title: Consumption of barley beta-glucan ameliorates fatty liver and insulin resistance in mice fed a high-fat diet.
abstract: 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.
authors.affiliation: Division of Metabolic Diseases, Center for Biomedical Science, National Institute of Health, Tongillo, Eunpyung-gu, Seoul 122-701, Korea.
authors.forename: Joo Sun
authors.initials: JS
authors.lastname: Choi
authors.forename: Hyunsook
authors.initials: H
authors.lastname: Kim
authors.forename: Myeong Ho
authors.initials: MH
authors.lastname: Jung
authors.forename: Shinhee
authors.initials: S
authors.lastname: Hong
authors.forename: Jihyun
authors.initials: J
authors.lastname: Song
mesh_terms: D000818:Animals; D001835:Body Weight; D004041:Dietary Fats / Q000008:administration & dosage*; D005234:Fatty Liver / Q000097:blood / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D005749:Gastric Inhibitory Polypeptide / Q000097:blood; D015971:Gene Expression Regulation, Enzymologic; D018149:Glucose Intolerance / Q000517:prevention & control; D001467:Hordeum / Q000737:chemistry*; D055504:Insulin Receptor Substrate Proteins / Q000378:metabolism; D007333:Insulin Resistance; D050356:Lipid Metabolism / Q000235:genetics; D008099:Liver / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000517:prevention & control; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D012639:Seeds / Q000737:chemistry; D015398:Signal Transduction; D047071:beta-Glucans / Q000008:administration & dosage*
chemical_list: D004041:Dietary Fats; D055504:Insulin Receptor Substrate Proteins; C526295:Irs1 protein, mouse; D012333:RNA, Messenger; D047071:beta-Glucans; D005749:Gastric Inhibitory Polypeptide; D051057:Proto-Oncogene Proteins c-akt