title: Glucan-rich polysaccharides from Pleurotus sajor-caju (Fr.) Singer prevents glucose intolerance, insulin resistance and inflammation in C57BL/6J mice fed a high-fat diet.
abstract: BACKGROUND
  Pleurotus sajor-caju (P. sajor-caju) has been extremely useful in the prevention of diabetes mellitus due to its low fat and high soluble fiber content for thousands of years. Insulin resistance is a key component in the development of diabetes mellitus which is caused by inflammation. In this study, we aimed to investigate the in vivo efficacy of glucan-rich polysaccharide of P. sajor-caju (GE) against diabetes mellitus and inflammation in C57BL/6J mice fed a high-fat diet.
  
  
  METHODS
  Diabetes was induced in C57BL/6J mice by feeding a high-fat diet. The mice were randomly assigned to 7 groups (n=6 per group). The control groups in this study were ND (for normal diet) and HFD (for high-fat diet). The treated groups were ND240 (for normal diet) (240 mg/kg b.w) and HFD60, HFD120 and HFD240 (for high-fat), where the mice were administrated with three dosages of GE (60, 120, 240 mg GE/kg b.w respectively). Metformin (2 mg/kg b.w) served as positive control. The glucose tolerance test, glucose and insulin levels were measured at the end of 16 weeks. Expressions of genes for inflammatory markers, GLUT-4 and adiponectin in the adipose tissue of the mice were assessed. One-way ANOVA and Duncan's multiple range tests (DMRT) were used to determine the significant differences between groups.
  
  
  RESULTS
  GE treated groups improved the glucose tolerance, attenuated hyperglycemia and hyperinsulinemia in the mice by up-regulating the adiponectin and GLUT-4 gene expressions. The mice in GE treated groups did not develop insulin resistance. GE also down-regulated the expression of inflammatory markers (IL-6, TNF-α, SAA2, CRP and MCP-1) via attenuation of nuclear transcription factors (NF-κB).
  
  
  CONCLUSIONS
  Glucan-rich polysaccharide of P. sajor-caju can serve as a potential agent for prevention of glucose intolerance, insulin resistance and inflammation.
authors.affiliation: 1Institute of Biological Sciences, University of Malaya, 50603 Kuala Lumpur, Malaysia.
authors.forename: Gowri
authors.initials: G
authors.lastname: Kanagasabapathy
authors.forename: Umah Rani
authors.initials: UR
authors.lastname: Kuppusamy
authors.forename: Sri Nurestri
authors.initials: SN
authors.lastname: Abd Malek
authors.forename: Mahmood Ameen
authors.initials: MA
authors.lastname: Abdulla
authors.forename: Kek-Heng
authors.initials: KH
authors.lastname: Chua
authors.forename: Vikineswary
authors.initials: V
authors.lastname: Sabaratnam
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D018932:Chemokine CCL2 / Q000235:genetics / Q000276:immunology; D004041:Dietary Fats / Q000378:metabolism; D005260:Female; D048690:Fruiting Bodies, Fungal / Q000737:chemistry; D055951:Functional Food / Q000032:analysis; D015870:Gene Expression / Q000187:drug effects; D005936:Glucans / Q000008:administration & dosage / Q000032:analysis*; D018149:Glucose Intolerance / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism / Q000517:prevention & control*; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D015850:Interleukin-6 / Q000235:genetics / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000235:genetics / Q000276:immunology; D020076:Pleurotus / Q000737:chemistry*; D011134:Polysaccharides / Q000008:administration & dosage* / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology
chemical_list: D001786:Blood Glucose; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D004041:Dietary Fats; D005936:Glucans; D007328:Insulin; D015850:Interleukin-6; D016328:NF-kappa B; D011134:Polysaccharides; D014409:Tumor Necrosis Factor-alpha