title: Curcumin improves glucose tolerance via stimulation of glucagon-like peptide-1 secretion.
abstract: Glucagon-like peptide-1 (GLP-1) is a type of incretin secreted from enteroendocrine L-cells. Our previous studies demonstrated that curcumin (a yellow pigment of turmeric) significantly increases the secretion of GLP-1 in enteroendocrine L cell line (GLUTag cells). However, it is not clear whether its action in vivo directly enhances GLP-1 secretion, which then leads to a reduction in blood glucose levels via the stimulation of insulin secretion. In addition, the molecular target of curcumin-induced GLP-1 secretion has not been clarified.
  
  
  
  Glucose tolerance was significantly improved in rats after pre-administered curcumin (1.5 mg/kg) followed by intraperitoneal glucose injections via the stimulation of GLP-1 secretion and the induction of insulin secretion. In GLUTag cells, curcumin-induced GLP-1 secretion was associated with G protein-coupled receptor (GPR) 40/120. Furthermore, the glucose-lowering effect induced by curcumin was significantly reduced after the administration of a GPR40/120 antagonist in rats.
  
  
  
  These findings demonstrate the biological function of curcumin as a GLP-1 secretagogue and the possible molecular target that mediates GLP-1 secretion. Increases in the secretion of endogenous GLP-1 induced by curcumin may allow the dosages of other diabetic medicines to be reduced and aid in the prevention of diabetes.
authors.affiliation: College of Bioscience and Biotechnology, Chubu University, Kasugai, Aichi, Japan.
authors.forename: Masaki
authors.initials: M
authors.lastname: Kato
authors.affiliation: College of Bioscience and Biotechnology, Chubu University, Kasugai, Aichi, Japan.
authors.forename: Sho
authors.initials: S
authors.lastname: Nishikawa
authors.affiliation: College of Bioscience and Biotechnology, Chubu University, Kasugai, Aichi, Japan.
authors.forename: Akiho
authors.initials: A
authors.lastname: Ikehata
authors.affiliation: College of Bioscience and Biotechnology, Chubu University, Kasugai, Aichi, Japan.
authors.forename: Kojiro
authors.initials: K
authors.lastname: Dochi
authors.affiliation: College of Bioscience and Biotechnology, Chubu University, Kasugai, Aichi, Japan.
authors.forename: Tsubasa
authors.initials: T
authors.lastname: Tani
authors.affiliation: Theravalues Corporation, Tokyo, Japan.
authors.forename: Tsukasa
authors.initials: T
authors.lastname: Takahashi
authors.affiliation: Theravalues Corporation, Tokyo, Japan.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Imaizumi
authors.affiliation: College of Bioscience and Biotechnology, Chubu University, Kasugai, Aichi, Japan.
authors.forename: Takanori
authors.initials: T
authors.lastname: Tsuda
mesh_terms: D000284:Administration, Oral; D000818:Animals; D001565:Benzoates / Q000494:pharmacology; D001786:Blood Glucose / Q000378:metabolism; D002460:Cell Line; D003474:Curcumin / Q000008:administration & dosage / Q000494:pharmacology*; D052216:Glucagon-Like Peptide 1 / Q000097:blood / Q000378:metabolism*; D005947:Glucose / Q000008:administration & dosage; D005951:Glucose Tolerance Test; D007003:Hypoglycemia / Q000188:drug therapy / Q000378:metabolism; D007274:Injections, Intraperitoneal; D007328:Insulin / Q000097:blood; D008297:Male; D051379:Mice; D011743:Pyrimidines / Q000494:pharmacology; D017207:Rats, Sprague-Dawley; D043562:Receptors, G-Protein-Coupled / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D001565:Benzoates; D001786:Blood Glucose; C498007:FFAR4 protein, mouse; C473036:Ffar1 protein, mouse; C515631:GW1100; D007328:Insulin; D011743:Pyrimidines; D043562:Receptors, G-Protein-Coupled; D052216:Glucagon-Like Peptide 1; D003474:Curcumin; D005947:Glucose
keywords: Curcumin; Diabetes; G protein-coupled receptor 40/120; Glucagon-like peptide-1; Glucose tolerance