Oya Sayin

Investigation of adropin and leptin levels in pediatric obesity-related nonalcoholic fatty liver disease.

Abstract Aim: Nonalcoholic fatty liver disease (NAFLD) is the accumulation of excess fat in the liver in the absence of alcohol consumption, which is commonly associated with obesity and increased risk of atherosclerosis as well as insulin resistance. Adropin is a recently identified protein encoded by the gene related with energy homeostasis, which is expressed in the liver and the brain and has a role in preventing insulin resistance and obesity. The aim of this study was to investigate the serum adropin and leptin levels in obese adolescents and compare the patients with, and without, NAFLD and with healthy controls. Methods: Sixty-four obese adolescents (30 with NAFLD, 34 without NAFLD) and 36 healthy controls were enrolled in the study. Serum adropin and leptin levels were evaluated by sandwich enzyme-linked immunosorbent assay. Results: Serum adropin levels were significantly lower in obese children than healthy controls (3.2±1.0 and 9.2±1.2 ng/mL, respectively, p=0.001). Serum leptin levels were significantly higher in patients than in controls (12.4±1.1 and 4.1±3.1 pg/mL, respectively; p=0.000). Serum adropin levels of patients with NAFLD were significantly lower than in patients without NAFLD (2.9±0.5 and 3.5±1.2 ng/mL, respectively; p=0.023) and healthy controls (p=0.000). Logistic regression analysis showed that a decrease in adropin levels was the only independent factor for fatty liver disease in obese adolescents (odds ratio: 3.07, 95% confidence interval 1.14–8.2, p=0.026). Leptin, relative weight and HOMA-IR of the patients were not independent risk factors for NAFLD. Conclusions: In this study, serum adropin levels were significantly lower in obese adolescents with fatty liver disease compared to patients without fatty liver disease and healthy controls. Lower adropin level was an independent risk factor for NAFLD in obese adolescents in logistic regression analysis. Assessment of serum adropin concentrations may provide a reliable indicator of fatty liver disease in obese adolescents.

A Comparison Study of Growth Factor Expression following Treatment with Transcutaneous Electrical Nerve Stimulation, Saline Solution, Povidone-Iodine, and Lavender Oil in Wounds Healing

This study compared the effects of transcutaneous electrical nerve stimulation (TENS), saline solution (SS), povidone-iodine (PI), and lavender oil (Lavandula angustifolia) through expression of growth factors in a rat model of wound healing. Six experimental groups were established, each containing 8 rats: a healthy group with no incision wounds, an incision-control group, an incision and TENS group, an incision and SS group, an incision and PI group, and an incision and lavender oil group. Experiments continued for 5 days, after which the skin in the excision area was removed. Tissue concentrations of epidermal growth factor (EGF) and platelet-derived growth factor (PDGF)-A were measured using enzyme-linked immunosorbent assay (ELISA). Tissue expressions of EGF, PDGF-A, and fibroblast growth factor (FGF)-2 were determined using immunohistochemistry. Wound closure progressed more rapidly in the TENS and lavender oil groups than in the control and other study groups. In particular, PDGF-A expressions in the dermis and EGF expression in the epidermis were significantly intense in the TENS group (P < 0.05). In addition, ELISA levels of growth factors such as PDGF-A and EGF were significantly higher in TENS group compared to the control group (P < 0.05). These immunohistochemical and ELISA results suggest that TENS may improve wound healing through increasing growth factors in the dermis and epidermis more than other topical applications.

Neuroprotective effects of MK-801 against traumatic brain injury in immature rats.

Traumatic brain injury (TBI) is a major health problem in pediatric ages and also has major social, economic, and emotional outcomes, with diverse sequelae in many spheres of everyday life. We aimed to investigate the effect of MK-801, a competitive NMDA receptor antagonist, on hippocampal damage and behavioral deficits on 10-day-old rat pups subjected to contusion injury. The aims of the present study were to determine: (i) the short term effects of MK-801 on hippocampal BDNF, NGF and NMDA receptor immunoreactivity and neuron density in hippocampus (ii) long term effects of MK-801 on cognitive dysfunction following TBI in the immature rats. MK-801, was injected intraperitoneally at the doses of 1mg/kg of body weight immediately after induction of traumatic injury. Hippocampal damage was examined by cresyl violet staining, BDNF, NGF and NMDAR receptor immunohistochemistry on P10 day and behavioral alterations were evaluated using elevated plus maze and novel object recognition tests two months after the trauma. Histopathological and immunohistochemical evaluations showed that treatment with a single dose of 1mg/kg MK-801 (i.p.) significantly ameliorated the trauma induced hippocampal neuron loss and decreased BDNF, NGF and NMDAR expressions in CA1, CA3 and DG hippocampal brain regions. Additionally, treatment with MK-801 ameliorated anxiety and hippocampus dependent memory of animals subjected to trauma. These results show that acute treatment of MK-801 has a neuroprotective role against trauma induced hippocampal neuron loss and associated cognitive impairment in immature rats.

Evaluation of the relationship between serum adropin levels and blood pressure in obese children.

Abstract Background: The prevalence of obesity and related cardiovascular comorbodities is increasing rapidly. Adipokines play a major role in the pathogenesis of obesity-related inflammation and hypertension. Aim: The aim of this study was to evaluate the serum adropin levels in obese children and to determine the relationship between adropin levels and blood pressure (BP) in the pediatric age group. Methods: Forty obese children (mean age: 12.5±2.5 years; male/female ratio: 18/22) and 15 healthy controls (mean age: 15±3.14 years; male/female ratio: 5/15) were included in the study. Serum adropin levels, and a number of laboratory and clinical variables were compared. Ambulatory blood pressure monitoring was performed on obese subjects. Relationship between adropin levels and BP variables was examined. Results: Serum adropin levels were significantly lower in obese subjects than in healthy controls (193.56±94 vs. 289±187 pg/mL, p=0.03). Adropin levels were correlated negatively with body mass index z-score (r=−0.56; p=0.034). There was no correlation between serum adropin levels and laboratory variables in obese subjects. Five of the patients (12.5%) were nondipper, and nine of the patients (22.5%) had hypertension. There was no significant correlation between serum adropin levels and BP variables. Conclusion: Serum adropin levels were significantly lower in obese children; however, there was no correlation between serum adropin levels and BP variables. Further studies are needed to determine the role of adipokines on BP.

Resveratrol Reduces Matrix Metalloproteinase-2 Activity Induced by Oxygen-Glucose Deprivation and Reoxygenation in Human Cerebral Microvascular Endothelial Cells

The main pathophysiology in cerebral ischemia is the structural alteration in the neurovascular unit, coinciding with neurovascular matrix degradation. Among the human matrix metalloproteinases (MMPs), MMP-2 and -9, known as gelatinases, are the key enzymes for degrading type IV collagen, which is the major component of the basal membrane that surrounds the cerebral blood vessel. In the present study, we investigated the effects of resveratrol on cytotoxicity, reactive oxygen species (ROS), and gelatinases (MMP-2 and -9) in human cerebral microvascular endothelial cells exposed to 6 hours of oxygen-glucose deprivation and a subsequent 24 hours of reoxygenation with glucose (OGD/R), to mimic ischemia/reperfusion in vivo. Lactate dehydrogenase increased significantly, in comparison to that in the normoxia group. ROS was markedly increased in the OGD/R group, compared to normoxia. Correspondingly, ROS was significantly reduced with 50 μM of resveratrol. The proMMP-2 activity in the OGD/R group showed a statistically significant increase from the control cells. Resveratrol preconditioning decreased significantly the proMMP-2 in the cells exposed to OGD/R in comparison to that in the OGD/R group. Our results indicate that resveratrol regulates MMP-2 activity induced by OGD/R via its antioxidant effect, implying a possible mechanism related to the neuroprotective effect of resveratrol.

Evaluation of serum neopterin levels and its relationship with adipokines in pediatric obesity-related nonalcoholic fatty liver disease and healthy adolescents.

Abstract Aim: Nonalcoholic fatty liver disease (NAFLD) is associated with inflammation and increased risk of atherosclerosis. Neopterin is regarded as a biochemical marker of cell-mediated immunity, which is secreted by monocytes and macrophages, mainly in response to interferon-gamma. The aim of the present study was to investigate the serum neopterin levels in obese adolescents and compare the neopterin levels in patients with and without NAFLD and also with healthy controls. The second aim of the study was to research the possible relationship between neopterin levels and adipokines (leptin, adiponectin, resistin, and ghrelin). Methods: Ninety-three obese adolescents (39 with NAFLD, 54 without NAFLD) and 55 healthy controls were enrolled in the study. Serum levels of neopterin and adipokines were measured with high-performance liquid chromatography and sandwich enzyme-linked immunosorbent assay, respectively. Results: Serum neopterin levels were significantly higher in patients with NAFLD (3.20±0.09 nmol/L) than in their healthy peers (2.91±0.08 nmol/L) (p=0.020). Neopterin levels were positively correlated with leptin levels in obese patients (r=0.380, p<0.001) and in the group comprising all individuals (r=0.206, p<0.05). There was no correlation between neopterin concentrations and relative weight, alanin aminotransferase, adiponectin, resistin, and ghrelin levels. Conclusion: The serum neopterin levels were significantly higher in obese adolescents with fatty liver disease compared to controls, and this may be related to increased cell-mediated immunity in fatty liver disease.

Lipoic acid decreases peritoneal adhesion formation in a rat uterine scar model

OBJECTIVE To investigate the effects of lipoic acid in the prevention of postoperative pelvic adhesions by a visual scoring system and immunohistochemistry in a rat uterine horn model with full thickness injury. MATERIAL AND METHODS Twenty-eight female Wistar albino rats were randomised into four groups: uterine trauma control, 15 days and 30 days, and uterine trauma + lipoic acid, 15 days and 30 days. A full thickness defect was established by incising a segment of approximately 1.0 cm in length from each uterine horn, leaving the mesometrium intact. Extension and severity of the adhesions in each group were scored by a visual scoring system and evaluated immunohistochemically. RESULTS Adhesion scores were 2.00±0.81, 2.14±0.69 0.71±0.75, and 0.85±0.69 for extent and 2.28±0.48, 2.14±0.69, 0.85±0.69, and 1.14±0.69 for severity in Groups 1, 2, 3 and 4, respectively. Adhesion extent and severity were significantly less for groups treated by lipoic acid but no difference was observed between long and short administration. Both Vitronectin and u-PAR staining were significantly increased in treatment groups when compared to the control group. CONCLUSION Lipoic acid was found to be effective in reducing postoperative adhesion formation in a rat model.

SERUM NESFATIN-1 LEVELS IN GIRLS WITH IDIOPATHIC CENTRAL PRECOCIOUS PUBERTY

Objective: Nesfatin-1, an anorexigenic neuropeptide, is expressed mainly in the central nervous system and in some peripheral tissues. The role of nesfatin-1 in energy balance has been investigated. Despite the suggestion of a role for nesfatin-1 in reproductive function, data are limited on the role of nesfatin-1 in human puberty. Methods: The aim of this study was to investigate the following: i) the role of nesfatin-1 in puberty, and ii) relationship between nesfatin-1 and anthropometric measurements and gonadotropin levels in girls with idiopathic central precocious puberty (CPP). Twenty-four girls with CPP (7.68±1.02 years) and 20 female, prepubertal, healthy controls (7.48±0.88 years) were enrolled in the study. All patients with CPP were treated by the intramuscular administration of leuprolide acetate at a daily dose of 3.75 mg for 28 days. Nesfatin-1 was measured before and during treatment. Results: There was no difference in serum nesfatin-1 levels in girls with CPP and healthy controls [5.67 (2.5-20.6) mmol/L and 5.75 (2.51-9.64) mmol/L], respectively. There was a negative correlation between nesfatin-1 levels and body weight and body mass index-standard deviation score (p=0.01, r=-0.83; p=0.025, r=-0.81, respectively). No correlation was found between nesfatin-1 and gonadotropin, estradiol levels, uterine length or endometrial thickness. Conclusion: The results of this study suggest that there are no differences between girls with CPP and healthy, prepubertal girls regarding nesfatin-1 levels.

In Vitroeffects of Selenium on Human Glioblastoma Multiforme Cell Lines: A Preliminary Study

Glioblastoma multiforme (GBM) is caused by the central nervous system-derived glial cells, and represents the most common (50%-60%) form of primary brain tumors. The aim of this study was to investigate the in vitro effects of selenium on human GBM cells. In the present study, GMS-10 and DBTRG-05MG human GBM cell lines were used as a model to examine selenium entering the cell, cell proliferation, cytotoxicity, DNA fragmentation and Ki-67 protein expression in selenomethionine treated and non-treated groups. Seleno-L-methionine (SeMet) as the organic source of selenium exerted effects on cell proliferation and cytotoxicity, as assessed with WST-1 and lactate dehydrogenase (LDH) tests, respectively. Apoptosis was assessed by DNA fragmentation with an enzyme-linked immunosorbent assay. Ki-67 protein expression was determined by Western blotting, while selenium measurements were performed in the supernatants and lysates by using Graphite Furnace Atomic Absorption Spectrometry. This is the first study to examine the effects of SeMet on cell proliferation and death in GMS-10 and DBTRG-05MG cells. Both GBM cell lines responded to SeMet in a dose- and time-dependent manner. WST-1 test showed that low-dose SeMet treatment (50 and 100 μM) increased cell proliferation. Analysis of intracellular SeMet levels by using AAS showed results consistent with viability and cytotoxicity tests. SeMet treatment for 72h caused increased DNA fragmentation in both cell lines. In conclusion, our results suggest that SeMet induces cell death at high doses, while increasing cell proliferation at low doses. In the view of the data obtained in this investigation, further studies focusing on the possibility of using SeMet against different types of GBM and in combination with prospect synergic compounds are considered to be worthwhile.

Relationship of serum ghrelin, leptin, resistin, adiponectin levels with nutritional status and inflammatory determinants in juvenile idiopathic arthritis

levels were statistically significant between control group and inactive disease group (p=0.000). We also compared the patients whose weight for height were 90-110 with healthy controls in order to make a comparement independent from the effects of adipose tissue on levels of leptin and adiponectin: levels of adiponectin were significantly lower in patients than controls (p=0.005), levels of leptin were significantly lower in patients than controls (p=0.000), levels of relative adiponectin were significantly lower in patients than controls (p=0.007) and levels of relative leptin were significantly lower in patients than controls (p=0.000). Conclusion In this study, we showed that levels of relative leptin and adiponectin of JIA patients were lower than controls. This may be related to the inhibition of leptin and adiponectin production per unit of fat mass in the existence of disease. Further prospective studies including larger number of patients are required to demonstrate the effect of the disease and the treatments on adipokines in JIA patients.