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Miroslav Zeman, Marek Vecka, František Perlík, Barbora Staňková, Robert Hromádka, Eva Tvrzická, Jakub Širc, Jakub Hrib and Aleš Žák
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Maryana Kondro, Nazarii Kobyliak, Oleksandr Virchenko, Tetyana Falalyeyeva, Tetyana Beregova and Petro Bodnar
Considering the association between microflora and obesity, and the significantly higher prevalence of non-alcoholic fatty liver disease (NAFLD) in obese people, the aim of our study was to investigate the preventive effect of multiprobiotics on the monosodium glutamate (MSG) induced NAFLD model, in rats. The work was carried out on 60 rats placed into three groups: the Control group, the MSG-group and the MSG-probiotic group. The MSG-group and the MSG-probiotic group were injected with 4 mg/g of MSG subcutaneously neonatally on the 2nd-10th days of life. The MSG-probiotic rats were also treated with 140 mg/kg of multiprobiotic “Symbiter” from the 4th week of life. In the 4-month-old rats, biochemical and morphological changes in liver were assessed, and steatosis was confirmed by the NAFLD activity score (NAS). Our results reveal that the multiprobiotic lowered total NAS, the degree of steatosis and the liver lobular inflammation caused by MSG. It also brought about decreased liver total lipids and triglycerids content, as well as decreased visceral adipose tissue mass. However, there was no difference in the liver serum biochemical indicators between all experimental groups. The obtained data does suggest the efficacy of probiotics in the prevention of NAFLD.
Katarzyna Kot-Bakiera, Ewelina Wawryk-Gawda, Beata Cichacz-Kwiatkowska and Barbara Jodlowska-Jedrych
Hepatic stellate cells (HSC) are a nonparenchymal population of liver cells. In normal conditions, they store vitamin A, control the turnover of the extracellular matrix, and regulate the contractility of the sinusoids. Acute and chronic damage such as that brought about by alcohol activates the stellate cells and they are then responsible for the liver's inflammatory fibrotic response. Hence, alcohol consumption leads to hepatitis, steatosis, fibrosis and cirrhosis of liver by way of different mechanisms depending on effect upon the nonparenchymal cells of the liver.
The aim of our study was to assess the histological changes in the liver of rats after chronic alcohol consumption. In our work, we evaluated the intensity of liver fibrosis and the number of Kupffer cells and active hepatic stellate cells present within a test population. In the experiment, we used 10 Wistar rats of 250 gram weight. The animals were placed within one of two groups: A (experimental) and C (control). Group A received alcohol for 4 weeks, while group C received just water. The rats of both groups were decapitated 24 hours after the end of the experiment. The samples of liver were then evaluated after H&E, Masson’s trichrome staining and an immunohistochemical reaction to desmin (a marker of quiescent HSC) and α-smooth muscle actin (marker of active HSC) antibody. In our work, we observed intensive fibrosis in the portal spaces and perivenular areas in group A samples. Moreover, Kupffer cells and stellate cells with positive α-SMA expression were more numerous in group A than in the group C, and these correlate with the area of intensive fibrosis. The expression of desmin in the HSC was seen in both groups to a similar level.
Conclusion: Chronic alcohol consumption activates the transdifferentiation of hepatic stellate cells into the positive α-SMA myofibroblast-like cells which are responsible for fibrogenesis.
Elina G. Manzhalii, Valentyna O. Moyseyenko, Tetyana M. Falalyeyeva, Olena I. Tsyryuk, Vitaliy E. Kondratiuk and Taras D. Nykula
electron transport chain of rat hepatocytes under different steatosis. Research Journal of Pharmaceutical, Biological and Chemical Sciences . 2016;7(4):752-5.
12. Kondro M., Kobyliak N, Virchenko O, Falalyeyeva T, Beregova T, Bodnar P. Multiprobiotic therapy from childhood prevents the development of nonalcoholic fatty liver disease in adult monosodium glutamate-induced obese rats. Curr Issues Pharm. Med. Sci. 2014;2(4):243-5.
13. Baykova IE, Nikitin IG. [Drug liver]. Ross. Med. Zhurn . 2009;1. Article in Russian
14. Buyeverov AO, Yeshanu VS
Regina S. Komsa-Penkova, Georgi M. Golemanov, Zdravka V. Radionova, Pencho T. Tonchev, Sergej D. Iliev and Veselin V. Penkov
poor outcome only in the presence of inflammation in prevalent haemodialysis patients. Eur J Clin Invest. 2008;38(11):804-11.
58. Peter A, Kovarova M, Staiger H, Machann J, Schick F1, Königsrainer A, et al. The Hepatokines Fetuin-A and Fetuin-B are up- regulated in the State of Hepatic Steatosis and have an impact on Glucose Homeostasis in Humans. Am J Physiol Endocrinol Metab. 2017 Nov 14:ajpendo002622017. doi: 10.1152/ajpendo00262.2017.
59. Reinehr T, Roth CL. Fetuin-A and its relation to metabolic syndrome and fatty liver disease in obese children