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Background. Chronic alcohol use leads to alcoholic liver fibrosis. Today, a sufficient number of scientific studies are focused on the pathometabolic mechanisms of liver fibrosis development and formation in animal models. The purpose of our study was to investigate structural changes and liver stiffness, biochemical markers of fibrosis in rats with chronic alcoholic liver injury (CALI) modeling and to evaluate the changes of these parame­ters with different types of treatment. Materials and methods. Eighty-nine rats were divided into experimental groups depending on the duration of alcohol exposure (4 and 12 weeks) and the corresponding type of correction (metadoxine and prebiotic). Results. When modeling CALI at week 4, morphological studies revealed moderate large-droplet fatty hepatosis and mild fibrosis in the central venule of the liver lobes. After 12 weeks of forced alcoholization, with more pronounced general intoxication, hepatocytes have dystrophic changes such as appearance of single or grouped dystrophic cells in the parenchyma. A combination of protein and fatty dystrophy was more common. Elastography allowed to detect structural changes in the liver at the early stages of fibrosis formation when modeling CALI for 12 weeks. There were also changes in the levels of biochemical parameters: free and protein-bound hydroxyproline, glycosaminoglycans. According to the results of elastography, liver stiffness in rats increased maximally after prebiotic correction in all approaches compared to the controls. After correction of CALI, both early- and long-term, fibrosis markers normalized in rat liver homogenate after administration of metadoxine and prebiotic. After prebiotic correction at week 12 of alcoholization, we observed a 12% decrease in liver parenchymal stiffness in the CALI modeling group and a 19% decrease (p

The article deals with the study on the content of fecal short-chain fatty acids (SCFA) and their association with insulin resistance in obese children. It was found that intestinal microflora in obese children is characterized by changes in the qualitative composition and increased metabolic activity of the intestinal microflora. A moderate increase of HOMA-IR is accompanied by elevated concentration of anti-inflammatory cytokines, the content of which correlates with that of acetic, propionic acid and a decrease in the metabolic activity of intestinal microflora. The progression of insulin resistance is accompanied by a further increase in the concentration of anti-inflammatory cytokines, the level of HOMA-IR correlates with the level of propionic SCFA. Thus, modulation of SCFA content may be a promising way of therapeutic influence to correct insulin resistance and obesity in children.

Background. Today most of the scientists are studying the processes of hepatocyte damage under the influence of free fatty acids (FFA) in vitro conditions. Therefore, in vivo studies of the spectrum of FFA in liver pathologies of different genesis, including toxic ones, are of considerable interest. Materials and methods. Toxic liver damage was simulated by subcutaneous injection of CCl4 solution in olive oil into rats. The following groups were formed: control (healthy; n = 15); I — CCl4-induced liver damage without drug correction (n = 6); III — CCl4-induced liver damage + metadoxin (Liveria IC; n = 8); III — CCl4-induced liver damage + metabiotic (Hilac forte) (n = 7). For morphological assessment of steatosis and fibrosis we used three-color qualitative staining of liver samples by Mallory-Slinchenko. Quantitative content of monounsaturated fatty acids (MUFA) in liver homoge­nate was determined by gas chromatography. Results. Evaluation of hepatobioptates in group I rats revealed tissue disorganization with macrovesicular steatosis in the cytoplasm of hepatocytes, the formation of interparticle multiple fibrous septa and inflammatory cell infiltration. The use of metadoxin (group II) and metabiotic (group III) improved the morphological picture of the liver, which was damaged by CCl4. Total MUFA content increased significantly in 118 (p

Background. Changes in the intestinal microbiome trigger the development and progression of non-alcoholic fatty liver disease (NAFLD). Adverse fluctuations in intestinal microbiota are associated with increased intestinal permeability, activation of mucosal and adaptive immunity, increase in production and intestinal absorption of short-chain fatty acids (SCFA). The ratio of acetic, propionic, butyric acid is an important indicator of the integrity of the microbial community of the intestine. Thus, the study of the gut microbiota composition and short-chain fatty acids production represents a very appealing approach to increasing our knowledge about the mechanisms leading to NAFLD in children. The purpose of the study was to determine the features of the fecal short-chain fatty acids (fSCFA) content and the colonic microbiota composition in children with NAFLD. Materials and methods. A comprehensive examination of 102 children was provided in the Department of Pediatric Gastroenterology of the Institute of Gastroenterology of the National Academy of Medical Sciences of Ukraine. According to the presence of obesity, transient elastography data and alanine aminotransferase levels the patients were divided into four groups: I group — children with simple hepatic steatosis (n = 24); II group — children with nonalcoholic steatohepatitis (NASH) (n = 14); III group — children with obesity without steatosis (n = 48), IV group — children with normal weight (n = 16). Chromatographic study of fSCFA was conducted using gas chromatograph Chromatec-Crystal 5000. The microorganisms were identified using a microbiological study of the colon content. Diagnosis of NAFLD was established with FibroScan 502 Touch (Echosens, France) with the determination of the controlled attenuation parameter. Results. Significant changes in the spectrum of fSCFA were observed in children of the III group with acetic acid content increased by 4.8 times (р

There were studied the features of changes in the factors of aggression and protection in the gastric juice of 91 patients with gastroesophageal reflux disease (GERD) combined with sphincter of Oddi dysfunction. It was determined the pH, concentration of pepsin, glycoproteins, bile acids, sialic acids, fucose, hexosamines, the level of nitric oxide metabolites. It has been found that increased levels of nitric oxide metabolites and bile acids in gastric juice enhances the inflammatory processes in the gastric mucosa irrespective of the functional state of the sphincter of Oddi. Aggressive properties of gastric contents were increased in patients with GERD associated with both hypertonic and hypotonic sphincter of Oddi. The deficit and imbalance of protection factors in most patients in all groups were manifested by reduction in the concentration of carbohydrate terminal residues of glycoproteins as compared to the control group.