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Oś mózgowo-jelitowa w regulacji apetytu

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EN
Brain-gut axis is of great importance in regulation of appetite and gastrointestinal functions. Impulses coming from sense organs such as sight, sound and smell are modified in central nervous system and then they are transmitted to enteric nervous system (ESN) through efferent pathways involving the spinal cord and the autonomic nervous system. There are many hormones, peptides and neurotransmitters involved in the neurohormonal regulation of appetite among them the predominant role is attributed to enterohormones such as: ghrelin, leptin, corticoliberin (CRH), neuropeptides orexins and peptides such as peptide YY, human pancreatic polypeptide (PP), glucagon-like peptide-1 (GLP 1), cholecystokinin (CCK) and neuropeptide Y (NPY). The short overview presents the advances in our understanding of brain-gut axis with major focus being addressed to the recent developments in the control of appetite by brain centers and the central as well as peripheral hormonal mechanisms.
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2018
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vol. 65
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issue 3
359-366
EN
Selenium compounds have been implicated as anticancer agents; however, the mechanism of their inhibitory action against cancer development has not been extensively investigated. A constitutive activation of the Wnt/β-catenin pathway is a central event in colorectal carcinogenesis. In this pathway, excessive cell proliferation is initiated by generation of β-catenin followed by overexpression of proto-oncogenes, such as c-Myc. It is believed that under physiological conditions the level of c-Myc is efficiently controlled by accessibility of the β-catenin protein through the process of phosphorylation by glycogen synthase kinase 3β (GSK-3β). Here, we determined whether selenomethionine (SeMet) can inhibit cell growth and affect the Wnt/β-catenin pathway in the HT-29 human colorectal cancer cells in vitro. The effective cytotoxic doses of SeMet have been selected after 48 h of incubation of this compound with colorectal cancer HT-29 cell line. MTT assay was used to assess cell viability and the protein and mRNA levels of β-catenin and c-Myc were determined by Western blotting and qPCR, respectively. SeMet potently inhibited growth of HT-29 cells, significantly decreased level of the β-catenin protein and mRNA concentration, down-regulated the c-Myc gene expression and up-regulated the pro-apoptotic Bax protein level. Moreover, SeMet increased the level of GSK-3β phosphorylated at serine 9 (S9) and significantly increased the level of β-catenin phosphorylated at S33 and S37. We conclude that SeMet suppresses growth of HT-29 colorectal cancer cells by a mechanism linked to the Wnt/β-catenin pathway, however, degradation of β-catenin may occur independently of GSK-3β catalytic activity and its phosphorylation status.
EN
Following genetic immunization of laying ducks with a plasmid expressing Helicobacter pylori UreB (large subunit of urease), IgY against UreB were obtained from egg yolks. These polyclonal and monospecific IgY antibodies are of higher-titer and specifically recognize recombinant H. pylori urease purified from Escherichia coli. To our knowledge this is the first report describing generation of IgY antibodies directed against antigens of H. pylori by DNA-based immunization.
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