. Out of which 71 (age 31.59 ± 4.88 years) were with MetS and 99 (age 31.75 ± 6.34 years) were without MetS. Different parameters of MetS and serum resistin level were measured according to the standard protocols as given in NCEP ATP III 2001 guideline. Serum resistin levels were significantly higher in subjects with MetS when compared with subjects without MetS [13.54 ± 4.14 ng/ml (n = 71) vs. 7.42 ± 2.31 ng/ml (n = 99); P ≤ 0.001]. Resistin levels were positively associated with waist circumference, systolic and diastolic blood pressure, plasma glucose, waist/hip ratio, serum triglycerides, serum cholesterol, serum VLDL, plasma insulin, and insulin resistance, while it was negatively associated with high-density lipoprotein. This study demonstrates a positive correlation between resistin and factors of MetS except high-density lipoprotein which was found to be negatively correlated in Indian female subjects.

Patients with nonalcoholic fatty liver disease display increased serum resistin levels and decreased adiponectin levels

Resistin and adiponectin are recently discovered protein hormones, which are produced and secreted by adipocytes. Nonalcoholic fatty liver disease (NAFLD) is a metabolic syndrome, which is associated with obesity. The aim of this study was to evaluate the changes of serum adiponectin and resistin in patients with NAFLD and to determine the relationship between serum adipokine levels and clinicopathologic parameters of NAFLD. Forty-three patients with NAFLD and 43 controls were enrolled in this pair-matched study. Body weight, height, body mass index, abdominal wall fat thickness, waist circumference, hip circumference, and the percentage of body fat were measured. Additionally, serum lipid, glucose, alanine aminotransferase, aspartate aminotransferase, adiponectin, and resistin were determined in all individuals. Serum adiponectin and resistin levels were determined using ELISA kits. Serum adiponectin levels were significantly lower in patients with NAFLD compared to the control group (control: 2.01+/-1.10 mg/l vs. NAFLD: 1.38+/-0.65 mg/l, P<0.01). Serum resistin levels were significantly elevated in patients with NAFLD compared to the control group (control: 4.70+/-3.30 ng/ml vs. NAFLD: 9.20+/-7.20 ng/ml, P<0.05). Serum adiponectin concentration was negatively correlated with the waist circumference (rho=-0.425), body mass index (rho=-0.329), percentage of body fat (rho=-0.256), abdominal wall fat thickness (rho=-0.226), and fasting blood glucose concentration (rho=-0.242), but was positively correlated with HDL (rho=0.226). Serum resistin concentration was positively correlated with waist circumference (rho=0.237). No correlation was found between resistin levels and blood pressure, fasting blood glucose concentration, triglyceride, total cholesterol, and HDL. NAFLD patients had lower adiponectin levels and higher resistin levels. A positive correlation was found between resistin and waist circumference, whereas a negative correlation was found between adiponectin and waist circumference, body mass index, percentage of body fat, abdominal wall fat thickness, and fasting blood glucose concentration. These data suggested that hypoadiponectinemia and hyperresistinemia might be involved in the development of NAFLD.

The relationship between periodontal condition and serum levels of resistin and adiponectin in elderly Japanese

Diabetes and periodontitis are associated with each other. Adipokines, specifically adiponectin and resistin, are secreted from adipocytes and are thought to cause insulin resistance in rodents. Additionally, adiponectin and resistin may play a role in inflammation and immune responses. The aim of this study was to clarify the relationship between serum levels of adipokines and periodontal conditions in elderly Japanese people with and without periodontitis. A total of 158 Japanese men and women (76 years old) with or without periodontitis were selected for the study. Serum adiponectin, resistin, interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) concentrations were compared between subjects with and without periodontitis. Serum resistin levels and total leukocyte counts in subjects with periodontitis were higher than in control subjects. No significant differences were observed in adiponectin, IL-6 and TNF-alpha levels between subjects with and without periodontitis. Logistic regression analysis showed that periodontitis with at least one tooth that displayed a probing pocket depth of > or =6 mm was significantly associated with higher serum resistin levels (odds ratio, 2.0; 95% confidence interval, 1.0-4.0). When excluding periodontitis subjects with < or =10% of bleeding on probing and excluding control subjects with >10% bleeding on probing, differences between groups and odds ratio increased. Serum adiponectin tended to decrease in patients with periodontitis, albeit not significantly. Increased serum resistin levels were significantly associated with periodontal condition, especially when considering bleeding on probing, in elderly Japanese people. There was also a trend, though non-significant, toward decreased levels of adiponectin in subjects with periodontitis.

Insulin sensitivity and resistin levels in gestational diabetes mellitus and after parturition

Resistin is expressed and secreted by the placenta during pregnancy. Increased serum resistin levels have been found in the second half of normal pregnancy, but its role in the pathogenesis of the insulin resistance of pregnancy is undetermined. The objective of the study was to assess the relationship between circulating resistin levels and insulin sensitivity in gestational diabetes mellitus (GDM). A case (n=23)-control (n=35) study was performed at the obstetrics and endocrinology clinic of a university hospital. In total, 58 Caucasian women with a singleton pregnancy who had been referred for a 100 g oral glucose tolerance test were enrolled between the weeks 26 and 30, and 22 women with GDM were also evaluated after pregnancy. Serum resistin and insulin sensitivity in GDM during and after pregnancy. The relationship of resistin to metabolic abnormalities was evaluated. Resistin levels were lower in GDM women than in pregnant women with normal glucose tolerance (NGT) (4.32+/-1.56 vs 9.30+/-1.32 ng/ml, P<0.001), and experienced a further decrease after parturition (4.24+/-1.56 vs 3.11+/-1.63 ng/ml, P=0.003). The association between low serum resistin levels and the diagnosis of GDM was independent of the degree of insulin sensitivity. Lower resistin levels were observed in GDM than in NGT women and decreased after parturition, suggesting a role for resistin in the development of this disease. But we have failed to find an independent relationship between resistin levels and insulin sensitivity during pregnancy.

Plasma resistin levels correlate with determinants of the metabolic syndrome

The role of resistin in insulin sensitivity and obesity is controversial. Some authors suggest that increased serum resistin levels are associated with obesity, visceral fat, insulin resistance, type 2 diabetes and inflammation, while others failed to observe such correlations. The aim of the present study was to investigate the relationship of plasma resistin levels with markers of the metabolic syndrome and atherosclerosis in a large population-based study. Plasma resistin levels were determined in 1090 subjects free of any medication selected from the PLIC study (designed to verify the presence of atherosclerotic lesions and progression intima-media thickness (IMT) in the common carotid artery in the general population) and related to the presence of obesity, metabolic syndrome, metabolic abnormalities, cardiovascular risk, and progression of IMT. Plasma resistin levels were highly positively correlated with triglycerides, waist circumference, waist/hip ratio, systolic blood pressure, and ApoAI/ApoB ratio, while they were inversely correlated with high density lipoprotein and ApoAI levels. This finding was gender specific (mainly in women). Plasma resistin levels were significantly higher in women with the metabolic syndrome compared with controls (4.90 (0.24) ng/ml vs 3.90 (0.11) ng/ml; P<0.01), while no difference was observed in obese subjects. Finally, plasma resistin levels were significantly correlated with cardiovascular risk calculated according to the Framingham algorithm (P<0.01). Plasma resistin levels are increased in presence of the metabolic syndrome and are associated with increased cardiovascular risk.

Increased serum resistin levels in patients with type 2 diabetes are not linked with markers of insulin resistance and adiposity

The role of resistin in human biology remains uncertain. We measured serum resistin levels in Japanese patients with (n=111) and without (n=98) type 2 diabetes mellitus and investigated the significance of this hormone in the pathophysiology of diabetes. The levels of serum adiponectin and leptin were also measured. Resistin levels were increased significantly in patients with type 2 diabetes compared with non-diabetic subjects (24.7+/-2.6 vs. 15.0+/-1.2 ng/ml, p=0.0013). However, there was no correlation in either patient group between serum resistin levels and markers of insulin resistance, obesity or hyperlipidaemia. These results were in direct contrast to the data of leptin or adiponectin, both of which were closely related to these clinical markers of diabetes. Multivariate regression analysis on the combined data of the two groups demonstrated that the presence of diabetes and HDL cholesterol levels were significant predictors of serum resistin levels (diabetes: beta=0.159, p=0.035; HDL: beta=-0.172, p=0.039). No correlation was observed between C-reactive protein and resistin adjusted for BMI. Taken together, these findings demonstrate that serum resistin levels are increased in patients with type 2 diabetes, but this increase is not linked to markers of insulin resistance or adiposity. Further studies are necessary to elucidate the significance of serum resistin concentration in human pathophysiology.