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Background To investigate serum levels of brain injury markers in diabetic ketoacidosis (DKA) and the relation of these markers with clinical and radiological findings of brain injury and laboratory results. Methods Twenty-nine patients with DKA, 30 with type 1 diabetes mellitus (T1DM), and 35 healthy children were included. Clinical and laboratory findings, and the Glasgow Coma Scale (GCS) were recorded. In the DKA group, neuron-specific enolase (NSE), S100 calcium-binding protein B (S100B) and glial fibrillary acidic protein (GFAP) levels were measured at baseline and 6 and 12 hours after treatment. Magnetic resonance imaging was performed in the DKA group to demonstrate any brain injury. Results No clinical or radiological findings of brain injury were found in any of the patients with DKA. In the DKA group, S100B was significantly higher than the healthy control and T1DM groups, while GFAP and NSE levels were not different from controls and T1DM patients. No significant differences were found in GFAP, NSE and S100B levels according to severity of DKA, diabetes duration and GCS. Conclusion NSE and GFAP levels do not increase in DKA patients without overt brain injury. Elevated levels of S100B, which is also synthesized from non-neuronal tissues, might arise from peripheral sources. A lack of concurrent increase in serum levels of these brain injury markers might result from the yet intact blood brain barrier or a true absence of neuronal damage. In order to reveal subclinical brain injury related to DKA, there is a need for studies concurrently assessing neurocognitive functions.

Objective: To investigate the relationship between zonulin levels and clinical and laboratory parameters of childhood obesity. Methods: The study included obese children with a body mass index (BMI) >95th percentile and healthy children who were of similar age and gender distribution. Clinical (BMI, waist circumferences, mid-arm circumference, triceps skinfold, percentage of body fat, systolic blood pressure, diastolic blood pressure) and biochemical (glucose, insulin, lipid levels, thyroid function tests, cortisol, zonulin and leptin levels) parameters were measured. Results: A total of 43 obese subjects (23 males, mean age: 11.1±3.1 years) and 37 healthy subjects (18 males, mean age: 11.5±3.5 years) were included in this study. Obese children had significantly higher insulin, homeostasis model assessment of insulin resistance, triglyceride, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (HDL-C), zonulin and leptin levels than healthy children (p0.05). Comparison of the obese children with and without insulin resistance showed no statistically significant differences for zonulin levels (p>0.05). Zonulin levels were found to negatively correlate with HDL-C and positively correlate with leptin levels, after adjusting for age and BMI. Conclusion: To the best of our knowledge, this is the first study investigating the relationship between circulating zonulin level (as a marker of intestinal permeability) and insulin resistance and leptin (as markers of metabolic disturbances associated with obesity) in childhood obesity. The results showed that zonulin was significantly higher in obese children when compared to healthy children, a finding indicating a potential role of zonulin in the etiopathogenesis of obesity and related disturbances.

This study aimed to investigate the relationship between serum irisin level and metabolic and anthropometric parameters in obese children.The study included 36 obese children with a body mass index (BMI) of ≥95th percentile and 30 healthy children with a BMI ranging from the 5th to the 85th percentile. Healthy and obese children had similar age, gender and pubertal stage distribution. Anthropometric and biochemical parameters (fasting glucose, insulin, lipid profile, leptin and irisin levels) were measured. Bioelectric impedance analysis was used to determine the body composition parameters, including body fat percentage and fat mass.Serum irisin and leptin levels of the obese children were significantly higher than those of the healthy children [median irisin levels, 141.2107.6ng/mL, p=0.024; median leptin levels, 10.92.9pg/mL, P0.001, respectively). No statistically significant difference was found when leptin and irisin levels were compared among obese patients in terms of the presence of insulin resistance. Irisin levels significantly correlated with high-density lipoprotein cholesterol (HDL-C), fasting insulin and homeostasis model assessment-insulin resistance (HOMA-IR) with adjustment for age and BMI. The multivariate regression analysis showed that age, HOMA-IR and HDL-C had a significant association with the serum irisin level, which explained 30.6% of the variance.This study demonstrated that obese children had significantly higher irisin levels than healthy children. Additionally, it provides evidence regarding the role of irisin on insulin sensitivity and lipid metabolism in childhood obesity.

Increased amyloid beta (AB) peptide concentration is one of the initiating factors in the neurodegeneration process. It has been suggested that cholesterol induces the synthesis of AB peptide from amyloid precursor protein or facilitates the formation of amyloid plaque by lowering the aggregation threshold of the peptide. It is also shown that AB peptides may affect cholesterol metabolism and the synthesis of steroid hormones such as progesterone and estradiol. Pregnenolone (P) and pregnenolone sulfate (PS) are the major steroids produced from cholesterol in neural tissue. In toxicity conditions, the effect of AB peptides on P and PS levels has not yet been determined. Furthermore, it has not been clearly defined how changes in cellular P and PS levels affect neuronal cell survival. The aim of this study was to determine the effects of AB peptides on cellular changes in P and PS levels depending on the level of their main precursor, cholesterol. Cholesterol and toxic concentrations of AB fragments (AB 25-35, AB 1-40 and AB 1-42) were applied to PC-12 and SH-SY5Y cells. Changes in cellular cholesterol, P and PS levels were determined simultaneously in a dose-and time-dependent manner. The cell viability and cell death types were also evaluated. AB peptides affected both cell viability and P/PS levels. Steroid levels were altered depending on AB fragment type and the cholesterol content of the cells. Treatment with each of the AB fragments alone increased P levels by twofold. However, combined treatment with AB peptides and cholesterol increased P levels by approximately sixfold, while PS levels were increased only about 2.5 fold in both cell lines. P levels in the groups treated with AB 25-35 were higher than those in AB 1-40 and AB 1-42 groups. The cell viabilities were significantly low in the group treated by AB and cholesterol (9 mM). The effect of AB peptides on P levels might be a result of cellular self-defense. On the other hand, the rate of P increase might be playing a key role in the cell death mechanism of AB toxicity depending on cellular cholesterol levels.

Introduction: Several case reports stress that high-dose biotin causes incorrect laboratory results. However, the extent of this interference in children is not systematically studied. Aim: To assess factors associated with biotin interference on thyroid function tests in subjects with biotinidase deficiency. Method: The study included 44 children who were treated with oral biotin (Group 1, median dose: 10 mg/day [25–75p; 10–10], age: 1.83 years [1.04–2.90]) and 30 healthy subjects (Group 2, age: 1.05 years [0.37–3.37]). Thyroid function tests were performed with two different assays, and streptavidin-coated particles were used in order to remove biotin from serum samples of cases with biotin interference. Results: The measurements were first performed with Beckman Coulter. In Group 1, remarkably high levels of fT3 and fT4 were found in 26 (59.1%) and 25 (56.8%) patients, respectively. Thyroid hormone functions were all normal in Group 2. Significantly higher serum biotin levels were detected in interference-positive children (p < 0.001). The serum biotin levels in Group 1 showed a strong positive correlation with fT3 (r = 0.867, p < 0.001) and fT4 levels (r = 0.905, p < 0.001). A serum biotin level of 80.35 µg/L was found to be the best cut-off value for predicting interference (sensitivity: 96.2% and specificity: 94.4%). When analyzed with Siemens Advia Centaur XP, all thyroid function tests were normal in both groups except in one patient (2.27%) with slightly elevated fT3 level in Group 1. Repeated tests with Beckman Coulter after neutralization of biotin with streptavidin magnetic particles in serum samples of the interference-positive cases revealed normal thyroid hormone levels. Conclusion: Interference is an important problem in thyroid function tests in nearly 60% of all children receiving biotin treatment for biotinidase deficiency. Serum levels of biotin rather than the dosage are the main determinant of interference, which can be eliminated by choosing appropriate laboratory methods.

Background/aim: Galanin is a neuropeptide that is shown to be involved in the regulation of food intake and glucose homeostasis. The objective of this study was to evaluate the relation of serum galanin levels with anthropometric and metabolic parameters in obese and healthy children. Material and methods: The cross-sectional study consisted of 38 obese children (mean age: 11.9 ± 3.0 years) and 30 healthy children (mean age: 11.4 ± 2.0 years). Clinical and biochemical parameters [glucose, insulin, homeostasis model assessment-insulin resistance (HOMA-IR), lipids, galanin, and leptin levels] were assessed. Results: Serum galanin and leptin levels were significantly higher in obese children. In obese children, galanin levels were positively correlated with fasting glucose (r = 0.398, p = 0.013), insulin (r = 0.383, p = 0.018), HOMA-IR (r = 0.375, p = 0.020), and triglycerides (r = 0.391, p=0.015). Multivariate backward regression analysis revealed that galanin levels were significantly associated with fasting glucose, insulin, HOMA-IR, and triglyceride, which explained 42.0% of the variance (r2 = 0.483, P < 0.001). Conclusions: Serum galanin levels were significantly higher in obese children than healthy controls and positively correlated with insulin resistance and triglycerides in obese children. This study suggests that galanin is associated with glucose homeostasis and lipid metabolism in childhood obesity.

Background/aim: Nesfatin-1, an anorexigenic molecule, seems to play a role in appetite regulation and energy homeostasis. e goal of this study was to evaluate the relation of nesfatin-1 with anthropometric and metabolic (ghrelin, leptin) parameters in children with idiopathic chronic malnutrition. Materials and methods: The study included 37 underweight and 38 healthy children who were similar regarding age, sex, and pubertal status. Anthropometric and biochemical (nesfatin-1, ghrelin, and leptin levels) variables were assessed. Results: A total of 37 underweight subjects (mean age 10.5 &pm; 2.6 years) and 38 heathy subjects (mean age 10.3 ± 2.3 years) were recruited. Underweight children had signi cantly higher nesfatin-1 (2.76 &pm; 0.4 vs. 1.56 &pm; 0.7, P < 0.001) and lower leptin levels (2.21 &pm; 2.0 vs. 5.21 &pm; 2.4, P < 0.001) than those of the control subjects. Nesfatin-1 levels were signi cantly associated with only leptin levels, a er adjusting for age and BMI (r = ?0.371, P = 0.001). Conclusion: The present study is the rst to evaluate nesfatin-1 levels in relation with anthropometric and metabolic parameters in children with chronic malnutrition, who were subsequently found to have signi cantly higher nesfatin-1 levels. Our study underlines that nesfatin-1 may play a role in the development of malnutrition by inhibiting food intake in children.

Galectin-1, a recently identified peptide, is primarily released from the adipose tissue. Although galectin-1 was shown to have an anti-inflammatory effect, its specific function is not clearly understood. We aimed to evaluate the relationship of serum galectin-1 levels with clinical and laboratory parameters in childhood obesity. A total of 45 obese children (mean age: 12.1 +/- 3.1 years) and 35 normal-weight children (mean age: 11.8 +/- 2.2 years) were enrolled. Clinical [body mass index (BMI), waist circumference (WC), percentage of body fat and blood pressure] and biochemical [glucose, insulin, lipids, galectin-1, high-sensitive C-reactive protein (hsCRP) and leptin levels] parameters were assessed. Serum galectin-1, hsCRP and leptin levels were significantly higher in obese children than those in normal-weight children (12.4 vs 10.2 ng/mL, p < 0.001; 3.28 vs 0.63 mg/L, p < 0.001; 8.3 vs 1.2 ng/mL, p < 0.001, respectively). In obese children, galectin-1 levels correlated negatively with fasting glucose (r = 0.346, p = 0.020) and positively with fat mass (r = 0.326, p = 0.026) and WC standard deviation score (SDS) (r = 0.451, p = 0.002). The multivariate regression analysis demonstrated that serum galectin-1 levels were significantly associated with fasting glucose and WC SDS. This study showed that obese children had significantly higher galectin-1 levels in proportion to fat mass in obese cases than those in healthy children, which may be interpreted as a compensatory increase in an attempt to improve glucose metabolism.

Aim: The aim of the study was to evaluate the macular pigment optical density (MPOD) levels in patients with wet age-related macular degeneration (AMD), dry AMD, and also in healthy controls. Settings and Design: This study was conducted at Department of Ophthalmology, and the study design was a prospective study. Patients and Methods: Forty-eight patients with wet AMD, 51 patients with dry AMD, and 50 controls were included in the study. All patients were naive to both previous lutein or zeaxanthin administration and any previous intravitreal injections. Fundus reflectance (VISUCAM 500, reflectance of a single 460 nm wavelength) was used to measure the MPOD levels. Three groups were compared regarding age, gender, serum lutein, and zeaxanthin concentrations as well as MPOD levels. Results: Serum lutein and zeaxanthin levels were significantly higher in control group when compared with wet AMD (Group 1) and dry AMD (Group 2) (P = 0.001 and P < 0.001, respectively). Mean MPOD was found to be similar in all of the three study subgroups (P = 0.630). However, maximum MPOD was significantly higher in control group when compared with Group 1 and 2 (P = 0.003). There was no correlation between serum lutein or zeaxanthin concentrations and mean MPOD levels (P = 0.815, r = 0.014 and P = 0.461, r = 0.043, respectively), but there was a weak correlation between serum zeaxanthin concentration and maximum MPOD level (P = 0.042, r = 0.124). Maximum MPOD level was found to be correlated with the level of AMD (Group 1, 2, and 3; r = 0.184, P = 0.041). Conclusion: Maximum MPOD level was found to be lower in patients with AMD when compared with control cases. Mean MPOD and maximum MPOD levels were similar in wet and dry AMD Groups. These results can be applied clinically keeping in mind that MPOD measurements with one wavelength reflectometry may not be completely reliable.

UrotensinII (UII), one of the most potent vasoconstrictor proteins, may be associated with insulin resistance. The objective of our research was to determine the level of UII in sera of patients with PCOS and to investigate the relationship between UII and insulin resistance in patients with PCOS. Fourty seven PCOS patients and 42 healthy women were included in the study. Serum fasting glucose, insulin, UII, free testosterone and hs-CRP levels of the patients were examined. The HOMA-IR formula was used to calculate insulin resistance. Insulin sensitivity was calculated by using the QUICKI-IS formula. The two groups did not show any a significant difference in terms of age and BMI (p 0.05). Serum UII, hs-CRP, insulin levels and the HOMA-IR were significantly higher in the patients with PCOS (p 0.05). In the analysis of the correlation, UII and HOMA-IR showed statistically significant, moderately strong and positive correlation(r = 044, p 0.001). UII and QUICKI-IS showed statistically significant, moderately strong and negative correlation(r = -0.44, p 0.001). Also, a significant and positive correlation was found between with UII and hs-CRP(r = 0.51, p 0.001). Our study data suggested that UII may have a role in the pathophysiology of insulin resistance and increased cardiovascular risk, which are commonly found in patients with PCOS.

Context Adipsin, a protein secreted mainly from the adipose tissue, is a structural homologous of complement factor D, a rate-limiting enzyme of the alternative complement system. Growing evidence suggests that the alternative complement system plays a role both in the regulation of energy homeostasis and the atherosclerosis. Polycystic ovary syndrome (PCOS) is a reproductive and metabolic disease. Objective To ascertain whether circulating adipsin levels are altered in women with PCOS, and whether there is association between adipsin and metabolic parameters or carotid intima media thickness (CIMT). Participants 144 women with PCOS and 144 age- and BMI-matched controls without PCOS were recruited for this cross-sectional study. Main Outcome Measures Circulating adipsin levels were measured using ELISA. Metabolic, hormonal parameters and CIMT were also determined. Results Adipsin levels were significantly elevated in women with PCOS compared with controls (91.52 ± 14.11 vs. 60.31 ± 9.71 ng/ml, P

The current study aimed to investigate the relationship between serum betatrophin levels and metabolic and anthropometric parameters in obese children.The study included 40 obese children with a body mass index (BMI) above 95th centile, and 35 non-obese subjects with a BMI 3-85th centile, whose age and gender were similar to those of the patient group. Fasting serum glucose, insulin, lipid profile, alanine aminotransferase, aspartate aminotransferase, serum betatrophin, and leptin levels were measured to evaluate the metabolic parameters. Total cholesterol:high-density lipoprotein cholesterol and low-density lipoprotein cholesterol:high-density lipoprotein cholesterol ratios were calculated as "atherogenic indices".Serum betatrophin levels of the obese subjects were significantly lower than that of non-obese subjects (p0.05). Insulin resistant subjects had significantly lower betatrophin concentrations than those of non-insulin resistant subjects (p0.05). Betatrophin levels were negatively correlated with the fasting serum insulin and, accordingly insulin resistance index.Serum betatrophin levels are lower in obese and insulin resistant subjects and betatrophin might act as a potential biomarker of insulin resistance in obese children or adolescents.

Adropin is a peptide hormone implicated in the regulation of insulin sensitivity and energy homeostasis. Polycystic ovary syndrome (PCOS) is a metabolic and reproductive disease associated with insulin resistance. It has been demonstrated that various inflammatory markers increased in PCOS including TNF-α. TNF-α regulates the secretion of certain peptides which play a crucial role in glucose and lipid homeostasis. There is also some evidence of a link between TNF-α and adropin. To ascertain whether there is an association between circulating adropin levels and TNF-α in PCOS. 152 women with PCOS and 152 age- and body mass index-matched controls without PCOS were recruited for this cross-sectional study. Adropin and TNF-α levels were measured using ELISA. Adropin levels were lower in the PCOS group compared with the control group (7.43 ± 0.79 vs. 9.42 ± 0.76 ng/ml, P

OBJECTIVE: The objective of this trial was to determine the levels of inflammatory markers, high-sensitivity C-reactive protein and fetuin-A pre- and post-levothyroxine treatment in cases of subclinical hypothyroidism. MATERIALS AND METHODS: A total of 32 patients with a diagnosis of subclinical hypothyroidism and a control group of 30 healthy individuals were tested for high-sensitivity C-reactive protein and fetuin-A, followed by the administration of 50 µg of levothyroxine in the patient group for 3 months. During the post-treatment stage, high-sensitivity C-reactive protein and fetuin-A levels in the patient group were re-assessed and compared with pre-treatment values. RESULTS: Pre-treatment levels of both high-sensitivity C-reactive protein and fetuin-A were observed to be higher in the patient group than in the control group. The decrease in high-sensitivity C-reactive protein levels during the post-treatment stage was not statistically significant. However, the decrease observed in post-treatment fetuin-A levels was found to be statistically significant. CONCLUSION: The decrease in fetuin-A levels in subclinical hypothyroidism cases indicates that levothyroxine treatment exerts anti-inflammatory and anti-apoptotic effects. Although the decrease in high-sensitivity C-reactive protein levels was statistically non-significant, it is predicted to reach significance with sustained treatment.

We aimed to investigate serum nesfatin-1 level in girls with premature thelarche (PT) and its relationship with anthropometric parameters and leptin, which are involved in the initiation of pubertal process.Non-obese girls who presented with the complaint of early (2-8 years) and isolated breast development were included in the study. The control group consisted of age-matched healthy prepubertal girls. Auxological measurements were performed in all subjects. Gonadotropin-releasing hormone (GnRH) stimulation test and bone age assessment were conducted in subjects with early breast development. Girls with a bone age/chronologic age ratio1.2 and a peak luteinizing hormone (LH) response to GnRH stimulation5 mIU/L were included in the PT group.The study included 22 non-obese girls with PT and 24 healthy prepubertal controls. Body mass index (BMI), BMI-standard deviation score (SDS) and height SDS were similar between the groups (p0.05). Serum leptin and nesfatin-1 levels were found significantly higher in the PT group compared to controls (p0.05). No correlation was detected between nesfatin-1 and basal LH, basal follicle stimulating hormone (FSH), stimulated peak LH, peak FSH, leptin levels and anthropometric parameters in the PT group (p0.05).Results of the present study showed that serum nesfatin-1 and leptin levels are significantly higher in girls with PT than in prepubertal controls. This finding suggests that similar to leptin, nesfatin-1 may also have a central or peripheral role in the initiation of pubertal process and may be related to PT pathogenesis.

The aim of the present study was to investigate the diagnostic role of serum neurokinin B level and its relationship with kisspeptin and leptin, which are known to be involved in the initiation of pubertal process. Girls who presented with breast development (1 and a peak luteinizing hormone response in gonadotropin releasing hormone stimulation test >5 mIU/L were included in the central precocious puberty group, while patients who did not meet these criteria were included in the premature thelarche group. Patients with organic pathologies were excluded. Healthy prepubertal girls with similar age were included as the control group. Leptin, kisspeptin and neurokinin B levels were measured by ELISA method. The study included 20 girls with idiopathic central precocious puberty 22 girls with premature thelarche and 24 prepubertal controls. While serum kisspeptin, leptin and neurokinin B levels were significantly higher in central precocious puberty and premature thelarche groups compared to controls, no significant difference was found between central precocious puberty and premature thelarche groups. Increased serum levels of leptin, kisspeptin and neurokinin B in patients with premature thelarche and central precocious puberty suggest that they take part during the initiation of pubertal process, however, these markers are not able to differentiate patients with central precocious puberty from premature thelarche. (C) 2015 Elsevier Inc. All rights reserved.

Objective Adhesion molecules are involved in inflammation, atherosclerosis and malignancy. This study measured levels of adhesion molecules before and after levothyroxine therapy in patients with subclinical hypothyroidism (SHO). Methods Levels of soluble (s) intracellular adhesion molecule (ICAM)-1, s vascular cell adhesion molecule (sVCAM) VCAM-1 and sE-selectin were analysed in patients diagnosed with SHO, prior to administration of 50 µg/day levothyroxine orally for 3 months. Subsequently, levels of sICAM-1, sVCAM-1 and sE-selectin were reanalysed then compared with the pretreatment levels. Results In 30 patients with SHO, levels of sICAM-1 were found to be significantly higher than those in healthy controls, ( P = 0.001). Post-treatment sICAM-1 levels were significantly lower than pretreatment levels ( P = 0.001). No significant differences were found in sVCAM-1 or sE-selectin levels between healthy controls and patients with SHO before treatment, or between patients with SHO pre- and post-treatment. Conclusions Patients with SHO had significantly higher levels of sICAM-1 compared with controls. Levels became normal after treatment with levothyroxine. These findings emphasize the need for levothyroxine therapy in cases of SHO to normalize sICAM-1 levels. Such treatment helps to prevent the future development of atherosclerosis or cancer.

Background: High levels of adhesion molecules are known to result in inflammation of the vascular cells through endothelial dysfunction and thus atherogenesis. To this end, this trial was performed to investigate whether a cause of the accelerated atherogenesis in cases with non-alcholic fatty liver disease (NAFLD) was the increase in the levels of the adhesion molecules. Material and Methods: 53 cases with NAFLD diagnosed using ultrasonography and biopsy and 46 control cases were enrolled in the trial. Soluble intercellular adhesion molecule (sICAM-1), Vascular adhesion molecule (sVCAM) and sE-selectinconcentrations were determined by using an enzyme linked immunosorbent assay (ELISA) kit from Biosource (Bender MedSystems GmbH, Vienna Austria) according to the manufacturer’s instructions. Results: The levels of these adhesion molecules in patients with NAFLD were higher than those in the control subjects but only a significant difference in sE-selectin levels between the NAFLD and control groups was observed (p 0.05). Conclusions: The high levels of adhesion molecules and particularly of the sE-selectin statistically suggest that endothelial dysfunction and inflammation occur, which may represent a major factor in accelerating the atherogenesis process. We believe that detection of a high sE-selectin level would be leading the way when developing new therapeutical modalities for cases with NAFLD.

OBJECTIVE: Fetuin-A is a protein secreted from the liver that inhibits arterial calcification deposition and can contribute to insulin resistance. Hyperthyroidism is also associated with insulin resistance. It is not known whether hyperthyroidism has an effect on fetuin-A levels. METHODS: We measured fetuin-A levels and homeostasis model of assessment-insulin resistance before hyperthyroidism treatment was initiated and after euthyroidism was achieved. A total of 42 patients diagnosed with hyperthyroidism were enrolled in this study. Fetuin-A, insulin, high-sensitivity C-reactive protein, fasting blood glucose, free T3 (fT3), free T4 (fT4), and thyrotropin were measured before and after euthyroidism was established. RESULTS: Basal fasting blood glucose, high-sensitivity C-reactive protein, insulin, c-peptide, homeostasis model of assessment-insulin resistance, fT3, fT4 and fetuin-A levels were significantly decreased after euthyroidism was achieved (Table 1). Basal fasting blood glucose (r:0.407, p:0.008), high-sensitivity C-reactive protein (r:0.523, p

This study was designed to show the effect of propylthiouracil treatment on sCD40L, high-sensitivity C-reactive protein, and fetuin-A levels on subjects with subclinical hyperthyroidism. After checking sCD40L, high-sensitivity C-reactive protein, and fetuin-A levels of 35 patients with subclinical hyperthyroidism, each was given 50 mg tablets of propylthiouracil three times daily. After 3 months, sCD40L, high-sensitivity C-reactive protein, and fetuin-A levels were then compared to the levels before treatment. Although high-sensitivity C-reactive protein and sCD40L levels were normal in the subclinical hyperthyroidism patients compared to the healthy controls, fetuin-A levels were statistically significantly higher (*p = 0.022). After treatment, fetuin-A levels of subclinical hyperthyroidism patients decreased statistically significantly compared to the levels before treatment (**p = 0.026). sCD40L and high-sensitivity C-reactive protein levels did not have a statistically significant difference compared to the control group and post-propylthiouracil treatment. In subclinical hyperthyroidism patients, high fetuin-A levels before propylthiouracil treatment and decreases in these levels after treatment in cases with subclinical hyperthyroidism indicated the possibility of preventing long-term cardiac complications with propylthiouracil treatment.

WOS: 000294257800004, PubMed: 21804277, Background Increased levels of selectins, adhesion molecules, hs-CRP and homocysteine are considered important as indicators of atherosclerosis. There is a significant amount of evidence that high LDL-C levels are a risk factor for coronary artery disease, whereas the relevance of isolated triglycerides is controversial. The present study aims to compare the levels of homocysteine, hs-CRP, E-selectin, sP-selectin, VCAM-1, ICAM-1 in patients with isolated hypertriglyceridemia and polygenic hypercholesterolemia. Methods The following three groups were formed: polygenic hypercholesterolemia group (n=30), isolated hypertriglyceridemia group (n=30) and control group (n=30). These three groups were matched in terms of BMI, waist circumference and gender. Plasma high sensitive CRP, homocysteine, sVCAM-1, sICAM-1, sP-selectin, sE-Selectin levels of patients in these three groups were measured. Results In the present study, mean values for sE-selectin, sVCAM-1 and sICAM-1 in the polygenic hypercholesterolemia group were significantly higher than in the other two groups (p0.05), where as the hs-CRP value was significantly higher in patients with isolated hypertriglyceridemia compared to the control group (p=0.001). Conclusion The increase of adhesion molecules, homocysteine and hs-CRP in polygenic hypercholesterolemia subjects compared to the isolated hypertriglyceridemia group reflects their high cardiovascular risk.

Our aim was to investigate the protective effect of wheat germ oil (WGO) at different doses on diabetes mellitus (DM)-induced erectile and endothelial dysfunction. Twenty-four male Wistar rats weighing 250-300 g were divided into four groups as; control group treated with saline, DM group, DM group treated with 3 ml/kg WGO (DM + 3WGO group), DM group treated with 6 ml/kg WGO. Type 1 DM was induced by intraperitoneal injection of 60 mg/kg streptozotocin (STZ). STZ-induced diabetic rats received saline, 3 ml/kg WGO, and 6 ml/kg WGO via oral gavage daily for 5 weeks. The density of WGO used was 0.92 g/ml. The protective effect of WGO was evaluated by (i) in vitro vascular function, (ii) in vivo erectile function, and (iii) oxidative stress parameters in both aorta and penile tissue. Acetylcholine-mediated relaxation in the aorta and erectile functions decreased significantly in the DM group (p = 0.018 and p = 0.005). WGO (3 and 6 ml/kg) improved vascular functions in the DM groups (p = 0.001 and p = 0.014). The beneficial effect of WGO on erectile function appeared at higher doses of WGO. However, a higher dose of WGO substantially increased the oxidative stress parameters in both aorta and penile tissue. These findings suggest that the improvement in vascular or erectile function by WGO was not related to antioxidant effects, and new studies are needed to clarify the mechanism.