title: A polysaccharide from Grifola frondosa relieves insulin resistance of HepG2 cell by Akt-GSK-3 pathway.
abstract: Grifola frondosa is an important fungal research resource. However, there was little report about hyperglycemic activity of Grifola frondosa polysaccharide on insulin resistance in vitro. In this study, the hypoglycemic activity of a polysaccharide obtained from Grifola frondosa (GFP) on HepG2 cell and hpyerglycemic mechanism were investigated. The purity of the isolated polysaccharides was examined by HPLC. In this research, it was found that GFP enhanced the absorption of glucose of HepG2 cells in a dose dependent manner at 24 h of 30 ugmL⁻¹. GC-MS and FT-IR spectroscopy analysis results showed that glucose and galactose were the dominant monosaccharides in GFP and the major component of GFP was β-pyranoside. Western-blotting results showed that the HepG2 cell model treated with GFP activated the insulin receptor protein (IRS) in the cell membrane and increased phosphorylated-AktSer473 expression, which had an inhibition of glycogen synthase kinase (GSK-3). The down-regulation of GSK-3 stimulated synthesis of intracellular glycogen. The results above suggested that the GFP increased the metabolism of glucose and stimulated synthesis of intracellular glycogen through the Akt/GSK-3 pathway.
authors.affiliation: Key Laboratory of Food Nutrition and Safety, Ministry of Education, College of Food Engineering and Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, People's Republic of China.
authors.forename: Xiaolei
authors.initials: X
authors.lastname: Ma
authors.forename: Fuchuan
authors.initials: F
authors.lastname: Zhou
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Chen
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Zhang
authors.forename: Lihua
authors.initials: L
authors.lastname: Hou
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Cao
authors.forename: Chunling
authors.initials: C
authors.lastname: Wang
mesh_terms: D065567:Absorption, Physiological / Q000187:drug effects; D015703:Antigens, CD / Q000378:metabolism; D002240:Carbohydrate Sequence; D002681:China; D055808:Drug Discovery; D062610:Fungal Polysaccharides / Q000737:chemistry / Q000302:isolation & purification / Q000378:metabolism / Q000494:pharmacology*; D005947:Glucose / Q000378:metabolism; D038362:Glycogen Synthase Kinase 3 / Q000037:antagonists & inhibitors / Q000378:metabolism; D048691:Grifola / Q000737:chemistry* / Q000378:metabolism; D056945:Hep G2 Cells; D022781:Hepatocytes / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D007004:Hypoglycemic Agents / Q000737:chemistry / Q000302:isolation & purification / Q000378:metabolism / Q000494:pharmacology*; D007333:Insulin Resistance; D007700:Kinetics; D008112:Liver Glycogen / Q000096:biosynthesis; D010766:Phosphorylation / Q000187:drug effects; D011134:Polysaccharides / Q000032:analysis; D011499:Protein Processing, Post-Translational / Q000187:drug effects; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D011972:Receptor, Insulin / Q000819:agonists / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*
chemical_list: D015703:Antigens, CD; D062610:Fungal Polysaccharides; D007004:Hypoglycemic Agents; D008112:Liver Glycogen; D011134:Polysaccharides; C435941:INSR protein, human; D011972:Receptor, Insulin; C494918:AKT1 protein, human; D051057:Proto-Oncogene Proteins c-akt; D038362:Glycogen Synthase Kinase 3; D005947:Glucose