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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.


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.


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<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<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.


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.


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.


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).


Adipose tissue expresses all the renin-angiotensin system (RAS) components that play an important role in the adipogenesis, lipid and glucose metabolism regulation in an auto/paracrine manner. The classical RAS has been found to be over-activated during the adipose tissue enlargement, thus elevated generation of angiotensin II (Ang II) may contribute to the obesity pathogenesis. The contemporary view on the RAS has become more complex with the discovery of alternative pathways, including angiotensin-converting enzyme 2 (ACE2)/angiotensin (Ang)-(1-7)/Mas receptor, (pro)renin receptor, as well as angiotensin IV(Ang IV)/AT4 receptor. Ang-(1-7) via Mas receptor counteracts with most of the deleterious effects of the Ang II-mediated by AT1 receptor implying its beneficial role in the glucose and lipid metabolism, oxidative stress, inflammation, and insulin resistance. Pro(renin) receptor may play a role (at least partial) in the pathogenesis of the obesity by increasing the local production of Ang II in adipose tissue as well as triggering signal transduction independently of Ang II. In this review, modulation of alternative RAS pathways in adipose tissue during obesity is discussed and the involvement of Ang-(1-7), (pro)renin and AT4 receptors in the regulation of adipose tissue homeostasis and insulin resistance is summarized.


A 46 year-old female patient presented to the hospital with ongoing and progressively increasing fatigue, severe nausea and vomiting, loss of appetite, constipation, palpitations and somnolence. Laboratory evaluation revealed a severe hypercalcaemia and overt hyperthyroidism. She was diagnosed with primary hyperparathyroidism accompanied by Graves’ disease. The patient underwent total thyroidectomy and right inferior parathyroid gland adenoma excision on the 24th day of her admission to the hospital after calcium levels and free thyroid hormone levels were brought to normal ranges. We suggest that a possibility of simultaneous thyrotoxicosis and primary hyperparathyroidism in cases presenting with a hypercalcaemic crisis should be considered


Objectives. A number of recently published studies have shown that the sympathetic nervous system may influence cancer progression. There are, however, some ambiguities about the role of the parasympathetic nerves in the modulation of growth of different tumor types. Moreover, tumor models used for investigation of the autonomic neurotransmission role in the processes related to the cancer growth and progression are mainly of the solid nature. The knowledge about the nervous system involvement in the modulation of the development and progression of malignant ascites is only fragmental. Therefore, the aim of the present article was to summarize the results of our experimental studies focused on the elucidation of the role of the autonomic nervous system in the modulation of tumor growth in animals. We are summarizing data from studies, in which not only different experimental approaches in order to influence the autonomic neurotransmission, but also different tumor models have been used.

Methods. Three different types of tumor models, namely solid rat intra-abdominal fibrosarcoma, solid murine subcutaneous melanoma, and rat ascites hepatoma, and three types of interventions have been used in order to modulate the autonomic neurotransmission, specifically chemical sympathectomy, subdiaphragmatic vagotomy, or the electric stimulation of the vagus nerve.

Results. We have proved a strong stimulatory effect of the sympathetic nerves on the development and growth in both solid tumors, rat fibrosarcoma as well as murine melanoma, and significant inhibitory impact on the survival time of tumor-bearing animals. The progression of ascites hepatoma in rats was not influenced by chemical sympathectomy. Modulation of parasympathetic signalization by vagotomy or vagal nerve stimulation does not affect fibrosarcoma and ascites hepatoma growth and survival of the tumor-bearing rats.

Conclusions. Based on the obtained data, it seems that the solid types of tumors are suitable substrate for the direct action of neurotransmitters released especially from the sympathetic nerves. In contrast, it appears that the malignant ascites are not under the direct autonomic nerves control; however, an indirect action via the immune functions modulation cannot be excluded.


Objectives. Elevated total serum free fatty acids (FFAs) concentrations have been suggested, controversially, to enhance insulin resistance and decrease percent remaining β-cell function. However, concentrations of individual serum FFAs have never been published in terms of their relationship (correlation) to homeostatic model assessment-insulin resistance (HOMA-IR) and percent remaining β-cell function (HOMA-%β) in the type 2 diabetics (T2Ds). Alpha-linolenic acid consumption has a negative correlation with the insulin resistance, which in turn is negatively correlated with the remaining β-cell function. The primary objective was to test the hypothesis that there would be different relationship (correlation) between the blood serum individual free FFA mol % levels and HOMA-IR and/or HOMA-%β in T2D. The secondary objective was to test the hypothesis that flaxseed oil, previously being shown to be ineffective in the glycemic control in T2Ds, may alter these correlations in a statistically significant manner as well as HOMA-IR and/or HOMA-%β.

Methods. Patients were recruited via a newspaper advertisement and two physicians have been employed. All the patients came to visit one and three months later for a second visit. At the second visit, the subjects were randomly assigned (double blind) to flaxseed or safflower oil treatment for three months, until the third visit.

Results. Different statistically significant correlations or trends towards among some serum individual free FFA mol % levels and HOMA-IR and HOMA-%β, pre- and post-flaxseed and safflower oil supplementation were found. However, flaxseed oil had no impact on HOMA-IR or HOMA-%β despite statistically significant alterations in correlations compared to baseline HOMA-IR.

Conclusions. The obtained data indicate that high doses of flaxseed oil have no statistically significant effect on HOMA-IR or HOMA-%β in T2Ds, probably due to the additive effects of negative and positive correlations.