<abstract xmlns="http://www.w3.org/1999/xhtml"> Objective. The aim of the present study was to determine the irisin levels in patients with the type 1 diabetes mellitus (T1DM) and to examine the relation of irisin levels with the inflammation and autoimmunity.Methods. This study included 35 cases diagnosed with T1DM and 36 healthy volunteers. Antiglutamic acid decarboxylase (anti-GAD), islet cell antibody (ICA), and insulin autoantibody levels were measured in patients at the time when they were included into the study and recorded from the patient files. Serum irisin levels were measured by ELISA kit.Results. The median irisin levels were determined higher in T1DM group compared to the control one (6.8 ng/ml vs. 4.8 ng/ml, p=0.022; respectively). Median irisin levels were higher in anti-GAD (p=0.022) and ICA (p=0.044) positive groups compared to negative groups. In T1DM group, irisin levels displayed positive correlation with glycosylated hemoglobin (HbA1c) (r=0.377, p&lt;0.001) and anti-GAD (r=0.392, p=0.020) and negative correlation with creatinine (r=-0390, p=0.021). In multivariate regression model, HbA1c (B±SE: 2.76±17683, p&lt;0.001), and anti-GAD (B±SE: 2.311±0.610, p=0.001) were determined as independent predictors for predicting the irisin levels.Conclusion. In patients with T1DM, which chronic inflammation and autoimmunity take part in their etiopathogenesis, anti-GAD levels were an independent risk factor for the irisin. Th is may suggest that factors such as inflammation and autoimmunity can be effective in the synthesis of irisin.</abstract>

Ankara Numune Training and Research Hospital, Department of Internal Medicine, Ankara,

Turkey Yuksek Ihtisas Training and Research Hospital, Department of Gastroenterology, Ankara,

Ankara Numune Training and Research Hospital, Department of Biochemistry, Ankara,

Ankara Numune Training and Research Hospital, Department of Biochemistry, Ankara, Turkey

Hitit University School of Medicine, Department of Endocrinology and Metabolism, Çorum,

Factors associated with increased irisin levels in the type 1 diabetes mellitus

<abstract xmlns="http://www.w3.org/1999/xhtml"> Objective. The aim of the present study was to examine the effect of inhibition of endoplasmic reticulum stress signaling, mediated by IRE1 (inositol requiring enzyme 1), which is a central mediator of the unfolded protein response on the expression of genes encoded estrogen related proteins (NRIP1/RIP140, TRIM16/EBBP, ESRRA/NR3B1, FAM162A/E2IG5, PGRMC2/PMBP, and SLC39A6/LIV-1) and their hypoxic regulation in U87 glioma cells for evaluation of their possible significance in the control of glioma cells proliferation.Methods. The expression of NRIP1, EBBP, ESRRA, E2IG5, PGRMC2, and SLC39A6 genes in U87 glioma cells, transfected by empty vector pcDNA3.1 (control) and cells without IRE1 signaling enzyme function (transfected by dnIRE1) upon hypoxia, was studied by a quantitative polymerase chain reaction.Results. Inhibition of both enzymatic activities (kinase and endoribonuclease) of IRE1 signaling enzyme function up-regulates the expression of EBBP, E2IG5, PGRMC2, and SLC39A6 genes is in U87 glioma cells in comparison with the control glioma cells, with more significant changes for E2IG5 and PGRMC2 genes. At the same time, the expression of NRIP1 and ESRRA genes is strongly down-regulated in glioma cells upon inhibition of IRE1. We also showed that hypoxia increases the expression of E2IG5, PGRMC2, and EBBP genes and decreases NRIP1 and ESRRA genes expression in control glioma cells. Furthermore, the inhibition of IRE1 in U87 glioma cells decreases the eff ect of hypoxia on the expression of E2IG5 and PGRMC2 genes, eliminates hypoxic regulation of NRIP1 gene, and enhances the sensitivity of ESRRA gene to hypoxic condition. Furthermore, the expression of SLC39A6 gene is resistant to hypoxia in both the glioma cells with and without IRE1 signaling enzyme function.Conclusions. Results of this investigation demonstrate that inhibition of IRE1 signaling enzyme function affects the expression of NRIP1, EBBP, ESRRA, E2IG5, PGRMC2, and SLC39A6 genes in U87 glioma cells in gene specific manner and these changes possibly contribute to the suppression of the cell proliferation. Most of these genes are regulated by hypoxia and preferentially through IRE1 signaling pathway of endoplasmic reticulum stress.</abstract>

Department of Molecular Biology, Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv, Ukraine

Department of Pediatrics, National Bohomolets Medical University, Kyiv,

Department of Molecular Biology, Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv,

Hypoxic regulation of the expression of genes encoded estrogen related proteins in U87 glioma cells: eff ect of IRE1 inhibition

<abstract xmlns="http://www.w3.org/1999/xhtml"> Objective. The aim of the current study was to assess the protective outcome of hemin, a heme oxygenase-1 (HO-1) inducer on L-arginine-induced acute pancreatitis in rats. Acute pancreatitis (AP) is considered to be a critical inflammatory disorder with a major impact on the patient health. Various theories have been recommended regarding the pathophysiology of AP and associated pulmonary complications.Methods. Twenty-four adult male albino rats were randomly divided into four groups: control group, acute pancreatitis (AP), hemin pre-treated AP group, and hemin post-treated AP group.Results. Administration of hemin before induction of AP significantly attenuated the L-arginine- induced pancreatitis and associated pulmonary complications characterized by the increasing serum levels of amylase, lipase, tumor necrosis factor-α, nitric oxide, and histo-architectural changes in pancreas and lungs as compared to control group. Additionally, pre-treatment with hemin significantly compensated the deficits in total antioxidant capacities and lowered the elevated malondialdehyde levels observed with AP. On the other hand, post-hemin administration did not show any protection against L-arginine-induced AP.Conclusions. The current study indicates that the induction of HO-1 by hemin pre-treatment significantly ameliorated the L-arginine-induced pancreatitis and associated pulmonary complications may be due to its anti-inflammatory and antioxidant properties.</abstract>

Assistant Professor, Department of Physiology, Faculty of Medicine, Minia University, 61111, Minia,

Departments of Physiology, Pharmacology and Histology, Faculty of Medicine, Minia University, Minia,

Eff ects of hemin, a heme oxygenase-1 inducer in L-arginine-induced acute pancreatitis and associated lung injury in adult male albino rats

<abstract xmlns="http://www.w3.org/1999/xhtml"> Objective. Melatonin is a hormone predominantly synthesized and secreted during the night by the pineal gland. Artificial light at night, especially its blue part, acutely suppresses the melatonin production. Th e aim of the present study was to find out, whether an intense blue light phototherapy of severe hyperbilirubinemia, may suppress the melatonin production during the night when the eyes will be properly protected by a sleep mask.Methods. The main melatonin metabolite, 6-sulphatoxymelatonin was measured in urine in a nine-year old boy suffering from the Crigler-Najjar syndrome type I. The boy was treated during the sleep period with an intense blue light (to 1800 lx) 10 h/day, since his birth. During the phototherapy, his eyes were protected with a sleep mask. The concentration of 6-sulphatoxymelatonin was determined in the first morning urine and urine collected afternoon during the six days. The patient was exposed to phototherapy for three nights, two nights without and the last one with the treatment. The control urine samples were obtained from 8 healthy nine-year old boys. The level of 6-sulphatoxymelatonin was measured by radioimmunoassay and the data were normalized to urinary creatinine.Results. A distinct melatonin production rhythm was found and 6-sulphatoxymelatonin concentration in urine of the patient was comparable with the values obtained by the control group. No differences in 6-sulphatoxymelatonin levels were found between the nights with and without the phototherapy applied.Conclusions. We conclude that the whole night treatment of hyperbilirubinemia with intense blue light has negligible side effect on the rhythmic melatonin production, when the eyes are sufficiently protected by the sleep mask.</abstract>

PhD., Department of Animal Physiology and Ethology, Faculty of Natural Sciences, Comenius University in Bratislava, Ilkovicova 6, 842 15 Bratislava,

1st Department of Pediatrics, University Children’s Hospital, Bratislava,

Department of Animal Physiology and Ethology, Faculty of Natural Sciences, Comenius University, Bratislava,

Intense blue light therapy during the night-time does not suppress the rhythmic melatonin biosynthesis in a young boy

<abstract xmlns="http://www.w3.org/1999/xhtml"> The term “adrenal incidentaloma” is a radiological term. Adrenal incidentalomas are adrenal tumors discovered in an imaging study that has been obtained for indications exclusive to adrenal conditions (Udelsman 2001; Linos 2003; Bulow et al. 2006; Anagnostis et al. 2009). This definition excludes patients undergoing imaging testing as part of staging and work-up for cancer (Grumbach et al. 2003; Anagnostis et al. 2009). Papierska et al. (2013) have added the prerequisite that the size of a tumor must be “greater than 1cm in diameter”, in order to be called incidentaloma. Although in the most cases these masses are non-hypersecreting and benign, they still represent an important clinical concern because of the risk of malignancy or hormone hyperfunction (Barzon et al. 2003). Th e adrenal tumors belong to the commonest incidental findings having been discovered (Kanagarajah et al. 2012).</abstract>

General Surgeon, Demergi 6, Athens 10445,

Third Department of Surgery, University of Athens, ATTIKON Hospital, Athens,

Radiology of the adrenal incidentalomas. Review of the literature

<abstract xmlns="http://www.w3.org/1999/xhtml"> The maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive. Th e body weight depends on the balance between the energy intake and energy expenditure. Increased food intake over the energy expenditure of prolonged time period results in an obesity. Th e obesity has become an important worldwide health problem, even at low levels. The obesity has an evil effect on the health and is associated with a shorter life expectancy. A complex of central and peripheral physiological signals is involved in the control of the food intake. Centrally, the food intake is controlled by the hypothalamus, the brainstem, and endocannabinoids and peripherally by the satiety and adiposity signals. Comprehension of the signals that control food intake and energy balance may open a new therapeutic approaches directed against the obesity and its associated complications, as is the insulin resistance and others. In conclusion, the present review summarizes the current knowledge about the complex system of the peripheral and central regulatory mechanisms of food intake and their potential therapeutic implications in the treatment of obesity.</abstract>

Physiology Department, Faculty of Medicine, MAHSA University, Malaysia

Physiology Department, Faculty of Medicine, Minia University,

Central and peripheral control of food intake

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