title: Antihyperglycemic effect of equol, a daidzein derivative, in cultured L6 myocytes and ob/ob mice.
abstract: METHODS
  Molecular mechanisms for the potential antihyperglycemic effect of equol remain to be elucidated. In this study, we investigated the in vitro effect of equol on glucose uptake, AMP-activated protein kinase (AMPK) phosphorylation, and glucose transporter 4 (GLUT4) translocation to plasma membrane in L6 myocytes, and its in vivo antihyperglycemic effect in obese-diabetic model ob/ob mice.
  
  
  RESULTS
  Equol was found to promote glucose uptake, AMPK phosphorylation, and GLUT4 translocation detected by Western blotting analyses in L6 myotubes under a condition of insulin absence. Equol (0.05% in diet) suppressed the rise in serum glucose, cholesterol, triglyceride, and lipid peroxide concentrations and the hepatic triglyceride level as compared with those in the control group. Moreover, equol treatment suppressed the rises in fasting blood glucose level and improved the impaired glucose tolerance in ob/ob mice. Furthermore, equol treatment was demonstrated to improve expression of hepatic gluconeogenesis- and lipogenesis-related genes in terms of glucose and lipid metabolism.
  
  
  CONCLUSIONS
  The hypoglycemic effect of equol is related to increased GLUT4 translocation to the plasma membrane via AMPK activation. In addition, equol suppresses the fasting blood glucose level and gene expression of hepatic enzymes related to glucose metabolism. These results strongly suggest that equol has antidiabetic potential.
authors.affiliation: Department of Applied Biological Chemistry, Tokyo University of Agriculture and Technology, Fuchu, Tokyo, Japan; Department of Biotechnology, Konkuk University, Chungju, Republic of Korea.
authors.forename: Sun Hee
authors.initials: SH
authors.lastname: Cheong
authors.forename: Keisuke
authors.initials: K
authors.lastname: Furuhashi
authors.forename: Katsuki
authors.initials: K
authors.lastname: Ito
authors.forename: Masato
authors.initials: M
authors.lastname: Nagaoka
authors.forename: Takayuki
authors.initials: T
authors.lastname: Yonezawa
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Miura
authors.forename: Kazumi
authors.initials: K
authors.lastname: Yagasaki
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism; D052242:Adiponectin / Q000097:blood; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002460:Cell Line; D018932:Chemokine CCL2 / Q000097:blood; D002784:Cholesterol / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy; D060754:Equol / Q000494:pharmacology*; D018149:Glucose Intolerance / Q000188:drug therapy; D051275:Glucose Transporter Type 4 / Q000235:genetics / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007328:Insulin / Q000097:blood; D050356:Lipid Metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008820:Mice, Obese; D032342:Muscle Cells / Q000187:drug effects* / Q000378:metabolism; D018485:Muscle Fibers, Skeletal / Q000187:drug effects / Q000378:metabolism; D010766:Phosphorylation; D051381:Rats; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D051275:Glucose Transporter Type 4; D007004:Hypoglycemic Agents; D007328:Insulin; C495693:Slc2a4 protein, mouse; D017392:Thiobarbituric Acid Reactive Substances; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D060754:Equol; D002784:Cholesterol; D055372:AMP-Activated Protein Kinases
keywords: AMPK; Equol; Glucose transporter 4; Glucose uptake; L6 myocytes