title: Hypoglycemic effect and mechanism of a proteoglycan from ganoderma lucidum on streptozotocin-induced type 2 diabetic rats.
abstract: OBJECTIVE
  Diabetes mellitus inducing a leading cause of morbidity are widespread in the entire globe. The present study was to investigate the antidiabetic potency and mechanism of a proteoglycan extract, named FYGL (Fudan-Yueyang-G. lucidum), from the fruiting bodies of Ganoderma Lucidum as published recently, using streptozotocin-induced type 2 diabetic mellitus (T2DM) rats.
  
  
  METHODS
  The T2DM model rats were treated with FYGL as well as metformin and rosiglitazone. The levels of plasma glucose and insulin were measured, and the expression and activity of the protein tyrosine phosphatase 1B (PTP1B) and the tyrosine phosphorylation level of the insulin receptor (IR) 3-subunit in the livers and skeletal muscles of the T2DM rats were analyzed by immunoprecipitation and Western blotting methods. In addition, the levels of free fatty acid and serum lipid profile were measured using commercial kits for those trailed rats.
  
  
  RESULTS
  The decrease in fasting plasma glucose and the increase in insulin concentration dose- and time-dependently in the T2DM rats treated by FYGL, comparable with that by the clinical drugs, metformin and rosiglitazone. The levels of the PTP1B expression and activity were decreased, and the tyrosine phosphorylation level of the IR 1-subunit was increased in the skeletal muscles of the T2DM rats. Furthermore, FYGL significantly decreased the levels of free fatty acid, triglyceride, total cholesterol and low density lipoprotein-cholesterol as well as increased the level of high density lipoprotein-cholesterol.
  
  
  CONCLUSIONS
  It is suggested that the hypoglycemic mechanisms of FYGL are caused by inhibition of the PTP1B expression and activity, consequently, regulation of the tyrosine phosphorylation level of the IR 13-subunit. As those results, FYGL also controlled the plasma biochemistry indexes relative to the type 2 diabetes-accompanied metabolic disorders. This is possibly the first report on the underlying mechanisms responsible for the antidiabetic effect of Ganoderma lucidum.
authors.affiliation: The Key Laboratory of Molecular Engineering of Polymers, Department of Macromolecular Science, Fudan University, Shanghai, PR China.
authors.forename: B S
authors.initials: BS
authors.lastname: Teng
authors.forename: C D
authors.initials: CD
authors.lastname: Wang
authors.forename: D
authors.initials: D
authors.lastname: Zhang
authors.forename: J S
authors.initials: JS
authors.lastname: Wu
authors.forename: D
authors.initials: D
authors.lastname: Pan
authors.forename: L F
authors.initials: LF
authors.lastname: Pan
authors.forename: H J
authors.initials: HJ
authors.lastname: Yang
authors.forename: P
authors.initials: P
authors.lastname: Zhou
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D015153:Blotting, Western; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000188:drug therapy*; D003924:Diabetes Mellitus, Type 2 / Q000139:chemically induced / Q000188:drug therapy*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D048690:Fruiting Bodies, Fungal / Q000737:chemistry; D007004:Hypoglycemic Agents; D007328:Insulin / Q000097:blood; D008055:Lipids / Q000097:blood; D008099:Liver / Q000378:metabolism; D008297:Male; D008687:Metformin / Q000494:pharmacology; D018482:Muscle, Skeletal / Q000378:metabolism; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1 / Q000096:biosynthesis; D011509:Proteoglycans / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020940:Reishi / Q000737:chemistry*; D000077154:Rosiglitazone; D045162:Thiazolidinediones / Q000494:pharmacology
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007004:Hypoglycemic Agents; D007328:Insulin; D008055:Lipids; D011509:Proteoglycans; D045162:Thiazolidinediones; D000077154:Rosiglitazone; D008687:Metformin; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1