![]() FOS increased not only the fecal concentrations of n-butyric acid (0.04 ± 0.01 vs. In addition, FOS inhibited adipocyte enlargement and formation of crown-like structures and reduced the M1 macrophage frequency in the epididymal fat of the MSG mice (39.4% ± 3.0% vs. FOS treatment improved the liver pathology and blunted the increases in the mRNA expression levels of lipid metabolism enzymes. Hepatic steatosis, inflammatory cell infiltration, and hepatocyte ballooning in the liver and increased hepatic mRNA expression of fatty acid synthase and glycerol-3-phosphate acyltransferase were observed in the MSG-treated mice. Hepatic mRNA expression of lipid metabolism enzymes and SCFA in feces and sera were measured. At 18 weeks, histological characteristics of the liver and epididymal fat were compared between the groups. Six mice were also administered 5% FOS via drinking water from 10 weeks of age. Twelve newborn C57BL/6 J male mice were subcutaneously injected with monosodium glutamate (MSG) to induce obesity on a conventional diet. This study aimed to determine the effects of fructo-oligosaccharides (FOS) on steatohepatitis and visceral adiposity in an obese mouse model of NASH. Dysbiosis was reported to contribute to NASH pathogenesis. Within the spectrum of NAFLD, non-alcoholic steatohepatitis (NASH) in combination with hepatic inflammation and fibrosis can lead to liver cirrhosis and hepatocellular carcinoma. Non-alcoholic fatty liver disease (NAFLD) is a hepatic manifestation of metabolic syndrome.
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