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Currently, obesity is an important health problem in all countries, both developed and developing. Dietary habits and neurohormonal imbalances play a critical role in obesity. Circulating amounts of ghrelin, which is a neurohormonal hormone, decrease with obesity and increase with weight loss. Although it is known that both mRNA and peptide version of the ghrelin hormone are expressed in almost all tissues of both humans and animals, it is not known how obesity changes the expression of this hormone in the tissues, with the exception of the gastrointestinal system tissues. Therefore, the objective of the present study is to show how diet-induced obesity in rats changes ghrelin expression in all system tissues, and thus, to shed light on the etiopathology of obesity. The study included 12 male and 12 female 2-month-old Wistar albino species rats. The animals in the control group were fed on standard rat pellet, while those in the experiment group were fed ad libitum on a cafeteria-style diet for 2 months. When their body mass index reached 1 g/cm(2), diet-induced obese (DIO) rats were sacrificed in a sterile environment after one night fasting. Ghrelin localizations in the tissues were studied immunohistochemically using avidin-biotin-peroxidase complex (ABC) method, while tissue ghrelin amounts were analyzed using radioimmunoassay (RIA) method. When the ghrelin amounts in the urogenital system (with the exception of kidney tissues), sensory organs, respiratory system, immune system, skeletal muscle system, cardiovascular system, nervous system, and adipose tissue of rats analyzed by RIA method were compared to those in the control group, tissue ghrelin amounts in the DIO group were found lower. Immunohistochemical findings which showed a similar fall in ghrelin concentrations in the tissues were parallel to RIA results. In addition, ghrelin was shown to be synthesized in the cardiovascular system, heart muscle cells, tails of the sperms, hair follicles, lacrimal glands, tongue, and teeth of rats for the first time in this study and ghrelin syntheses in these tissues were found to decrease in obesity. Nutritional obesity is among the most common causes of obesity and the findings we have obtained through diet-induced obesity will contribute to the illumination of the etiopathology of obesity.

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The aims of the present study were to examine ghrelin expression in serum and gastrointestinal tract (GIT) tissues, and to measure tissue ghrelin levels and obesity-related alterations in some serum biochemical variables in rats with diet-induced obesity (DIO). The study included 12 male rats, 60 days old. The rats were randomly allocated to two groups (n = 6). Rats in the DIO group were fed a cafeteria-style diet to induce obesity, while those in the control group were fed on standard rat pellets. After a 12 week diet program including an adaptation period all rats were decapitated, tissues were individually fixed, ghrelin expression was examined by immunohistochemistry , and tissue and serum ghrelin levels were measured by radioimmunoassay. Serum biochemical variables were measured using an autoanalyzer. When the baseline and week 12 body mass index and GIT ghrelin expression were compared between DIO and control rats, BMI had increased and ghrelin expression decreased due to obesity. The RIA results were consistent with these findings. Serum glucose, LDL cholesterol, and total cholesterol levels were elevated and HDL cholesterol significantly decreased in the DIO group. A comparison of GIT tissues between the control and obese groups demonstrated that ghrelin was decreased in all tissues of the latter. This decrease was brought about a decline in the circulating ghrelin pool. This suggests that rather than being associated with a change in a single tissue, obesity is a pathological condition in which ghrelin expression is changed in all tissues.

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Although immune-mediated pathogenesis in adriamycin (ADR)-induced nephropathy has been proposed recently, studies are lacking about the effects of immunmodulators, such as vitamin D, on ADR-induced nephrotoxicity. We hypothesized that vitamin D(3) (cholecalciferol) would be beneficial on ADR-induced nephropathy because of its immunmodulatory properties. Eighteen male Wistar rats were divided into three groups (n = 6): group 1 (control), group 2 (single ADR injection intravenously), and group 3 (similar single ADR injection intravenously + daily oral cholecalciferol for 21 days) were used in the study. A single high dose of ADR resulted in increased urinary protein: creatinine ratio for all three weeks of the experiment in both groups 2 and 3 compared with the controls. Histological examination of the kidney tissue revealed distinct tubular lesions as tubular necrosis, hyaline casts in tubular lumen, tubular degeneration, tubular dilatation, and tubular vacuolization in group 2 compared with group 1. These tubular lesions were significantly reduced in group 3 compared to group 2. The results of this study indicate that cholecalciferol causes satisfactory tubulointerstitial recovery in ADR-induced nephrotoxicity in rats.

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Nonseminomatous germ cell tumors of the testis are common and are very aggressive malignant tumors. Most of the cases have metastases at the time of diagnosis, and involvement of the posterior mediastinum in particular is well known. A 33 year-old male patient presented with complaints of a swelling on the right side of the neck that had been growing for the last month, as well as shortness of breath and cough. His thoracic computed tomography (CT) showed a 1.5 cm lymph node on the anterior mediastinum and a mass of about 11 × 10 × 8 cm extending from the right lung apex to the right hilus, with regular contours and without contrast enhancement. The patient, who was given the preliminary diagnosis of a mixture metastatic bronchial tumor plus lymphoma, was subjected to transthoracic fine needle aspiration cytology (FNAC). His abdominal CT revealed a hypodense, heterogeneous and cystic necrotic mass of about 10 × 7 × 5 cm that was para-aortic at the infrarenal level (initially predicted as a lymphoma). The patient, who could not be typed in his cytopathological examination, was diagnosed with malignant epithelial tumor and was recommended to undergo a genitourinary system examination. Upon finding a high alpha fetoprotein (AFP) value, a scrotal ultra sonography was performed which showed a mass filling the right testis. Histopathological examination of the orchiectomy material resulted in the diagnosis of mixed germ cell tumor (60% mature teratoma and 40% yolk sac tumor). Even though metastatic lesions are mostly seen in the posterior mediastinum, our findings reveal that specimens obtained with FNAC from the anterior mediastinum bear discohesive, pleomorphic, small nuclei in epithelial cells with microvacoules in the cytoplasm. These cytopathological alterations in specimens from the anterior mediastinum might promote germ cell and yolk sac tumors.

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Ghrelin belongs to the family of a gut-brain hormone that promotes food intake and controls energy balance. Recently, it has also been shown to regulate bone formation directly. Dental tissue shares several functional, developmental and anatomical similarities with bone, and in the present study we have investigated the presence of ghrelin in 44 human teeth using immunocytochemistry and radioimmunoassay. Both methods showed that the hormone is present in canines and molars, mainly in the odontoblasts but also in the pulp. Ghrelin could potentially play interesting physiological roles in teeth.

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OBJECTIVE: To investigate the protective effect of instant coffee (IC) on acute liver injury induced by CCl(4). METHODS: The study included 32 rats which were allocated to four groups: control (n: 8), CCl(4) (n: 8), CCl(4)+IC (n: 8) and IC (n: 8). Malondialdehyde, which is a lipid peroxidation product, and levels of antioxidant capacity were measured and histopathological data were compared. RESULTS: It was seen in the study that lipid peroxidation products that increased in the plasma and liver tissue of the CCl(4) group decreased by IC administration. There was an increase in the measured antioxidant parameters, which were total antioxidant capacity (TAOC), sulphydryl (SH) and ceruloplasmin levels. Histopathologically, it was found that inflammation and necrosis which increased in the group administered CCl(4) decreased significantly with IC administration, but there steatosis did not change. CONCLUSIONS: It was seen that IC had a protective role in acute liver injury induced by CCl(4), but did not affect steatosis.