epiglucan and Fatty-Liver

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.

Topics: Animals; Avena; beta-Glucans; Disease Models, Animal; Dose-Response Relationship, Drug; Endotoxemia; Fatty Liver; Glucagon-Like Peptide 2; Glucose Intolerance; Inflammation; Insulin Resistance; Interleukin-1beta; Interleukin-6; Lipopolysaccharides; Liver; Male; Malondialdehyde; Mice; Mice, Inbred C57BL; Non-alcoholic Fatty Liver Disease; Oxidative Stress; Superoxide Dismutase; Transaminases; Triglycerides; Tumor Necrosis Factor-alpha; Weight Gain

The soluble fiber β-glucan, a natural component of barley, has been shown to lower the postprandial glucose response and is thought to improve insulin resistance.. This study examined the effect of chronic consumption of the high β-glucan barley flour on glucose control, liver lipids and markers of muscle fatty acid oxidation in the Zucker diabetic fatty (ZDF) rat. Two groups of ZDF rats were fed diets containing either 6% β-glucan in the form of barley flour or cellulose as a control for 6 weeks. A group of Zucker lean rats served as a negative control.. The barley flour group had an increased small intestinal contents viscosity compared to the obese control group. After 6 weeks, the barley flour group had reduced glycated hemoglobin, lower relative kidney weights and a reduced area under the curve during a glucose tolerance test, indicating improved glucose control. Fasting plasma adiponectin levels increased in the barley flour group and were not different than the lean control group. ZDF rats on the barley flour diet had lower relative epididymal fat pad weights than the obese control and a greater food efficiency ratio. The barley flour group also had reduced liver weights and a decreased concentration of liver lipids. The barley flour group had significantly higher concentrations of muscle acylcarnitines, a metabolite generated during fatty acid oxidation.. These results show that chronic consumption of β-glucans can improve glucose control and decrease fatty liver in a model of diabetes with obesity.

Topics: Adiponectin; Animals; beta-Glucans; Blood Glucose; Body Weight; Carnitine; Cholesterol; Diabetes Mellitus, Type 2; Dietary Fiber; Disease Models, Animal; Fatty Acids, Nonesterified; Fatty Liver; Flour; Glucose Tolerance Test; Hordeum; Insulin; Insulin Resistance; Intestine, Small; Ketones; Liver; Obesity; Organ Size; Postprandial Period; Rats; Rats, Zucker; Thiobarbituric Acid Reactive Substances; Triglycerides

Consumption of a diet high in barley beta-glucan (BG) has been shown to prevent insulin resistance. To investigate the mechanism for the effects of barley BG, three groups of male 7-wk-old C57BL/6J mice were fed high-fat diets containing 0, 2, or 4% of barley BG for 12 wk. The 2% BG and 4% BG groups had significantly lower body weights compared with the 0% BG group. The 4% BG group demonstrated improved glucose tolerance and lower levels of insulin-resistance index and glucose-dependent insulinotropic polypeptide. Consumption of the BG diet decreased hepatic lipid content. Mice on the BG diet also demonstrated decreased fatty acid synthase and increased cholesterol 7alpha-hydroxylase gene expression levels. The BG diet promoted hepatic insulin signaling by decreasing serine phosphorylation of insulin receptor substrate 1 and activating Akt, and it decreased mRNA levels of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase. In summary, consumption of BG reduced weight gain, decreased hepatic lipid accumulation, and improved insulin sensitivity in mice fed a high-fat diet. Insulin signaling enhanced due to the expression changes of glucose and lipid metabolism genes by BG consumption. Consumption of barley BG could be an effective strategy for preventing obesity, insulin resistance, and the metabolic syndrome.

Topics: Animals; beta-Glucans; Body Weight; Dietary Fats; Fatty Liver; Gastric Inhibitory Polypeptide; Gene Expression Regulation, Enzymologic; Glucose Intolerance; Hordeum; Insulin Receptor Substrate Proteins; Insulin Resistance; Lipid Metabolism; Liver; Male; Mice; Mice, Inbred C57BL; Obesity; Phosphorylation; Proto-Oncogene Proteins c-akt; RNA, Messenger; Seeds; Signal Transduction