An enormous amount of data has been published in recent years demonstrating melatonin's defensive role against toxic free radicals. In the present study, we examined the role of melatonin as an antioxidant against the effect of continuous light exposure. Rats were divided into three groups. Control rats (group A) were kept under natural conditions whereas other group of rats (group B and C) were exposed to constant light for inhibition of melatonin secretion by the pineal gland. Group C rats also received melatonin via s.c. injection (1 mg x kg(- 1) body weight x day(- 1)). At the end of experiment, all animals were sacrificied by decapitation, serum and tissue samples were removed for determination of malondialdehyde (MDA), a product of lipid peroxidation, conjugated dienes levels and glutathione peroxidase (GSH-Px) activity levels. It was found that lipid peroxidation was increased in the rats which were exposed to constant light. Melatonin injection caused a decrease in lipid peroxidation, especially in the brain. In addition, melatonin application resulted in increased GSH-Px activity, which has an antioxidant effect. Thus, melatonin is not only a direct scavenger of toxic radicals, but also stimulates the antioxidative enzyme GSH-Px activity to detoxify hydroxyl radical produced by constant light exposure.

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Aim: To investigate the effect of gabapentin on neural [neuron-specific enolase (NSE)] and glial markers [glial fibrillary acidic protein (GFAP) and S100B] in different brain regions of diabetic rats. Methods: Diabetes was induced by a single intraperitoneal injection of streptozotocine (50 mg/kg body weight). Rats in one diabetic group received gabapentin (50 mg·kg ) and rats in the other diabetic group received vehicle only for 6 weeks. The levels of GFAP, S100B, and NSE were determined by immunoblotting in the hippocampus, cortex, and cerebellum. Lipid peroxidation (LPO as malondialdehyde+ 4-hydroxyalkenals) and glutathione (GSH) levels were also determined in the same brain parts. Results: Total and degraded GFAP content and S100B protein expression in different areas of brain tissues significantly increased in diabetic rats compared to control rats. Similarly, NSE levels were also significantly elevated in hyperglycemic rats. In addition, there was a significant increase in LPO levels in the diabetic rat brain compared to control rat brains. Pretreatment with gabapentin prevented the upregulation of GFAP, S100B, and NSE in all brain regions of diabetic rats. The level of LPO was reduced, but not completely halted, by treatment with gabapentin. Conclusion: These results suggest that diabetes causes glial and neuronal injury, possibly as a result of elevated oxidative stress, and that gabapentin protects neurons and glial cells. Thus, we predict that gabapentin treatment will attenuate the hippocampal and cortical neurodegeneration observed during diabetes mellitus in rats. Key wordsgabapentin; glial fibrillary acidic protein; neurotrophic protein S100beta; phosphopyruvate hydratase; lipid peroxidation 1 Study supported by the Firat University R esear ch Fou nda t ion ( FUB AP Proj ect number 831).

Glial cells provide structural and metabolic support for neurons, and these cells become reactive to any insult to the central nervous system. The streptozotocin (STZ) rat model was used to study glial reactivity and the prevention of gliosis by alpha-lipoic acid (alpha-LA) administration. The expression of glial fibrillary acidic protein (GFAP), S100B protein, and neuron specific enolase (NSE) was determined as well as lipid peroxidation (LPO) and glutathione (GSH) levels in some brain tissues. Western blot analyses showed GFAP, S100B, and NSE levels significantly increased under STZ-induced diabetes in brain, and LPO level increased as well. Administration of alpha-LA reduced the expression both of glial and neuronal markers. In addition, alpha-LA significantly prevented the increase in LPO levels found in diabetic rats. GSH levels were increased by the administration of alpha-LA. This study suggests that alpha-LA prevents neural injury by inhibiting oxidative stress and suppressing reactive gliosis.

The underlying molecular mechanism of carcinogenesis in oral squamous cell carcinoma (OSCC) is poorly understood and appears to be controlled on many genetic, environmental, and hormonal factors. Obestatin and ghrelin, two recently discovered hormones, are co-expressed in endocrine cells. The purpose of this investigation was to examine the immunohistochemical features of OSCCs in relation to the tissue concentration of ghrelin and obestatin. The association between OSCC and Epstein Barr Virus (EBV) status was also explored. The expression of ghrelin and obestatin was examined by immunohistochemistry and immunoassay in oral biopsy specimens: 10 benign squamous epithelial cell samples, 10 microinvasive squamous cell carcinomas, and seven well-differentiated and seven poorly differentiated OSCCs. The presence of EBV was evaluated in these samples using immunohistochemistry. The concentrations of ghrelin and obestatin in tissue homogenates were measured by RIA and ELISA, respectively. Squamous cell carcinomas and benign tissue samples were positive for anti-EBV antibody, and obestatin and ghrelin were shown to be co-expressed in all stratified squamous epithelium samples. Expression of ghrelin and obestatin was decreased or absent in OSCCs in relation to the invasiveness of the carcinoma; ghrelin and obestatin levels in cancerous tissue homogenates were lower than in benign tissue homogenates. These results indicate that the concentrations and distribution of immunoreactive obestatin and ghrelin might be helpful in distinguishing OSCC from benign tumors. Maintaining normal levels of these hormones might be required for regulation of normal cell division. However, detailed studies will be required for better understanding of the complex mechanism of carcinogenesis relating to OSCCs.

Obesity, characterized by hyperleptinemia and hypoghrelinemia, has become a major health problem all over the world and is associated with an increased risk of complications including insulin resistance, hypertension, dyslipidemia, diabetes mellitus and atherosclerosis. The use of the pancreatic lipase inhibitor Orlistat can help seriously overweight people to achieve and maintain weight loss. The aim of our study was to compare the serum leptin and ghrelin levels in obese subjects who take orlistat with those receiving only dietary treatment. Twenty-one obese patients and 10 control subjects participated. The obese patients were divided into two groups; one group (n=11) took orlistat (120 mg, 3 times daily) and received dietary treatment and the other (n=10) only received the dietary treatment. The study lasted twelve weeks. The concentrations of serum ghrelin, leptin, insulin and C-peptide, and routine biochemical parameters, were measured in both groups. The serum ghrelin level was higher in control (183+/-62 fmol/ml) than obese (59+/-30 fmol/ml) subjects while the plasma leptin level was lower in control (8.7+/-12 microg/L) than obese (36.7+/-19 microg/L) subjects (all p<0.001). BMI and the total blood cholesterol, LDL and triglyceride levels fell significantly after both orlistat and dietary treatment in the obese subjects (all p<0.01), and the plasma ghrelin level rose (p<0.01). The leptin level demonstrated the opposite trend in both groups but only the patients taking orlistat showed a significant change (p<0.05).Taken together, these results show that orlistat has no effect on body weight in obese subjects additional to that conferred by a non-pharmacological life-style intervention. We therefore conclude that weight lost rather than type of treatment might be more valuable in obesity.

Renal Doppler ultrasonography can noninvasively identify a subgroup of nonazotemic patients with hepatic cirrhosis who are at high risk for subsequent development of renal dysfunction and hepatorenal syndrome.

Introduction: Meteorin-like (Metrnl), also known as subfatin, is a recently discovered adipokine with a favourable effect on insulin sensitivity. Studies have shown lower Metrnl levels in obese patients. However, data on its circulating levels in type 2 diabetes mellitus (T2DM) patients are contradictory. This study aims to evaluate serum Metrnl levels in T2DM patients and determine the relationship between serum Metrnl levels and insulin resistance in these patients. Material and methods: This cross-sectional study was conducted among 150 participants. The study was carried out between June 2019 and December 2019 at the internal medicine outpatient clinic of a tertiary university hospital. The participants were divided into three groups: group 1 (control group, n = 50), group 2 (newly diagnosed T2DM, n = 50), and group 3 (long-standing diagnosed T2DM, n = 50). An enzyme-linked immunosorbent assay (ELISA) was used to measure the serum levels of Subfatin (Metrnl), and the correlations of Metrnl level with anthropometric parameters, HOMA index, and biochemical measurements were assessed. Results: There was no statistically significant difference between the gender (p = 0.468) and age (p = 0.067) characteristics of the three groups. The Metrnl (subfatin) levels of the participants were as follows: control group-20.05 (1.56-103.78); newly diagnosed T2DM group-2.62 (1.25-103.78); and long-standing diagnosed T2DM group-2.01 (0.80-19.84) pg/mL. The Metrnl (subfatin) levels of the participants in the control group were higher than in the participants in the newly diagnosed T2DM and long-standing diagnosed T2DM groups (p < 0.001). Subfatin demonstrated a negative correlation with insulin and HOMA-IR in the control group and long-standing diagnosed T2DM group. Conclusions: The subfatin level was found to be higher in the healthy control group than in both diabetic patient groups. Subfatin level showed negative correlation with both insulin level and HOMA index. There was a relationship between subfatin and insulin resistance. Low levels of subfatin in the diabetic patient groups may play a role in the pathogenesis of T2DM by increasing insulin resistance.