Long-term liquid nutrition intake and development of obesity: differences between young and adult rats.

OBJECTIVE: Obesity is particularly associated with an increased consumption of palatable fat and sugar dense food and beverages. Therefore, we examined the effect of a normocaloric liquid diet (Fresubin) with increased carbohydrate content (constituting 55% of calories) on development of obesity in different developmental periods in male Wistar rats. METHODS: Fresubin was provided to 3 groups of rats: the first group received Fresubin immediately after weaning (21st day of age) to the end of experiment (150th day of age) for 5 months; the second group was fed with Fresubin from weaning to adulthood (90th day of age) for 3 months; and the third group received Fresubin only in adulthood (from 90th to 150th day of age) for 2 months. The control group was fed with standard pellet chow from weaning to the end of the experiment. Body weight, food and water intake were periodically measured. After terminating the experiment, the adiposity index was determined. RESULTS: Rats fed with liquid nutrition showed increased energy intake and body weight in comparison with the control rats. Interestingly, while obesity in the juvenile rats developed as late as of 13 weeks after the Fresubin intake, the adult rats fed with liquid nutrition had significantly elevated the body weight already 2 weeks after starting the treatment. Increased adiposity index was observed in both groups of rats fed with Fresubin during the whole study as well as the adulthood. CONCLUSIONS: Our data indicate that feeding of male Wistar rats with a high carbohydrate normocaloric diet results in a substantial development of obesity. Moreover, exposure of juvenile individuals to obesogenic environment leads, after a certain "latent period", to the development of obesity that may reflect low protein content of used liquid diet or higher resistance of juvenile organism to the obesogenic factors. Finally, based on the data obtained we suggest that Fresubin, with respect to its properties, may serve as a diet for the development of obesity which may exemplify an "obesity model" applicable in small laboratory animals.

Chemical sympathectomy suppresses fibrosarcoma development and improves survival of tumor-bearing rats.

Both experimental and clinical data indicate that the sympathetic nervous system may affect the development of certain tumors. To test this, in the present study we combined in vivo and in vitro approaches to study the effect of the sympathetic nervous system on proliferation of BP6-TU2 fibrosarcoma cells. First, we investigated the effect of 6-hydroxydopamine-induced sympathectomy on tumor development and survival of tumor-bearing rats. One week after chemical sympathectomy, we injected the BP6-TU2 fibrosarcoma cells intraperitoneally into male Wistar rats. The sympathectomy significantly reduced the incidence of intraperitoneal tumors and resulted in significantly improved survival of tumor-bearing rats compared to those with intact sympathetic innervation. Using immunohistochemical methods, we found neuron-specific enolase immunopositive structures within fibrosarcoma tissue, indicating innervation of tumors. Finally, an in vitro study showed elevated proliferation of BP6-TU2 fibrosarcoma cells in response to adding norepinephrine to the culture medium. Our findings indicate that sympathetic nerves directly potentiate the proliferation of BP6-TU2 fibrosarcoma cells in rats.

Brain-liver interactions during liver ischemia reperfusion injury: a minireview.

KEYWORDS: The liver is a vital organ, with a wide range of functions. This organ plays an important role in the metabolism, including the glycogen storage, decomposition of red blood cells, plasma protein synthesis, hormone production, and detoxification. The liver is innervated by sympathetic and parasympathetic nerves which are involved in the regulation of the hepatic metabolism. Tissue injury connected with ischemia and reperfusion has been implicated in several clinical settings, including myocardial infarction, brain ischemia, and organ transplantation. Consequences of the liver ischemia reperfusion injury (LIRI) induce first of all an organ failure and afterwards multiorgan system damages that may eventually lead to a death. Many models with an attempt to reduce harmful consequences of the LIRI, directing to develop a variety of prophylactic strategies, has been introduced including models of warm, cold or normothermic ischemia, ischemic pre- and post-conditionings, pharmacological interventions, etc. In spite of the improvements in the medical care and accumulation of a large amount of experimental data concerning the prevention of ischemia and reperfusion related injuries, many destructive processes explanation still remains problematic.

Activation of different neuronal phenotypes in the rat brain induced by liver ischemia­reperfusion injury: dual Fos/neuropeptide immunohistochemistry.

The aim of the present study was to reveal the effect of liver ischemia­reperfusion injury (LIRI) on the activity of selected neuronal phenotypes in rat brain by applying dual Fos-oxytocin (OXY), vasopressin (AVP), tyrosine hydroxylase (TH), phenylethanolamine N-methyltransferase (PNMT), corticoliberine (CRH), and neuropeptide Y (NPY) immunohistochemistry. Two liver ischemia­reperfusion models were investigated: (i) single ligation of the hepatic artery (LIRIa) for 30 min and (ii) combined ligation of the portal triad (the common hepatic artery, portal vein, and common bile duct) (LIRIb) for 15 min. The animals were killed 90 min, 5 h, and 24 h after reperfusion. Intact and sham operated rats served as controls. As indicated by semiquantitative estimation, increases in the number of Fos-positive cells mainly occurred 90 min after both liver reperfusion injuries, including activation of AVP and OXY perikarya in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, and TH, NPY, and PNMT perikarya in the catecholaminergic ventrolateral medullar A1/C1 area. Moreover, only PNMT perikarya located in the A1/C1 cell group exhibited increased Fos expression 5 h after LIRIb reperfusion. No or very low Fos expression was found 24 h after reperfusion in neuronal phenotypes studied. Our results show that both models of the LIRI activate, almost by the same effectiveness, a number of different neuronal phenotypes which stimulation may be associated with a complex of physiological responses induced by (1) surgery (NPY, TH, PNMT), (2) hemodynamic changes (AVP, OXY, TH, PNMT), (3) inflammation evoked by ischemia and subsequent reperfusion (TH), and (4) glucoprivation induced by fasting (NPY, PNMT, TH). All these events may contribute by different strength to the development of pathological alterations occurring during the liver ischemia­reperfusion injury.

Does incorporation of gene for green fluorescent protein in BP6 fibrosarcoma tumor cells depress their intraperitoneal growth in rats? (In honour of Nobel Prize laureates 2008--Osamu Shimomura, Martin Chalfie, Roger Y. Tsien).

This manuscript was in honour of Nobel Prize in chemistry "for the discovery and development of the green fluorescent protein, GFP" to Osamu Shimomura, Martin Chalfie, and Roger Y. Tsien, simultaneously a brief information about experience with GFP in experimental tumorigenesis used this study is also presented. The experimental data have showed that BP6 cells incorporated with GFP gene have had smaller ability to induce both experimental intraperitoneal and subcutaneous tumor process. It was anticipated that incorporation of GFP gene might change physiological properties of cytoskeleton and worsen adhesive characteristics of tumor cells. It was also supposed that aftertime GFP will enable to monitor proliferation of cells not only within experimental work, but also in human medicine. GFP could help (supposedly) as reporter of proliferation, but also can serve as "target" for guide of tumorigenesis inhibiting substances. These ideas which are consequences of our experiments we append as congratulation to Nobel Prize in chemistry of the 2008 (Fig. 2, Ref. 44). Full Text (Free, PDF) www.bmj.sk.