title: Salvianolic Acid B Ameliorates Hyperglycemia and Dyslipidemia in db/db Mice through the AMPK Pathway.
abstract: OBJECTIVE
  Salvianolic acid B (Sal B), a major polyphenolic compound of Salvia miltiorrhiza Bunge, has been shown to possess potential antidiabetic activities. However, the action mechanism of SalB in type 2 diabetes has not been investigated extensively. The present study was designed to investigate the effects of Sal B on diabetes-related metabolic changes in a spontaneous model of type 2 diabetes, as well as its potential molecular mechanism.
  
  
  METHODS
  Male C57BL/KsJ-db/db mice were orally treated with Sal B (50 and 100 mg/kg) or metformin (positive drug, 300 mg/kg) for 6 weeks.
  
  
  RESULTS
  Both doses of Sal B significantly decreased fasting blood glucose, serum insulin, triglyceride and free fatty acid levels, reduced hepatic gluconeogenic gene expression and improved insulin intolerance in db/db mice. High dose Sal B also significantly improved glucose intolerance, increased hepatic glycolytic gene expression and muscle glycogen content, and ameliorated histopathological alterations of pancreas, similar to metformin. Sal B treatment resulted in increased phosphorylated AMP-activated protein kinase (p-AMPK) protein expression in skeletal muscle and liver, increased glucose transporter 4 (GLUT4) and glycogen synthase protein expressions in skeletal muscle, and increased peroxisome proliferator-activated receptor alpha (PPARα) and phosphorylated acetyl CoA carboxylase (p-ACC) protein expressions in liver.
  
  
  CONCLUSIONS
  Our data suggest that Sal B displays beneficial effects in the prevention and treatment of type 2 diabetes at least in part via modulation of the AMPK pathway.
authors.affiliation: College of Pharmacy, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China.
authors.forename: Ming-Qing
authors.initials: MQ
authors.lastname: Huang
authors.forename: Cai-Jie
authors.initials: CJ
authors.lastname: Zhou
authors.forename: Yi-Ping
authors.initials: YP
authors.lastname: Zhang
authors.forename: Xiao-Qin
authors.initials: XQ
authors.lastname: Zhang
authors.forename: Wen
authors.initials: W
authors.lastname: Xu
authors.forename: Jing
authors.initials: J
authors.lastname: Lin
authors.forename: Pei-Jian
authors.initials: PJ
authors.lastname: Wang
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism*; D000818:Animals; D001572:Benzofurans / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*; D001835:Body Weight / Q000187:drug effects; D050171:Dyslipidemias / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000235:genetics; D005786:Gene Expression Regulation / Q000187:drug effects; D005943:Gluconeogenesis / Q000187:drug effects; D005947:Glucose / Q000378:metabolism; D018149:Glucose Intolerance / Q000097:blood / Q000150:complications / Q000188:drug therapy / Q000235:genetics; D051275:Glucose Transporter Type 4 / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism; D006006:Glycogen Synthase / Q000378:metabolism; D006019:Glycolysis / Q000187:drug effects; D006943:Hyperglycemia / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000235:genetics; D006946:Hyperinsulinism / Q000097:blood / Q000150:complications / Q000188:drug therapy; D008055:Lipids / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008810:Mice, Inbred C57BL; D018482:Muscle, Skeletal / Q000187:drug effects / Q000201:enzymology; D047493:PPAR alpha / Q000378:metabolism; D010179:Pancreas / Q000187:drug effects / Q000473:pathology; D010766:Phosphorylation / Q000187:drug effects; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D053630:Depsides
chemical_list: D055372:AMP-Activated Protein Kinases; D001572:Benzofurans; D005947:Glucose; D051275:Glucose Transporter Type 4; D006003:Glycogen; D006006:Glycogen Synthase; D008055:Lipids; D047493:PPAR alpha; D012333:RNA, Messenger; C076944:salvianolic acid B; D053630:Depsides