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In the present study, toxic effects, both alone and combined, of bisphenol A (BPA), lead (Pb) and endosulfan (ES) in the low doses were investigated in rat liver and kidney functions. In the study, bisphenol A (BPA), lead (Pb) and endosulfan (ES) were chosen because although they are the chemicals people are most frequently exposed to, no combined toxic effect studies were conducted with these chemicals. Sixty-four male Wistar albino rats were used in the study, and they were randomly divided into eight groups ( n = 8 per group); control, BPA (5 mg/kg), Pb (100 ppm), ES (0.61 mg/kg), BPA+Pb, BPA+ES, Pb+ES and BPA+P+ES. The rats were sacrificed after 65 days of treatment. Severe histopathological changes in the liver and kidney tissues were observed in the rats exposed to BPA+Pb+ES combination. Elevated malondialdehyde (MDA) in the liver and decreased superoxide dismutase activity (SOD) in the kidney tissue were detected in the BPA+Pb+ES group compared to those of the control group. It was found that serum alanine aminotransferase (ALT) and blood urea nitrogen (BUN) and creatinine (CREA) levels were higher in the BPA+Pb+ES combination group than the control group. Also, combined exposure of BPA, Pb and ES caused apoptotic cell numbers and inducible nitric oxide (iNOS) to increase in the liver and kidney tissues. The results of the present study suggested that the BPA, Pb and ES caused more dramatic changes to both histological architecture and cell apoptosis in the liver and kidney tissues when there was a combined exposure.

Background Childhood obesity leads to an increased inflammatory response, which in the long term can lead to serious health problems such as metabolic syndrome, diabetes, cancer and cardiovascular disease, and may also increase the risk of obesity in adulthood. Our aim was to evaluate inflammatory markers associated with pediatric obesity in 30 healthy children (BMI between the 15th–85th percentiles) and 30 obese children (BMI > 95th percentile) and to determine the possible associations of these markers. Methods Anthropometric measurements of the children were obtained. The serum preptin, peroxisome proliferator activated receptor gamma (PPARγ), nod-like receptor pyrin domain-containing 3 (NLRP3), and interleukin-18 (IL-18) levels of thirty children with obesity and thirty healthy children were determined using ELISA. Results NLPR3, preptin, and PPARγ levels were greater obese children than in healthy children ( p  < 0.05). We have shown that high PPARγ levels may have an inhibitory effect on the inflammatory activation of NLRP3. Conclusions In our study, the changes observed in preptin, NLRP3 and PPARγ parameters were found to be closely associated with pediatric obesity. These molecules may play an important role in understanding the relationship between pediatric obesity and inflammation and may be used as biomarkers in determining obesity treatment and complications in future studies.

Apelin is a bioactive mediator released by adipose tissue that can be involved in energy metabolism events and coronary artery disease. This study aims to investigate the role of serum apelin levels in patients with peripheral artery disease (PAD). The present observational case–control study consisted of 100 subjects (50 angiographically proven PAD patients and 50 healthy controls). Serum apelin and apelin receptor (APJ) levels were measured with blood samples. Clinical and laboratory findings were obtained from the hospital database system. The association between serum apelin levels, and PAD was investigated. The number of smokers and subjects with hypertension, coronary artery disease and diabetes mellitus was higher in the PAD group than in the control group ( P  < 0.05). Mean serum apelin levels were lower in the peripheral artery group than in the control group (mean: 13.94, SD 4.34 vs. mean: 16.79, SD 4.2, P  = 0.001). On the other hand, the mean APJ levels were higher in the control group (mean: 36.1, SD 19.1 vs. mean: 27.7, SD 13.1, P  = 0.019). There was no statistically significant difference between the two groups (20 (41.6%) vs. 21 (42%), P  = 973) regarding the obesity. Our findings revealed that hypertension, smoking and diabetes mellitus rates were higher among patients with PAD. In fact, the lower apelin levels and higher APJ levels were risk factors associated with PAD; the obesity was not related with development of PAD.

Irisin and oxytocin can affect energy homeostasis and it has been suggested that they may play an important role in reducing obesity and diabetes. In this study, we aimed to determine the relationship between metabolic parameters (including irisin and oxytocin levels) and anthropometric parameters in obese children. Ninety obese children (mean age, 13.85±1.63 years) and 30 healthy controls (mean age, 14.32±1.58 years) were enrolled in this study. Anthropometric and laboratory parameters (glucose, insulin, lipid, oxytocin, and irisin levels) were analyzed. The serum irisin and oxytocin levels were measured by enzyme-linked immunosorbent assay. Bioelectrical impedance was used to determine body composition. Irisin level was higher in the patients than in the controls (p=0.018), and this higher irisin level was correlated with increased systolic blood pressure, body mass index, waist/hip ratio, fat percentage, fat mass, glucose level, insulin level, and homeostasis model assessment of insulin resistance. Serum oxytocin level was significantly decreased in obese children compared to the controls (p=0.049). Also, among the 60 obese patients, oxytocin level was significantly lower in patients with than in those without metabolic syndrome (8.65±2.69 vs. 10.87±5.93 ng/L, respectively), while irisin levels were comparable (p=0.049 and p=0.104, respectively). There were no statistically significant relationships between oxytocin or irisin levels and lipid levels (p>0.05). Obese children had significantly higher irisin levels than the healthy controls. Additionally, this study shows for the first time that oxytocin level is significantly lower in obese compared with non-obese children and also lower in obese children with metabolic syndrome compared to those without.

ABSTRACT Background Although high‐dose biotin interference in automated immunoassays is now considered, there are very few studies showing biotin interference in manually operated research kits, especially with enzyme‐linked immunosorbent assay (ELISA). The aims of our study were to determine the effects of biotin interference on various parameters, including leptin, leptin receptor (LEPR), ghrelin, acylated ghrelin, deacylated ghrelin, ghrelin receptor (GHSR), kisspeptin (KISS1), kisspeptin receptor (KISS1R), preptin, peroxisome proliferator activated receptor gamma (PPARγ), nod‐like receptor pyrin domain‐containing 3 (NLRP3) and interleukin‐18 (IL‐18), which contribute to energy homeostasis in healthy and obese children. Methods Serum pools were prepared from healthy and obese individuals, and biotin concentrations in samples containing different amounts of biotin were measured via sandwich and competitive ELISA methods. In addition, possible biotin interactions were investigated by determining the concentrations of all the study parameters in serum pools containing different amounts of biotin. Results We found that the biotin‐competitive, ghrelin‐competitive, KISS1‐competitive, GHSR, leptin and LEPR ELISA kits were less affected by biotin interference and the results of these assay kits were more reliable. Unexpectedly, high levels were also measured in the biotin sandwich ELISA kit, indicating that biotin interference can also occur in manually operated assay kits. Conclusions Biotin exhibited an interference effect even in well‐functioning, qualified kits, and this negative effect was less common in competitive kits. Biotin interference was closely associated with the quality of the research kit, the parameters studied, and the presence of high biotin concentrations in the blood. In this study, we aimed for the first time to demonstrate biotin interference in ELISA research kits used in the analysis of pediatric obesity parameters other than routine testing. Our study revealed that biotin interaction may occur in manual ELISA kits and may cause erroneous test results. It will raise awareness among health professionals, researchers, and medical companies on this issue. By encouraging manufacturers developing medical products to take measures to reduce the effect of biotin interaction, it will prevent erroneous results in scientific studies and contribute to more precise measurements.

This study was designed to investigate the serum and synovial fluid leptin levels, and inflammatory markers in rheumatoid arthritis (RA) patients. Serum and synovial fluid leptin levels were significantly higher ( P  > 0.05) in RA patients than control group; RA patients with moderate disease activity (DAS < 2.7) having significantly higher leptin levels ( P  > 0.05) than those with low disease activity (DAS < 2.7). Leukocytes and erythrocyte sedimentation rate (ESR) were found to be significantly higher in moderate disease activity RA group compared to low activity group ( P  > 0.05, P  < 0.001, respectively). Serum leptin level is found to be independent of age and inflammatory markers. ESR is positively correlated with DAS activity and CRP values. Our finding of no correlation between leptin and BMI shows that regulation of leptinemia is complex, and leptin levels cannot be used to assess RA activity.

Background Childhood obesity leads to an increased inflammatory response, which in the long term can lead to serious health problems such as metabolic syndrome, diabetes, cancer and cardiovascular disease, and may also increase the risk of obesity in adulthood. Our aim was to evaluate inflammatory markers associated with pediatric obesity in 30 healthy children (BMI between the 15th-85th percentiles) and 30 obese children (BMI > 95th percentile) and to determine the possible associations of these markers. Methods Anthropometric measurements of the children were obtained. The serum preptin, peroxisome proliferator activated receptor gamma (PPAR[gamma]), nod-like receptor pyrin domain-containing 3 (NLRP3), and interleukin-18 (IL-18) levels of thirty children with obesity and thirty healthy children were determined using ELISA. Results NLPR3, preptin, and PPAR[gamma] levels were greater obese children than in healthy children (p < 0.05). We have shown that high PPAR[gamma] levels may have an inhibitory effect on the inflammatory activation of NLRP3. Conclusions In our study, the changes observed in preptin, NLRP3 and PPAR[gamma] parameters were found to be closely associated with pediatric obesity. These molecules may play an important role in understanding the relationship between pediatric obesity and inflammation and may be used as biomarkers in determining obesity treatment and complications in future studies. Keywords: Child, Obesity, Preptin, NLRP3, PPAR[gamma]

MicroRNAs (miRNAs) are non-coding RNA molecules that serve as regulators following gene expression transcription. While studies have investigated the role of miRNAs in the pathogenesis of essential hypertension (HT), very few have considered their place in the pathogenesis of resistant hypertension (RH). The purpose of this study was to investigate levels of miRNA 21 and miRNA 155 in RH and their relationships with aldosterone. Thirty-two normotensive patients, 30 newly diagnosed HT patients, and 20 RH patients were included in the study. Patients' demographic data were recorded, and office blood pressure measurement and 24-h ambulatory blood pressure monitoring (24-h ABPM) were performed. Blood specimens were collected for miRNA 21, miRNA 155 and aldosterone measurement. MiRNA 21 and miRNA 155 levels in the control and patient groups and their relations with other demographic and biochemical parameters were then subjected to analysis. No difference was determined in miRNA 155 levels between the groups, but miRNA 21 and aldosterone levels were significantly higher in the RH group (p < 0.001 and <0.05, respectively). At correlation analysis, miRNA 21 exhibited positive correlation with aldosterone, age, office SBP, 24-h ABPM all-day SBP. A 9.6 copy/uL level for miRNA 21 predicted presence or absence of RH with 95% sensitivity and 71% specificity (AUC:0.823, 95% CI (0.72-0.92). The study results revealed significantly higher miRNA 21 and aldosterone in RH patients than in healthy individuals and newly diagnosed hypertensives.

Advances in knowledge of neurotrophic factors are now revealing the complex control of energy homeostasis and appetite, as well as the crucial role these factors play in nervous system function. The aim of this study was to assess serum levels of neudesin in adolescents with obesity and to examine the relationship between these levels and metabolic outcomes. Adolescents, aged 10-17 years were enrolled. Subjects were divided into normal weight, obese and morbidly obese subgroups. Serum neudesin concentrations were compared between the groups. In total, 88 adolescents were recruited, of whom 30 (34.1%) were normal weight, 15 (17.0%) were obese and 43 (48.9%) were morbidly obese. Neudesin levels were significantly lower in obese adolescents than in the control group (p=0.013). A correlation analysis applied to the whole study group revealed a negative correlation between serum neudesin concentration and body mass index (BMI) z scores (r=-0.40, p<0.001). Serum neudesin levels tended to increase in adolescents with metabolic syndrome, insulin resistance, dyslipidaemia, and hypertension but the differences were not significant (p=0.259, p=0.246, p=0.259, and p=0.523, respectively). Serum neudesin levels were significantly correlated with BMI z score in obese adolescents. Generally, serum neudesin levels were low in obese and morbidly obese adolescents and tended to increase with the appearance of metabolic disorders. Both obesity and associated metabolic disorders have multifactorial causes. Therefore, we suggest that the role of the neudesin molecule in the regulatory mechanisms of obesity and metabolic disorders should be further investigated with well-designed studies enrolling larger groups.