NDLI: Oat β-glucan inhibits lipopolysaccharide-induced nonalcoholic steatohepatitis in mice

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Oat β-glucan inhibits lipopolysaccharide-induced nonalcoholic steatohepatitis in mice

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Oat β-glucan inhibits lipopolysaccharide-induced nonalcoholic steatohepatitis in mice

Content Provider	Royal Society of Chemistry (RSC)
Author	Zhao, Qiong Chen, Xingyun Hu, Xinzhong Xu, Chao You, Shuiping
Copyright Year	2013
Abstract	Nonalcoholic steatohepatitis (NASH) is part of the spectrum of nonalcoholic fatty liver disease. However, there are few suitable animal models to study the pathogenesis of NASH or very limited advances in the prevention. Our aims were to establish a mouse model of NASH by intraperitoneally injecting lipopolysaccharide (LPS) at a dose of 1.5 mg per kg body weight per day for 6 weeks and to investigate the potential inhibitory effects of oat β-glucan (1%, 5%, or 10%) added to a specific pathogen-free diet. Intraperitoneal injection of LPS for 6 weeks increased serum LPS levels; decreased serum glucagon-like peptide-2 levels; triggered abnormal aminotransferase activity, glucose intolerance, and insulin resistance; and increased hepatic proinflammatory cytokines (tumor necrosis factor-α, interleukin-6, interleukin-1β), triglyceride, and malonyl dialdehyde levels; but reduced hepatic superoxide dismutase activity. Histologic evaluation revealed evidence of hepatic steatosis, inflammation, and mild necrosis in LPS-treated mice. Dietary supplementation of oat β-glucan prevented most of the LPS-induced metabolic disorders, and improved hepatic steatosis and inflammation, although a dose-dependent effect was not observed. In conclusion, oat β-glucan could inhibit LPS-induced NASH in mice.
Starting Page	1360
Ending Page	1368
Page Count	9
File Format	HTM / HTML PDF
ISSN	20426496
Volume Number	4
Issue Number	9
Journal	Food & Function
DOI	10.1039/c3fo60081e
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	NASH Steatohepatitis Non-alcoholic fatty liver disease Mouse Lipopolysaccharide Intraperitoneal injection Glucagon-like peptide-2 Impaired glucose tolerance Insulin resistance Tumor necrosis factor alpha Interleukin 6 Triglyceride Superoxide dismutase Fatty liver Inflammation Necrosis
Content Type	Text
Resource Type	Article
Subject	Medicine Food Science

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Background on nafld/nash (2007).

Efficacy of Tumor Necrosis Factor and Interleukin-10 Analysis in the Follow-up of Nonalcoholic Fatty Liver Disease Progression.

Predictors of Insulin Secretion in Japanese Patients with Histopathologically-confirmed Non-alcoholic Fatty Liver Disease.

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Oat β-glucan inhibits lipopolysaccharide-induced nonalcoholic steatohepatitis in mice

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Background on nafld/nash (2007).

Efficacy of Tumor Necrosis Factor and Interleukin-10 Analysis in the Follow-up of Nonalcoholic Fatty Liver Disease Progression.

Predictors of Insulin Secretion in Japanese Patients with Histopathologically-confirmed Non-alcoholic Fatty Liver Disease.

Th17 involvement in nonalcoholic fatty liver disease progression to non-alcoholic steatohepatitis.

Glucagon-like peptide 1 decreases lipotoxicity in non-alcoholic steatohepatitis.

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Oat β-glucan inhibits lipopolysaccharide-induced nonalcoholic steatohepatitis in mice