title: Duodenal-Jejunal Bypass Improves Insulin Resistance by Enhanced Glucagon-Like Peptide-1 Secretion Through Increase of Bile Acids.
abstract: OBJECTIVE
  The aim of this study is to investigate the mechanisms of improvement in insulin resistance after duodenal-jejunal bypass (DIB), especially regarding the correlation between bile acids and glucagon-like peptide-1 (GLP-1).
  
  
  METHODS
  SD rats were divided into two groups: DIB or Sham group. Blood glucose, insulin, GLP-1, bile acids, and the number of L cells in the small intestine were investigated three weeks after the operations. Next, to assess the effect of the bile acids on GLP-1 secretion in ileum, bile diversion model (=inhibition of rapid bile exposure to the ileum; BD group) were performed and postoperative glycemic parameters were measured.
  
  
  RESULTS
  DJB improved insulin resistance and increased GLP-1 compared with sham. Higher bile acids in DJB were found than that in sham. The number of L cells in the common limb of DJB was increased compared with that in the distal segment of sham. In BD group, insulin resistance had not improved. GLP-1, bile acids, and the number of L cells revealed no significant changes compared with sham.
  
  
  CONCLUSIONS
  DJB has a potential to improve insulin resistance, which may be related to enhanced GLP-1 secretion through the increase of bile acids in the common limb of the small intestine.
authors.forename: Hideya
authors.initials: H
authors.lastname: Kashihara
authors.forename: Mitsuo
authors.initials: M
authors.lastname: Shimada
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Kurita
authors.forename: Takashi
authors.initials: T
authors.lastname: Iwata
authors.forename: Hirohiko
authors.initials: H
authors.lastname: Sato
authors.forename: Kozo
authors.initials: K
authors.lastname: Yoshikawa
authors.forename: Tomohiko
authors.initials: T
authors.lastname: Miyatani
authors.forename: Chie
authors.initials: C
authors.lastname: Takasu
authors.forename: Noriko
authors.initials: N
authors.lastname: Matsumoto
authors.forename: Hiroki
authors.initials: H
authors.lastname: Ishibashi
mesh_terms: D000714:Anastomosis, Surgical; D000818:Animals; D001647:Bile Acids and Salts / Q000097:blood / Q000378:metabolism*; D001786:Blood Glucose / Q000378:metabolism; D004386:Duodenum / Q000378:metabolism / Q000601:surgery*; D019858:Enteroendocrine Cells / Q000378:metabolism; D052216:Glucagon-Like Peptide 1 / Q000097:blood / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D007583:Jejunum / Q000378:metabolism / Q000601:surgery*; D008297:Male; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D015854:Up-Regulation
chemical_list: D001647:Bile Acids and Salts; D001786:Blood Glucose; D007328:Insulin; D052216:Glucagon-Like Peptide 1