Background. Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases, which has recently been mentioned as an independent cardiovascular risk factor. Objectives. Endocan is a novel molecule of endothelial dysfunction. We aimed to evaluate the associations of serum endocan levels with the hepatic steatosis index (HSI), fatty liver index (FLI), and degrees of hepatosteatosis in patients with metabolic syndrome with NAFLD. Design and Setting. This cross-sectional prospective study was performed in the outpatient clinic of an internal medicine department. Methods. The study included 40 patients with metabolic syndrome with NAFLD as noted using hepatic ultrasound and 20 healthy controls. Secondary causes of fatty liver were excluded. FLI and HSI calculations were recorded. Serum endocan level values were obtained after overnight fasting. Results. Higher values of HSI and FLI were found in the NAFLD groups than in the control groups (p<0.001). Five (12.5%) of 20 patients with liver steatosis had grade 1 liver steatosis, 15 (37.5%) patients had grade 2 liver steatosis, and 20 (50%) patients had grade 3 liver steatosis. Serum endocan levels were lower in patients with NAFLD compared with the healthy controls (146.56±133.29 pg/mL vs. 433.71±298.01 pg/mL, p<0.001). ROC curve analysis suggested that the optimum endocan value cutoff point for NAFLD was 122.583 pg/mL (sensitivity: 71.79%, specificity: 90%, PPV: 93.3%, and NPV: 62.1%). Conclusion. Serum endocan concentrations are low in patients with NAFLD, and the optimum cutoff point is 122.583 pg/mL. HSI and FLI were higher in patients with NAFLD; however, there was no correlation with serum endocan.
The Kütahya kaolinite deposits are the most important source of raw materials for the ceramics industry in Turkey. To date, no detailed mineralogical or geochemical characterizations of these materials have been carried out; the present study aims to fill that gap. The Kütahya kaolinite deposits formed by alteration of dacite and andesite tuffs related to Neogene volcanism whichwas associated withe xtensional tectonics. The kaolinite deposits contain silica and Fe- and Ti-bearing phases (pyrite, goethite, and rutile) in vertical and subvertical veins that diminish and then disappear upward. Mineralogical zonation outward from the main kaolinite deposit is as follows: kaolinite ± smectite + illite + opal-CT + feldspar; feldspar + kaolinite + quartz + smectite + illite; quartz + feldspar + volcanic glass. The veins and mineral distributions demonstrate that hydrothermal alteration was the main process in the development of the kaolinite deposits of the area. The very sharp, intense, diagnostic basal reflections at 7.2 and 3.57 Å, as well as non-basal reflections, well defined pseudohexagonal to hexagonal crystallinity with regular outlines, ideal differential thermal analysis-thermal gravimetric curves, and ideal, sharp, infrared spectral bands indicate well crystallized kaolinite. Micromorphologically, the development of kaolinite plates at the edges of altered feldspar and devitrified volcanic glass indicates an authigenic origin. Lateral increase in (SiO2+Fe2O3+MgO+Na2O+CaO+K2O)/(Al2O3+TiO2) from the center of the kaolinite deposit outward also indicates hydrothermal zonation. Enrichment of Sr in altered and partially altered rocks relative to freshvolca nic-rock samples demonstrates retention of Sr and depletion of Rb, Ba, Ca, and K during hydrothermal alteration of sanidine and plagioclase within the volcanic units. In addition, depletion of heavy rare earth elements (HREE) relative to light rare earth elements (LREE) in the kaolinized materials may be attributed to the alteration of hornblende. The negative Eu anomaly suggests the alteration of feldspar by hydrothermal fluids. The isotopic data from kaolinite and smectite indicate that hydrothermalalteration processes developed at 119.1–186.9°C and 61.8–84.5°C, respectively. Thus, the kaolinite deposits formed by hydrothermal alteration of volcanic glass, feldspar, and hornblende by a dissolutionprecipitation mechanism which operated under acidic conditions within Neogene dacite, andesite, and tuffs.
Obesity has recently been mentioned as a metabolic pandemic in developed and developing countries and is an important known risk factor for type 2 diabetes and cardiovascular diseases. The main mechanism responsible for obesity is insulin resistance. Adropin is a peptide-structured regulatory hormone that is suggested to play a role in insulin resistance and metabolic regulation. We aimed to evaluate the associations of serum adropin with insulin resistance and clarify the factors affecting serum adropin concentrations. The study included 50 obese patients and 22 healthy controls. Patients with chronic disease and drug use history were excluded. Serum adropin and other metabolic parameters were obtained after overnight fasting. ELISA was used to measure serum adropin concentrations. The homeostatic model assessment-insulin resistance (HOMA-IR) index was used to calculate insulin resistance. Insulin resistance was defined as HOMA-IR >2.5. Serum adropin values were found to be low in the obese otherwise healthy patient group (p<0.001). Linear regression analysis revealed that age, body mass index (BMI), waist circumference (WC), high-density lipoprotein cholesterol, fasting glucose, and HOMA-IR affect serum adropin level. In multiple regression analysis, age is the most significant factor affecting serum adropin concentration. Serum adropin concentrations were negatively correlated with BMI, WC, diastolic blood pressure, fasting glucose, and insulin. Serum adropin concentrations were low in obese patients and the optimum cut-off point for adropin to indicate HOMA-IR at 2.5 is 216.7 ng/L. The findings suggest that serum adropin may contribute to the regulation of glycolipid metabolism and insulin resistance in obese patients.
Effects of chito-oligosaccharides and L-carnitine supplementation in diets for ABSTRACTThe aim of this study was to determine effects of dietary supplementation with chitosanoligosaccharides (COS) and L-carnitine, individually or dually, on growth performance, carcass traits and some blood serum parameters in quails. A total of 192, four days old, Japanese quail chicks were allotted four groups, each of which included four replicates (12 birds per replicate). The groups received the same basal diet supplemented with 0 (Control), 150mg/kg chitosanoligosaccharides (COS), 150mg/kg L-carnitine (Carnitine), and 150 mg/kg chitosanoligosaccharides+150 mg/kg L-carnitine (COS+Car.) during the starter (1 to 21 days) and a grower (22 to 42 days) period. The feeding trial shoved that COS, L-carnitine and COS+L-carnitine had no significant effect on live weight, live weight gain, feed consumption and feed conversion. Supplementation with COS+L-carnitine induced higher leg ratio from than that of the Control. There were no differences on serum albumin, total protein, glucose and total cholesterol concentrations. It is concluded that due to the obtained higher leg ratio from COS+Car. group, after analysis of the profit and loss, if is economically profitable, chitosanoligosaccharides+L-carnitine could be added quail diets.Keywords: quail, chitosanoligosaccharides, L-carnitine, growth performance, carcass traits, blood parameters RESUMOO estudo objetivou determinar os efeitos da suplementação com chito-oligossacarídeos (COS) e Lcarnitina, individualmente ou em conjunto, sobre o desempenho, características de carcaça e alguns parâmetros sanguíneos em codornas. Um total de 192 codornas japonesas, com quatro dias de vida foi separado em quatro grupos, cada grupo com quatro repetições (12 aves por repetição). Os grupos receberam a mesma dieta basal suplementada com 0 (Controle), 150mg/kg chito-oligossacarídeos (COS), 150mg/kg L-carnitina (Carnitina), e 150mg/kg chito-oligossacarídeos +150 mg/kg L-carnitina (COS+Car.) durante o período inicial (1 a 21 dias) e de crescimento (22 a 42 dias). A fase de alimentação mostrou que COS, L-carnitina e COS+L-carnitina não tiveram efeito significativo no peso vivo, ganho de peso vivo, consumo de alimento e conversão de alimento. A suplementação com COS+L-carnitina induziu proporção de perna maior que o Controle. Não houve diferenças na concentração de albumina sérica, proteína total, glicose e colesterol total. Conclui-se que devido à proporção maior de perna obtida para o grupo COS+Car., após análise de perda e ganho, se for economicamente viável chitooligossacarídeos+L-carnitina pode ser adicionado à dieta de codornas.
IntroductionMetabolic syndrome has been recognized as a predictor of cardiovascular diseases. Epicardial fat tissue (EFT) thickness has recently been shown to be a predictor of cardiovascular diseases in metabolic syndrome patients. Endocan is a novel molecule which is considered to be an early marker of endothelial dysfunction. Our aim was to evaluate endocan serum levels for the first time in metabolic syndrome patients, in relation to EFT thickness.Material and methodsThe study included 44 patients with metabolic syndrome who had neither chronic kidney disease nor chronic inflammation and 26 healthy controls. Fasting blood samples were obtained from the groups. The serum levels of endocan were measured with a Sunred ELISA kit. EFT thickness of patients was measured by echocardiography.ResultsThe serum endocan levels were significantly lower in the metabolic syndrome patients compared to the healthy controls (120.71 ±90.17 pg/ml vs. 414.59 ±277.57, p < 0.001). Metabolic syndrome patients demonstrated significantly higher EFT (p = 0.042). EFT thickness had a positive correlation with age (r = 0.397, p = 0.008) and weight (r = 0.010). However, there was no correlation with serum endocan (r = –0.021, p = 0.893) or other parameters. Regression analysis revealed that waist circumference is the parameter among metabolic syndrome criteria having the strongest relationship with serum endocan levels ( = –0.499, p = 0.21).ConclusionsEFT thickness was high in metabolic syndrome patients and can be a useful marker for cardiovascular risk assessment. However, serum endocan levels were found to be low and there was no correlation with EFT thickness. Large sample sized prospective studies are needed to clarify the relation of endocan levels with the other clinical indicators of cardiovascular risk in metabolic syndrome.
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